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دراسات حديثة : الفيتامينات و الوقاية من سرطان الثدي

2010-05-06T14:06:00.000+04:00

دراسات حديثة : الفيتامينات و الوقاية من سرطان الثدي

يعتبر سرطان الثدي الخطر الذي يقض مضجع معظم النساء، يؤرق الكثيرات و يدفع الكثيرات الى أجراء فحوص دورية للكشف عنه في مراحله الأولى قبل أن يتطور و يستفحل و يصعب علاجه.
من منا لم يسمع عن قريبة أو جارة أو صديقة لم يصبها هذا المرض ؟ أعتقد أن التجربة تجعلنا ندرك خطر هذا المرض و تجعلنا أيضا نوقن بأن الوقاية منه هي بحد ذاتها وسيلة للشفاء منه.
الاحصائيات في عالمنا العربي تغيب كغياب الأشياء الكثيرة المهمة في هذا العالم المترامي الأطراف القليل الخيارات و الأهداف.
جمعية السرطان الأمريكية نشرت أحصاءات قد تكون مفزعة لهذا المرض ..لكن التوصيف الأبلغ لهذا المرض جاء في دراسة وصفته بأنه”أكثر الأمراض السرطانية المشخصة تهديدا لحياة النساء”.
من هنا نستطيع أن نعرف مدى خطر هذا المرض و مدى التهديد الذي يشكله و يجعله حديث النساء في مجالسهم و صالوناتهم.
لنعود الى الاحصائيات.. فجمعية السرطان الأمريكية قدرت عدد الحالت الجديدة لهذا المرض بحوالي 1.5 مليون حالة سنويا في أنحاء العالم و قدرته في الولات المتحدة لوحدها بحوالي 101 حالة /100.000 امرأة سنويا..
هذه الأرقام فقط لتوضيح مدى انتشاره و جديته… لن ندخل في هذه المقالة في عملية البحث عن علاجات لهذا المرض…فالعلاجات هي عملية معقدة و قد لا يكون التطرق اليها مفيدا في مثل هذه المواضع..
ما سنتطرق اليه هنا هي عملية الوقاية منه …فالوقاية دائما هي خط للدفاع …تقلل المخاطر و قد تدفع البلاء..
في دراسة جديدة قدمت في اللقاء السنوي لجمعية سرطان الثدي الأمريكية وصفت الفيتامينات” كأرخص أنواع التأمين ” على الثدي..
هذه الدراسة قالت بأن الفيتامينات نفسها تقوم بعملية اصلاح لحامض ال دي ان أي يفي الخلايا و و بالتالي تمنع تطورها لخلايا سرطانية.
دائما ما تحمل الفيتامينات خواص مضادة للأكسدة…هذه قد تكون عامل رئيسي في عملية منع تكون الخلايا السرطانية. فيتانين دي أيضا وجد في دراسة أخرى نشرت في المجلة الأمريكية للتغذية السريرية أن تناول جرعات يومية من هذا الفيتامين يقلل من الاصابة بالسرطان..الجرعات حددت بما يساوي 10 ميكرو غرام يوميا..
عملية أخذ الخلاصات من هذه الدراسات الحديثة توصل الى ذات النتيجة و هي أن الفيتامينات خط دفاع أول ضد هذا المرض ..و النصيحة للنساء” تناولي فيتامينك فانه بوليصة تأمينك”

Long-Term Use of Antidepressants For Depressive Disorders and the Risk of Diabetes Mellitus

2009-07-09T10:20:00.000+04:00

Andersohn F, Schade R, Suissa S, Garbe EAm J Psychiatry 2009 May 166(5):591-8
Commentary from Leo Sher and Maria Oquendo
Changes Clinical Practice: Patients receiving a moderate to high daily dose of antidepressants for greater than 12 months should be evaluated for impaired glucose tolerance/diabetes.
The authors of this study have shown that the long-term use of antidepressants in at least moderate daily doses was associated with an increased risk of diabetes. This finding indicates that blood glucose levels should be checked periodically in patients on long-term antidepressant therapy.
Depression is a severe condition that frequently requires a long-term treatment. The authors examined the relationships between the use of antidepressants and a risk of diabetes mellitus in patients of at least 30 years of age and whether the risk is influenced by treatment duration or daily dose. The authors used data from the UK General Practice Research Database (GPRD), which contains medical records for several million patients from about 450 general practices in the UK. Criteria for inclusion in the study included but were not limited to the following: (1) patients had to be at least 30 years of age at the time of cohort entry (only patients ≥30 years of age were included in the cohort to ensure that incident cases of diabetes were most likely to be type 2 diabetes); (2) have had no diagnosis of diabetes or impaired glucose tolerance and no treatment with oral antidiabetics or insulin before cohort entry; and (3) have had a diagnosis of depression within 180 days before or 90 days after cohort entry. Antidepressants were classified into tricyclic and tetracyclic antidepressants, selective serotonin reuptake inhibitors (SSRIs), monoamine oxidase (MAO) inhibitors, and the heterogeneous group of mixed-action "other antidepressants." Recent long-term use of antidepressants in moderate or high daily doses was associated with an increased risk of diabetes whereas recent use of shorter duration, use in lower daily doses, former use, and past use were not. This association was observed for both tricyclic antidepressants and SSRIs. In the analysis of individual antidepressants, increased risk estimates were observed for long-term use of amitriptyline, fluvoxamine, paroxetine, and venlafaxine. The results of this study are consistent with a recent report published by the Diabetes Prevention Program Research Group: the randomized Diabetes Prevention Program trial found an increased risk of diabetes in high-risk patients who used antidepressants.[1] A significant strength of this study is that all information was registered prospectively so that recall bias could be ruled out. An important limitation of this study is that weight gain during follow-up was not systematically recorded, and it was not included in the analysis. It is important to note that depression itself increases risk for diabetes. This may contribute to the results observed by the authors of the study. This study indicates that patients receiving antidepressants long-term should be evaluated for impaired glucose tolerance/diabetes. This study contributes to our knowledge of the use and possible adverse effects of antidepressants in the treatment of depression.

Alogliptin Delayed; Cancer Concerns With Insulin Glargine

2009-07-09T10:10:00.001+04:00

June 30, 2009 (Tokyo, Japan) — As expected, the US Food and Drug Administration has turned away the investigational diabetes drug alogliptin (Takeda Pharmaceutical) because of insufficient cardiovascular safety data [1]. The FDA decision will delay the drug's possible launch by at least two years, according to company officials.
Takeda received a "complete-response" letter on Friday, and the letter, according to a company press release, stated that existing clinical data were insufficient to meet the new cardiovascular safety requirements requested by the FDA.
The decision regarding alogliptin, a dipeptidyl peptidase-4 (DPP-4) inhibitor, was expected, given that the FDA issued a guidance document in December 2008 advising sponsors to conduct long-term clinical trials or provide equivalent evidence ruling out an unacceptable cardiovascular safety risk for new diabetes drugs seeking approval. Although the new drug application for alogliptin was filed in 2007, the new cardiovascular safety hurdle applied to all diabetes drugs, even those in development.
The recommendation emerged after concerns were raised about the cardiovascular safety of drugs in this field, especially the thiazolidinediones, including rosiglitazone (Avandia, GlaxoSmithKline). Takeda was informed in March that the available safety data were insufficient for approval and is currently in discussions with the FDA about the protocol for a new study.
Is There a Cancer Risk With Lantus?
The European Association for the Study of Diabetes (EASD) is urgently requesting further study into a possible link between insulin glargine (Lantus, Sanofi-Aventis) and cancer [2].
Concerns are raised based on a large German study of 127 000 patients that showed a dose-dependent increase in the risk of cancer among those treated with insulin glargine. The findings were replicated in a Swedish population-based study, while a Scottish study showed a nonsignificant increase in the risk of breast cancer. Data from a UK database showed no association between insulin glargine and cancer.
The EASD has communicated its concerns to European regulators but urges caution in interpreting the results. Further study is still needed, and in the meantime patients should continue taking the diabetes medication for glucose control or speak with their doctor if they are worried about the risk. The American Diabetes Association said the findings "are conflicting and inconclusive" and "cautions against overreaction until more information is available. [3]"

Vitamin D Deficiency Linked to Greater Risk for Primary Cesarean Delivery

2008-12-26T02:09:00.001+04:00

December 23, 2008 — Vitamin D deficiency in pregnancy is associated with increased odds of primary cesarean delivery, according to the results of a study reported in the December 23 Online First issue of the Journal of Clinical Endocrinology & Metabolism.

"At the turn of the 20th century, women commonly died in childbirth due to 'rachitic pelvis,' " write Anne Merewood, MPH, IBCLC, from Boston University School of Medicine in Massachusetts, and colleagues. "Although rickets virtually disappeared with the discovery of the hormone 'vitamin' D, recent reports suggest vitamin D deficiency is widespread in industrialized nations. Poor muscular performance is an established symptom of vitamin D deficiency, [and] the current US caesarean birth rate is at an all-time high of 30.2%."

The objective of this study was to determine the relationship between maternal serum 25-hydroxyvitamin D [25(OH)D] levels and the rate of primary cesarean delivery.

At an urban teaching hospital in Boston, with 2500 births per year, the investigators measured maternal and infant serum 25(OH)D at birth in 253 mother-infant pairs, of whom 43 (17%) had a primary cesarean delivery. Demographic and medical data were abstracted from the maternal medical record.

The rate of cesarean delivery was 14% in women with 25(OH)D levels of 37.5 nmol/L or higher and 28% in women with serum 25(OH)D levels less than 37.5 nmol/L (P = .012). The risk for cesarean delivery was nearly 4-fold higher in women with 25(OH)D levels less than 37.5 nmol/L vs those with 25(OH)D levels of 37.5 nmol/L or more, based on multivariable logistic regression analysis controlling for race, age, educational level, insurance status, and alcohol use (adjusted odds ratio [OR], 3.84; 95% confidence interval [CI], 1.71 - 8.62).

Limitations of this study include sample too small to determine whether vitamin D deficiency is related to specific types of cesarean deliveries, such as cephalopelvic disproportion or failure to progress.

"Vitamin D deficiency was associated with increased odds of primary caesarean section," the study authors write. "A randomized clinical trial is now needed to determine if adequate vitamin D supplementation during pregnancy to raise blood levels above 37.5 nmol/L can reduce the caesarean section rate."

More Research Urgently Needed on Off-Label Use of 14 Drugs

2008-12-07T01:19:00.001+04:00

November 25, 2008 — Fourteen drugs have been identified that most urgently require research regarding off-label uses, according to the results of a retrospective, cross-sectional study and quantitative analysis reported November 24 online ahead of print in the December issue of Pharmacotherapy. The lead author is Surrey Walton, PhD, an assistant professor of pharmacy administration at the University of Illinois at Chicago.

"The issue is that most off-label uses have less evidence and have been less rigorously scrutinized than indications that have gone through the [US Food and Drug Administration] FDA approval process," senior author Randall S. Stafford, MD, PhD, an associate professor of medicine at the Stanford Prevention Research Center in California, told Medscape Medical News. "It is not that there are necessarily harms associated with off-label use, but more that physicians are practicing without the usual reassurance that their use of these drugs is safe and efficacious. There are, of course, some examples of harms that have been identified, as with the use of the atypical antipsychotic medications in dementia."

Earlier research by Dr. Stafford's group suggested that 21% of drug use is for off-label indications, and that of these uses, 76% lack strong evidence. His current research suggests that the most common conditions prompting off-label use with limited evidence are psychiatric conditions, including depression and bipolar disorder.

"[The study authors] have applied their craft of pharmacoeconomic analysis and statistical modeling to a pertinent practice issue: how to rank order priorities for studying off-label prescribing," C. Lindsay DeVane, PharmD, professor and vice chair for research at the Department of Psychiatry & Behavioral Sciences, Medical University of South Carolina in Charleston, told Medscape Medical News when asked for independent comment.

"[They] have performed a service to the field by providing a quantitative approach to rank ordering off-label prescribing practices for further evaluation," Dr. DeVane said. "Their proposal of how to select marketed drugs for further evaluation is a welcome and informed scientific approach to translate clinical practice into evidence-based medicine."

The goal of this study was to develop a prioritized list of individual drugs for which future research regarding off-label uses is most warranted, using a commercial database providing ongoing estimates of drug prescribing practices of US office-based physicians and an Internet database of comprehensive evidence-based drug information.

"Presumably, the extent of off-label prescribing will vary according to where a specific drug resides in its life cycle," Dr. DeVane pointed out. "Early on, after initial marketing, off-label prescribing may be high as clinicians explore peripheral indications. Such an example would be prescribing for the anxiety disorders following the marketing of the selective serotonin reuptake inhibitors as treatments for depression."

Volume of off-label use with inadequate evidence, drug safety, and cost and market considerations were evaluated, and the number of off-label drug uses by indication from January 1, 2005, to June 30, 2007, in the United States were estimated from nationally representative prescribing data. These indications were then categorized based on the adequacy of scientific support, and a priority score was calculated from a model incorporating black-box warnings and safety alerts, drug cost, date of market entry, and marketing expenditures, as well as adequacy of scientific support. Varying key model parameters allowed performance of sensitivity analyses.

"Not surprisingly, high volume of use, safety issues, and cost and market considerations were the major factors that identified an off-label prescribing practice as a research priority," Dr. DeVane said. "The authors stayed within their scientific bounds and did not address the appropriateness of off-label prescribing, a practice that is sometimes common and extensive."

For a substantial number of drugs, there was a high volume of off-label prescribing despite the absence of good evidence, especially for antidepressants, antipsychotics, and anxiolytic-sedatives.

"The large magnitude of off-label use suggests that use is not limited to last-resort use in patients who have failed all approved medications," Dr. Stafford said. Although pharmaceutical companies are largely prohibited from marketing off-label uses, they may use exceptions, such as the ability to share published research that supports off-label uses with physicians, he said.

Quetiapine (Seroquel), which was FDA-approved in 1997 for treating schizophrenia, was found to have the highest rate of off-label uses with limited evidence (76% of all uses). Furthermore, this antipsychotic is expensive ($207 per prescription) and heavily marketed and carries a "black-box" warning from the FDA.

Both the base model and sensitivity analyses suggested a high priority for future research regarding 14 drugs. These drugs, and their most common off-label use, are quetiapine (bipolar maintenance), warfarin (hypertensive heart disease), escitalopram (bipolar disorder), risperidone (bipolar maintenance), montelukast (chronic obstructive pulmonary disease), bupropion (bipolar disorder), sertraline (bipolar disorder), venlafaxine (bipolar disorder), celecoxib (fibromatosis), lisinopril (coronary artery disease), duloxetine (anxiety disorder), trazodone (sleep disturbance), olanzapine (depression), and epoetin alfa (anemia of chronic disease).

Limitations of this study include the evaluation only of off-label use involving drugs used for indications not approved by the FDA, and not of other forms of off-label use; a systematic review of the clinical literature on specific drugs was not conducted; coding off-label uses was only applied to the available data on individual drugs and not to whether another drug in the same class was approved; the sample of physicians was not strictly random; and difficulty matching the International Classification of Diseases, Ninth Revision (ICD-9), codes from the National Disease and Therapeutic Index with the indications listed by the FDA and Drugdex.

Dr. Stafford recommends several forms of additional research, beginning with a rigorous systematic review of published and unpublished evidence.

"If evidence remains insufficient after this, then additional studies should be conducted," Dr. Stafford said. "These could take 2 forms: the use of observational data to assess safety and efficacy of off-label use or undertaking additional clinical trials on the off-label uses."

Soon after a new drug is introduced into clinical practice, anecdotal experiences of physicians attempting off-label use may suggest directions that should be explored in organized clinical trials, according to Dr. DeVane: If these trials indicate efficacy and safety, additional FDA-approved indications should result in a dramatic decline in off-label use.

"The ultimate value of this report will depend upon its adoption by the pharmaceutical industry, funding agencies, and consumer groups to guide investment of limited resources into postmarketing, phase 4 studies of already approved drugs," Dr. DeVane concluded. "Knowledge of a drug's pharmacology continues to accumulate throughout its availability for study. How we move from an initial approval to realization of the full extent of the medicinal value of drugs is a process that is both criticized and supported."

Obesity surgery helps diabetics, study finds

2008-01-23T02:41:00.001+04:00

CHICAGO, Jan 22 (Reuters) - Weight loss surgery can be especially helpful to patients with diabetes and can even help them reverse the disease, Australian researchers reported on Tuesday.

They found that obese patients with diabetes who had weight loss surgery were five times more likely to get their disease under control than those who dieted -- probably because they lost more weight.

The study, published in the Journal of the American Medical Association, is among the first to look at surgery as a potential treatment for obese patients with type 2 diabetes.

Type 2 diabetes, which is closely linked to obesity, is on the rise worldwide. At least 170 million people are estimated to have the disease and the number is predicted to at least double by 2030.

Bariatric surgery, which involves altering the digestive system to limit food intake, has been growing at a rapid pace, with the number of procedures rising to 200,000 in the United States in 2006, from just 13,000 in 1998.

John Dixon of Monash University in Melbourne and colleagues wanted to see if surgically induced weight loss could be an effective treatment for type 2 diabetes.

Dixon's team studied 60 obese people with a body mass index greater than 30 but less than 40. Body mass index or BMI is a ratio of height and weight. A BMI of 30 or greater is considered obese.

Patients got either surgery or a weight loss program that focused on diet and lifestyle changes.

Those in the surgery group were treated with an adjustable gastric banding device that limits food intake. Both groups also received conventional diabetes medications.

At the end of two years, 73 percent of the diabetics who had surgery no longer had diabetes, compared with 13 percent of those in the diet group. People who got surgery also needed far fewer diabetes medications.

The surgical group on average lost 20.7 percent of their body weight, compared with 1.7 percent in the diet and lifestyle group. There were no serious complications in either group.

It was the large weight loss, not the surgery per se, that helped the patients, the researchers said.

"This has important implications as it suggests that intensive weight-loss therapy may be a more effective first step in the management of diabetes than simple lifestyle change," they wrote.

In a commentary in the same journal, Drs. David Cummings and David Flum of the University of Washington in Seattle said policy and health leaders will need to balance the costs and risks of surgery against the chance of reversing diabetes.

But, they said, "the insights already beginning to be gained by studying surgical interventions for diabetes may be the most profound since the discovery of insulin."

(Editing by Maggie Fox and Cynthia Osterman)

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Zinc an Over view

2007-12-30T11:53:00.001+04:00

Zinc is an essential mineral that is important for immune function, wound healing, normal taste and smell, and is needed for DNA synthesis. Zinc also supports normal growth and development during pregnancy, childhood, and adolescence.

Zinc is a co-factor in DNA and protein synthesis and cell division. It is believed to be important in wound healing.

The UK recommended ranges are 5.5-9.5 mg/day for males and 4.0-7.0 mg/day for females.

The body contains 2 to 3 g of zinc (Zn), found mainly in bones, teeth, hair, skin, liver, muscle, leukocytes, and testes.

One third of the of zinc found in plasma is attached loosely to albumin, and about two thirds is firmly bound to globulins.

Absorption of zinc salts from food is approximately 20-40%. Absorption of zinc is higher from fish and meat but lower from whole-grain bread and cereals, where phytate content impairs absorption. Zinc is mainly lost from body in faeces

Meat, liver, peas, beans, eggs, and seafood (especially oysters) are good sources of zinc.

Mild deficiency of Zinc may cause no obvious symptoms, whereas severe deficiency may cause most or even all of the following features.

Anorexia, lethargy, diarrhoea

Growth retardation, delayed sexual maturation, hypogonadism and hypospermia

Alopecia, dermatitis, paronychia

Mental retardation, impaired nerve conduction and nerve damage

Hepatomegaly

Immune disorders and susceptibility to infections

Iron deficiency anaemia

Macular degeneration, night blindness

Impaired taste and smell

Impaired wound healing

Maternal zinc deficiency may cause anencephaly in the fetus.

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Antihypertensive Treatment May Help Maintain Memory

2007-10-05T01:53:00.000+04:00

Caroline Cassels
Medscape Medical News 2007. © 2007 Medscape

September 27, 2007 — New research indicates antihypertensive treatment leads to increased, joint activation of brain areas responsible for memory performance — a finding that suggests such treatment may help patients maintain cognition and memory.
A study led by J. Richard Jennings, PhD, from the University of Pittsburgh, in Pennsylvania, and presented at the American Heart Association (AHA) 61st Annual Fall Conference of the Council for High Blood Pressure Research, showed patients had a 2-fold increase in the joint activation of these areas of the brain after a year of treatment with either the angiotensin-converting enzyme lisinopril or beta blocker atenolol.
While there is an established link between hypertension and mild cognitive deficits, the mechanism has not been clear. Previous research by Dr. Jennings's team used brain imaging to examine the correlation among the activation of the prefrontal areas, parietal areas, and amygdala/hippocampus in hypertensives compared with controls and found it was higher in individuals with high blood pressure.

Vildagliptin: A Novel Oral Therapy for Type 2 Diabetes Mellitus

2007-07-21T12:58:00.000+04:00

In clinical trials of patients with type 2 diabetes mellitus, vildagliptin has been shown to reduce HbA_1c, fasting plasma glucose levels, prandial glucose levels, and prandial glucagon secretion and to improve ß-cell function. If vildagliptin is approved for marketing, it will add to the available treatment options for diabetes and will provide patients and health care providers with another noninjectable therapy option.

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Mechanism of action of vildagliptin. In response to a meal, active glucagon-like peptide-1 (GLP-1) is secreted by the L cells of the intestines. Without the presence of vildagliptin, GLP-1 is rapidly inactivated and degraded by the enzyme dipeptidyl peptidase IV (DPP4); when vildagliptin is present, vildagliptin binds to DPP4, allowing GLP-1 to remain active. Active GLP-1 causes the pancreas to increase insulin release and decrease glucagon release. Illustration by Marie Dauenheimer, CM

Three-Times-Daily Xylitol Does Not Prevent Acute Otitis Media

2007-05-19T16:21:00.001+04:00

NEW YORK (Reuters Health) May 18 - The sugar xylitol administered 3 times a day is not effective in preventing acute otitis media (AOM) in children attending day care, according to findings published in the May issue of the Pediatric Infectious Disease Journal.
"Xylitol administered regularly in the form of chewing gum or a mixture 5 times a day after each meal for 2 or 3 months was shown to reduce the occurrence of AOM by 30-40% in 2 previously published randomized trials," Dr. Matti Uhari and colleagues from the University of Oulu, Finland, write.
However, they note, "The practicability of giving xylitol 5 times per day for preventing AOM has been questioned, and following our initial findings, we have been evaluating more convenient ways of administering xylitol."
In a 3-month, randomized, double-blind study, the researchers examined whether xylitol administered 3 times daily reduced the occurrence of AOM. A total of 663 healthy day care children were randomized to receive either xylitol (9.6 g/d, n = 332) or placebo (0.5 g/d, n = 331). Xylitol was administered 3 times a day in chewing gum or in a mixture.
The average number of respiratory infection episodes was 2.4 in the control group and 2.2 in the test group. Of the 331 control subjects, 98 (30%) experienced at least one episode of AOM. Ninety-four (28%) of 332 xylitol-treated children had at least one episode of AOM. No significant differences were observed between the groups.
The investigators conclude that 5 daily doses of xylitol "remains the only regimen shown to be effective in preventing AOM."
They say that although the frequent dosing of xylitol might hinder its usefulness, it is noninvasive and doesn't increase microbial resistance. Furthermore, Dr. Uhari and colleagues point out, children "consider it to be fun and convenient, because they like the taste of xylitol chewing gum and mixture."

Theophylline Effective for Functional Esophageal Chest Pain

2007-05-19T16:12:00.000+04:00

NEW YORK (Reuters Health) May 18 - By relaxing the esophageal wall and decreasing hypersensitivity, theophylline may reduce non-cardiac, non-reflux esophageal chest pain, according to a research team at the University of Iowa in Iowa City.
As Dr. Satish S. C. Rao and colleagues note in the American Journal of Gastroenterology for May, adenosine is believed to be involved in visceral chest pain. They theorized that theophylline, an adenosine receptor antagonist, could reduce the pain.
To investigate, they recruited 21 patients with functional chest pain for a study involving esophageal balloon distention with impedance planimetry. The balloon was passed using a catheter into the lower part of the esophagus. Pressure in the balloon was increased in steps of 5 cm H2O up to a maximum of 65 cm H2O.
Sixteen subjects were deemed to have esophageal hypersensitivity, defined as 55 cm H2O pressure or less required to reproduce their typical chest pain. These subjects were randomly assigned to IV theophylline or placebo IV infusion.
"Theophylline significantly improved distension-induced esophageal chest pain," the investigators report. The threshold for chest pain increased significantly in six of eight patients given theophylline. In fact, five in the theophylline group felt no pain even at the maximum permissible distension pressure.
"The esophageal wall relaxed and became more deformable ... after theophylline infusion," Dr. Rao's team reports.
To test oral theophylline, patients with esophageal hypersensitivity participated in a cross-over study comparing twice daily doses of placebo or theophylline 200 mg. Treatment periods lasted for 4 weeks, with a 1-week washout period in between.
During the trial, the 19 patients kept diaries to record number, severity, and duration of chest pain. Compared with placebo, oral theophylline use was associated with fewer painful days (median 5 versus 10), number of chest pain episodes (8 versus 16), severity assessed on a scale of 0 to 3 (2 versus 3), and duration of episodes (6.5 versus 8.5 minutes).
Esophageal chest pain can be a frustrating problem, Dr. Rao and associates comment. "If a cardiac, pulmonary, musculoskeletal or esophageal source such as acid reflux disease can be excluded, our findings suggest that a trial of theophylline may be effective in relieving chest pain, " they advise.
But they caution that theophylline can potentiate gastroesophageal reflux, and patients should be carefully followed up.

New genes connected to diabetes identified

2007-04-29T22:06:00.001+04:00

Several teams, including one led by Harvard researchers, claimed Thursday that they had identified several new genes connected to the most common form of diabetes in a major collaborative effort.

The findings, presented in three reports by university scientists and one by a private company, offer novel insights into the biology of a disease that affects 170 million people worldwide.

The findings in the journals Science and Nature Genetics provided great insight into the role played by genes in a disease also tremendously influenced by behavior -- eating too much and exercising too little.

They identified three new genetic risk factors and confirmed five others that were discovered over the last few years. An additional risk factor identified by one group has not yet been confirmed by others.

They are all based on a new research technique called genome-wide association studies, in which scientists compare genetic samples from thousands of individuals with a specific illness to those without it. Differences between the two are examined as possible genetic causes of the disease.

"This is clearly a start in understanding the disease," said Dr. Larry Deeb, president for medicine and science at the American Diabetes Association. "Type 2 diabetes is multifactorial, there is not one gene associated with it, and yet we know it runs in families, so it has to be genetic."

More than 20 million Americans now have type 2 diabetes and scientists estimate that about 54 million more are at risk of getting the illness. The disease harms the body's ability to control blood sugar and can lead to heart disease, blindness and early death.

The new research is expected to provide leads for development of new treatments and possibly ways to prevent diabetes.

However, the variant genes found so far account for only 2 percent to 20 percent of the overall risk of diabetes, implying there are many more to be found. The present genes are not sufficient to distinguish reliably between people at low or high risk for diabetes.

(Agencies)

Antihypertensive Combination More Effective Than Single Agent

2007-02-08T01:54:00.000+04:00

NEW YORK (Reuters Health) Feb 07 - A low-dose quadruple antihypertensive drug combination appears to be more efficacious than treatment with individual agents, according to preliminary findings presented by Irish investigators.

"Most people with high blood pressure need two to three separate antihypertensive drugs," senior investigator Dr. John Feely told Reuters Health. "Combining low doses of established antihypertensive medicines in a single preparation or capsule can produce better blood pressure control than full doses of individual drugs."

In the January issue of Hypertension, Dr. Feely and Dr. Azra Mahmud of Trinity College, Dublin, investigated this approach by studying 108 untreated, white, hypertensive patients.

They were randomized to monotherapy with one of four agents -- amlodipine 5 mg; atenolol 50 mg; bendroflumethiazide 2.5 mg; captopril 50 mg twice daily -- or to a capsule containing all four drugs at one quarter of the dose used for monotherapy.

At 4 weeks, the reduction in mean arterial pressure with the combination treatment was 19 mm Hg, significantly greater than that seen with amlodipine (10 mm Hg), atenolol (10 mm Hg), bendroflumethiazide (6 mm Hg) or captopril (11 mm Hg).

The combination treatment also resulted in a greater percentage reduction of systolic (18 mm Hg) and diastolic blood pressure (17 mm Hg). Moreover, 60% of combination patients achieved a blood pressure of less than 140/90 compared with 15% to 45% of patients taking individual drugs.

The combination approach, Dr. Feely concluded, "has the potential to reduce costs, with possibly fewer side effects, and the number of medicines to be taken each day."

In an accompanying editorial, Dr. John L. Reid, of the University of Glasgow, agrees, pointing out in remarks to Reuters Health that "the paper provides new insights into potential approaches using very low doses of available drugs."

However, he added, "there is still a lot of work to be done in optimizing the drugs and doses and in confirming long-term benefit over months and years."

Assessing a Race-Based Pharmaceutical

2007-02-08T01:48:00.000+04:00

http://www.medscape.com/viewarticle/550182?src=mp

Introduction

Family physicians have no doubt been approached by their African American patients with congestive heart failure (and perhaps with other heart diseases), asking about the new "for blacks only" medicine, isosorbide dinitrate and hydralazine hydrochloride (BiDiL). Perhaps patients of other ethnic backgrounds have also asked their physicians about this drug. The media has covered the drug approval process extensively before and after a Food and Drug Administration (FDA) advisory committee recommended approval of BiDiL for the specific indication of congestive heart failure in African Americans -- the first drug to be approved for a single racial group. ^[1,2]

Advising our patients requires that we understand the science behind this new pharmaceutical development. It also requires that we be fully aware of the economic, social, cultural, and ethical issues lurking in the background of this purported discovery. In this article, we provide an overview of these issues and try to place the decision as to whether to recommend or prescribe BiDiL in context for family physicians.

Scientific Background

Understanding the science undergirding BiDiL requires a brief historical review, as well as a discussion of the scientific data. African American patients are more likely to die of heart failure compared with whites. Explanations are wide-ranging and include delay in diagnosis and treatment; limited access to coronary care; high prevalence of high-risk individuals with hypertension, diabetes, and dyslipidemia; and such related behavioral risk factors as physical inactivity and smoking. ^[3] One explanation focuses on impaired bioavailability of nitric oxide, which is thought to contribute to the structural remodeling of the left ventricle that increases the rate of death and complications. It has been proposed that African American patients may have a disproportionately lower nitric oxide bioavailability. Isosorbide acts as a nitric oxide donor and hydralazine as an antioxidant, and so together they might ameliorate the long-term effects of heart failure. ^[4]

A combination of isosorbide and hydralazine (160 mg and 300 mg total daily dose, respectively) was compared with enalapril (20 mg) in the second Vasodilator-Heart Failure Trial.^[5] Mortality at 2 years was significantly lower in the enalapril arm. A later retrospective review of those data, however, found that white patients had disproportionate benefit from enalapril, whereas the subset of African American patients appeared to receive substantially more benefit from the isosorbide-hydralazine therapy. ^[6] As of this point, no one had yet tested the hypothesis that isosorbide and hydralazine, added to a regimen that already included an angiotensin-converting enzyme (ACE) inhibitor, might provide benefit to patients with congestive heart failure.

The African American Heart Failure Trial (A-HeFT) was set up by the commercial sponsor, NitroMed, to test this hypothesis. Only African American patients were enrolled in the trial. About 1,000 patients were randomized to a fixed-dose combination of isosorbide and hydralazine (target daily dose, 120 mg and 225 mg, respectively) or placebo added to their existing medications (69% were on ACE inhibitors at baseline). Follow-up was planned for 18 months, but the study was stopped early (mean duration of follow-up, 10 months) because of excess mortality in the placebo group (54 vs 32 patients; 43% relative risk reduction; number needed to treat = 25). The composite outcome score (based on death, hospitalization, and quality of life) was significantly better in the drug group. ^[4]

Based on these impressive findings, an FDA advisory panel recommended on June 16, 2005, that BiDiL be approved specifically for the treatment of heart failure in African American patients. Because A-HeFT enrolled only African American subjects, the question of whether other patients might also benefit from adding isosorbide and hydralazine to their existing drug regimens for congestive failure remains unanswered at this time. ^[7]

Race as a Scientific Construct

As we begin to address the broader issues that frame the scientific discussion of BiDiL's uses and limits, we inevitably encounter the current debate over the use of race in medicine and medical science. This controversy may seem strange to many physicians, but it is currently a hotly debated issue amongst social and genetic scientists. For example, 2 prominent research journals recently devoted special issues to the controversy. ^[8,9] We will touch upon only a few highlights.

It has for some time been taken for granted that racial categories are of use to the physician in assessing the risks of various diseases. The latest genomic science has, however, failed to provide much support for our intuitions about racial categories in medicine. It has been shown generally that there is more genetic diversity within a so-called "racial" cohort than there is difference between 2 such cohorts. Nor does the human genome, in general, show the sorts of radical discontinuities among different racial groups that our commonplace intuitions would call for; instead, we see much more evidence of gradual blending. Craig Venter, who helped produce the first map of the human genome, commented regarding BiDiL, "It is disturbing to see reputable scientists and physicians even categorizing things in terms of race.... There is no basis in the genetic code for race." ^[10] Given the new genomic science, we must at least entertain the hypothesis that our intuitions were shaped, not by true empirical data, but in large part by vestiges of now-discredited biological theories of race, while acknowledging that most physicians today are not consciously racist nor intend racial discrimination.

A recent review of genomic science by a group of social scientists offered the conclusions that we must continue to do research on race in medicine, because whatever its biological basis (or lack of same), race remains a very important social construct, and as such, it has tremendous power to influence health and illness. ^[11] For example, some heart diseases may afflict African Americans more than whites because of the chronic stresses associated with being a member of a minority group rather than because of genetic factors. Simply eliminating race as a variable in medical research would undermine our ability to detect these factors and can therefore hardly be helpful in reducing the serious disparities that remain a problem in American medicine. At the same time we must actively avoid the intellectual trap of assuming that disease incidence disparities among racial or ethnic groups are rooted in genetic differences. We also must not assume that small effects may be attributable to sociocultural variables and that large effects always signal a biologic or genetic basis.

In the face of recent genomic data, some have felt the need to try to preserve our old intuitions and to rescue a concept of race that is, on the one hand, clearly biologically grounded, but on the other hand, avoids invidious discrimination. According to the view called "geographic race," self-ascribed racial groups tend to correspond reasonably well with the continent from which one's ancestors came. Continent of origin (and hence race) might then be a useful proxy indicator of important clusters of genetic traits. Data have been derived from haplotype mapping that appear at first glance to support such a view. ^[12] These findings, however, remain highly controversial and have been soundly challenged in terms of their practical generalizability and biomedical importance.^[13,14]

BiDiL and Past Invidious Discrimination

Many African American patients perceive that their community has historically been subjected to invidious racial discrimination by a white-dominated medical system. Whereas the infamous Tuskegee study has been the lightning rod for much of this sentiment, it is important to recall that many other events, both before and after Tuskegee, all served to create a well-grounded impression that the medical care received by African Americans fell short of what was available to white patients. ^[15] Even today, many life-extending procedures are used much less often among African American patients than among whites despite an absence of medical contraindications.^[16]

In the face of this unfortunate history, it is hard to avoid the conclusion that the emergence of an effective drug that is somehow "for blacks only" is a long overdue bit of poetic justice. Whatever one might think of the scientific pathway that led to BiDiL being approved specifically for African Americans, or of the other issues we will review below, the mere fact that a new drug seems to offer hope to African Americans with a serious chronic disease is a cause for celebration. It is very important that we not allow other legitimate concerns to make us appear insensitive to this unfortunate history of discrimination in health care.

The Economics of BiDiL

The great majority of clinical trials of drugs in the United States are now funded by the pharmaceutical industry.^[17] The average major drug firm spends 2 to 3 times as much on marketing as it does on research and development. ^[18] There is increasing evidence that all too often the industry allows the marketing tail to wag the research dog.^[19] Unfortunately, BiDiL provides several examples of this trend.

The African American cardiologists who participated in the BiDiL study had to walk a fine line -- avoiding too close an alliance with for-profit interests could easily have led to turning down a rare opportunity to do important research on heart disease in African American patients. As a rule, these investigators have been notably balanced and candid in assessing both the pros and cons of the research and its broader implications.

Nevertheless, BiDiL appears to be in large part a creature of marketing. The decision to seek a patent for a race-specific application extended the patent protection BiDiL will enjoy by 13 years.^[11] BiDiL reportedly will be marketed at $1.80 per pill (with means-based discounts offered by the company), roughly 4 to 7 times the cost of generic isosorbide plus hydralazine. ^[2] The African American Heart Failure Trial (A-HeFT) was designed to study a formulation of the 2 medications that did not match available generic doses (37.5 mg of hydralazine, instead of the most common available generic forms, 25 or 50 mg). If physicians, trying to save money for the patient or the insurer, attempt to substitute a generic dose, they are open to criticism if the patient does poorly, because they have failed to match precisely the dosage regimen that has been validated in a major controlled trial.

The present defenders of BiDiL have admitted that race is a poor scientific prop upon which to base the efficacy of a drug. They insist that eventually we will find the true genetic basis of the differential response to this medication; at that later date, some form of pharmacogenetic screening test will presumably identify all the patients, of whatever race, who will benefit from the drug. In the meantime, of course, they contend that we should not withhold an efficacious drug from a subgroup known to benefit, regardless of how crude a surrogate marker race may be.

What would be the financial incentive for the manufacturer to undertake the next round of pharmacogenetic research? Companies seek to expand, not to contract, the markets for their drugs. Under the present marketing structure, the company can sell BiDiL to African American patients; depending on how well the drug performs in practice, the company can also count on a certain amount of off-label prescribing as physicians elect to try it for patients of other races. To what extent would the identification of a specific genetic trait, correlated with positive therapeutic response, be likely to expand that market? As long as there is some probability that the results of that further research could cause the market to shrink, even if by a small amount, there is every incentive for the company to decline to undertake that research.

In sum, BiDiL is on the scene today mostly in answer to the question of how a company could generate a profit and much less in answer to the question of which drug would best help which group of patients and why. Family physicians might be leery of offering too much support to this so-called way of "advancing" medical knowledge.

Reinvigorating Race as a Medical Category

We have already reviewed the reasons as to why race, seen as a biological variable rather than as a social construct, is or should be falling out of favor in medical science. Given the history of how race has been used to justify differential treatment, almost always to the detriment of society's less powerful groups, we have good reason to welcome this development, even though it originates in a scientific understanding of genomics rather than in an urge for social reform.

By contrast, anything that seems likely to cement further the notion of race as a real biological variable in medicine, in addition to a marker of importance in diagnosis and therapeutics, might appear to be a retrogression. Despite the comforting claims that BiDiL is about race only as a matter of temporary convenience, the popularity of this drug is almost certain to prompt the general impression that race works as a medical category. As Kahn has stated, "The role of the federal legal and regulatory system in producing BiDiL as an ethnic drug is especially important because it lends the imprimatur of the state to the use of race as a biological category." ^[10,p33]

Perhaps any negative fallout from rediscovering race as a biological category will be readily contained in a society that is now better attuned to the dangers of racism. Or perhaps these ideas may have serious negative consequences that extend beyond the good that BiDiL might do for sufferers from congestive heart failure. Past history leads one to tread warily along such a path.

Ignoring Nongenetic Contributors to Disease

Family physicians, well schooled in the biopsychosocial model of health, ought especially to be concerned about an approach to research that de-emphasizes the search for social and cultural factors in disease.^[11,20] Advocates of BiDiL have promoted the notion that because African Americans die of heart failure at twice the rate as whites, such a great difference cannot be explained by sociocultural variables alone and must reflect underlying genetic differences.

Kahn has effectively questioned this entire line of reasoning.^[10] First, the 2:1 ratio of deaths among African Americans, a statistic used widely to raise investor capital for NitroMed and to secure political support for BiDiL, is derived from older data and looks only at people who are younger than 75 years. If one considers newer data among all age-groups, the ratio appears to be closer to 1.1:1. It is still true that African Americans tend to die of heart failure at younger ages than whites, and these data should not excuse us from continuing to battle the serious health disparities we know to exist. But the much-cited 2:1 ratio turns out to be highly questionable.

Second, regardless of the true ratio, the role of genetics in explaining the difference remains an untested hypothesis. For example, hypertension, one of the major risk factors for congestive heart failure, is more common within the African American community; and chronic social stress has been implicated as a possible contributor to the development of hypertension. Diet, exercise, and other environmental variables are also possible mediators. ^[3,11]

There is a danger that the apparent success of BiDiL will lead to a further de-emphasis of research into these social and environmental contributors to disease, while all the research funding is devoted to possible genetic bases. We already have seen a major shift in research funding in the United States as a result of the heavy influence of the pharmaceutical industry. A possibly highly effective nondrug treatment for a life-threatening disease is today less likely to receive research support than a slightly effective drug therapy for a minor lifestyle condition where a lucrative market exists. The BiDiL experience is likely to cause this disparity in research funding to grow.

Prescribing Issues

For suitable patients with heart failure and on optimal doses of other drugs, some might urge that we prescribe BiDiL specifically for those who can afford it as a way to reward the company for launching research specifically aimed at reducing health disparities on behalf of African Americans. We anticipate that the company will launch a publicity campaign among the African American community to make this case.

For patients unable to afford an expensive brand-name drug, or for family physicians less impressed with the scientific approach that the BiDiL research represents, it is important to consider possible lower-cost generic options. One could, or instance, prescribe isosorbide 20 mg and hydralazine 25 mg 3 times daily, and titrate as tolerated to a ceiling dose of 40 mg of isosorbide and 75 mg of hydralazine 3 times daily -- the same target dose used in the A-HeFT trial, which was achieved by about two thirds of the subjects. ^[4] Eventually using a 40-mg isosorbide tablet and 25-mg plus a 50-mg dose form of hydralazine could require that the patient take 3 pills 3 times a day, as compared to 2 BiDiL 3 times a day. In either case compliance will be a difficult issue with 3-times-a-day dosing. But patients need to be aware that the benefits seen in A-HeFT should be readily achieved with a cheaper dosage form.

In counseling patients and community groups, clinicians need to place BiDiL in its proper context. The medication appears to offer real benefits for some patients. Until more research is done, we will not know what population groups in addition to African Americans might enjoy those benefits. The family medicine community ought to encourage continued action to reduce health disparities, to promote research that addresses the psychological and social contributors to ill health alongside the biological factors, to propose reforms so that future pharmaceutical studies will be driven more by science and less by marketing, and generally to be skeptical of future claims for race-based therapeutics.

To read commentaries or to post a response to this article, see the online version at
http://annfammed.org/cgi/eletter-submit/4/6/556 .

Budesonide/Formoterol Effective as Asthma Maintenance and Reliever Therapy in Children

2007-01-04T04:14:00.001+04:00

NEW YORK (Reuters Health)

Budesonide/formoterol used for maintenance therapy, and as-needed for symptom relief as well, reduces the asthma exacerbation rate in children compared with conventional regimens, a group of European investigators report.

"A fixed combination of long-acting beta-2-agonists (LABA) plus inhaled corticosteroids (ICS) has never been proven to reduce asthma exacerbations versus ICS alone in children," Dr. Hans Bisgaard, of Copenhagen University Hospital, and colleagues report in the December issue of Chest.

To investigate alternatives, they conducted a 12-month, double-blind, study with 341children between the ages of 4 and 11 years who were uncontrolled on ICS. The researchers randomized the subjects to budesonide/formoterol for maintenance and reliever therapy (Symbicort maintenance and relief therapy; SMART) or to one of two alternative regimens. These included a fixed dose of budesonide/formoterol once daily plus terbutaline as rescue therapy or a fixed dose of budesonide once daily (at a four-fold higher dose) plus terbutaline as rescue therapy.

Exacerbations were observed in 14% of patients in the SMART group, 38% of patients in the fixed-dose combination group, and 26% of those in the fixed-dose budesonide group. The SMART regimen also reduced rates of exacerbation requiring medical intervention compared with two fixed-dose groups.

SMART significantly prolonged the time to first asthma exacerbation versus fixed-dose combination (p < 0.001) and fixed-dose budesonide (p = 0.02).

"Mild exacerbations occurred in 63% in SMART, 84% in fixed-dose combination, and 75% in fixed-dose budesonide regimen," Dr. Bisgaard's team reports. "The number of mild exacerbation days was also significantly reduced with SMART versus both fixed-dose groups."

Nighttime awakenings and the mean number of as-needed inhalations were lower in the SMART group compared with both of the fixed-dose groups. Greater improvement in yearly growth was also observed in the SMART group.

Serious adverse events occurred in two patients in the SMART group compared with 16 and 5 in the fixed-dose combination and fixed-dose budesonide groups, respectively. None of the patients in the SMART group experienced serious adverse events related to asthma worsening/exacerbation, compared with 6% and 2% of patients in the fixed-dose combination and fixed-dose budesonide groups, respectively.

The investigators believe that this is the first time this protocol has been used in children with asthma and conclude that it is "an effective and well-tolerated treatment approach that may greatly simplify pediatric asthma management in the future."

Adherence to Preventive Medications Reduces Risk of Diabetes

2006-09-11T21:48:00.000+04:00

NEW YORK (Reuters Health)

Adherence to a metformin-based preventive strategy in the Diabetes Prevention Program (DPP) was variable, depending on barriers and compliance strategies. However, participants who were adherent had a reduced risk of developing diabetes, according to findings published in the September issue of Diabetes Care.

The DPP investigated the value of intensive lifestyle intervention or metformin in delaying or preventing type 2 diabetes in high-risk individuals with impaired glucose tolerance.

Dr. Elizabeth A. Walker, of George Washington University, Rockville, Maryland, and colleagues examined medication adherence and health outcomes in the metformin and placebo arms of the DPP. They also assessed barriers to adherence and strategies for medication adherence.

A total of 2155 subjects who were randomly assigned to either the metformin or placebo treatment arms were included in the analysis. The overall adherence rates (the proportion of patients taking at least 80% of the prescribed dose) were 71% in the metformin group and 77% in the placebo group.

Among patients taking metformin, older age groups were more adherent than the youngest group (p = 0.01).

"Among both metformin and placebo arms, the most commonly reported barriers to taking DPP medication as prescribed were forgetting to take doses (22%), adverse effects (8%), and disruption of routines (8%)," Dr. Walker's team found. Overall, 15% of women and 10% of men reported adverse effects in the metformin group.

Participants who reported multiple strategies to take medications had increased odds of adherence (odds ratio 2.69, p < 0.0001).

Compared to patients who were adherent to placebo, those adherent to metformin had a 38.2% reduced risk of developing diabetes (p < 0.0003), the investigators report.

They conclude, "Our finding that the level of medication adherence predicted the primary outcome of diabetes lend support for future development and evaluation of brief, practical medication adherence interventions for primary care settings."

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Hypothyrodism

2006-09-06T04:29:00.000+04:00

Source: http://www.patient.co.uk/showdoc/23068762/

Thyroxine is a body chemical (hormone) made by the thyroid gland in the neck. It is carried round the body in the bloodstream. It helps to keep the body's functions (the metabolism) working at the correct pace. Many cells and tissues in the body need thyroxine to keep them going correctly.

Hypothyroidism is also known as an underactive thyroid. It occurs when the thyroid gland does not make enough thyroxine. This causes many of the body's functions to slow down. (In contrast, if you have hyperthyroidism, you make too much thyroxine. This causes many of the body's functions to speed up.)

What are the symptoms of hypothyroidism?

Many symptoms can be caused by a low level of thyroxine. Basically, everything 'slows down'. Not all symptoms develop in all cases.

Symptoms that commonly occur include: tiredness, weight gain, constipation, aches and pains, feeling cold, dry skin, lifeless hair, fluid retention, mental slowing, and depression.

Less common symptoms include: a hoarse voice, irregular or heavy menstrual periods in women, infertility, carpal tunnel syndrome (which causes pains and numbness in the hand), and memory loss or confusion in the elderly.

If you have angina, you may find that your angina pains become more frequent.

However, all these symptoms can be caused by other conditions, and sometimes the diagnosis is not obvious. Symptoms usually develop slowly, and gradually become worse over months or years as the level of thyroxine in the body gradually falls.

Possible complications
If you have untreated hypothyroidism:

You have an increased risk of developing heart disease. This is because a low thyroid level causes the blood lipids (cholesterol etc) to rise.

If you are pregnant, you have an increased risk of developing some pregnancy complications. For example: pre-eclampsia, anaemia, premature labour, low birth weight, stillbirth, and serious bleeding after the birth.

Hypothyroid coma (myxoedema coma) is a very rare complication.

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Imuran

2006-08-16T16:56:00.000+04:00

Wednesday, August 16, 2006

Before two weeks, a friend of mine had asked me about a drug called Imurane. He told me to search about its price and look if there is Syrian substitute of it with different brand name. I didn't hear about this drug before however my experience pushed me to ask my friend about the patient who is using such this drug. He told me that he had kidney transplantation and he used to use this drug. Directly I connected between what I have studied about kidney failure and its transplantation and this drug. Every patient who did kidney transplantation must use a kind of immunosuppressant which is used to decrease the efficacy of immune system toward the new alien body which is transplanted to the body.this is not the issue I want to talk about. The real issue is the expences of drugs in our countries and if the patient can really cover it in absence of real health insurance. This is the real reason of looking of a substitute for every expensive drug.

Imuran is Azathioprine is an immunosuppressant. Immunosuppressants decrease the effects of your body's immune system.

Saint Johns Wort

2006-07-22T21:20:00.000+04:00

Saint John's Wort
Saturday, July 22, 2006
Source :Aleppous Medica

It is an effective herb used widely for depression and anxiety. The effective compound in it is Hypericin . The only side effect for it is a disturbing in sleep; however, if people exceed the daily dose, they may get reddening on their skin. From my usage, another side effect may develop. An increasing in the blood pressure maybe noticed.

Rofecoxib but Not Other Coxibs Tied to Cardiovascular Risks

2006-06-24T03:41:00.000+04:00

By David Douglas

NEW YORK (Reuters Health)

Alone among selective cyclo-oxygenase 2 inhibitors (coxibs) and non-steroidal anti-inflammatory drugs (NSAIDs) evaluated in a new study, rofecoxib (Vioxx) use was significantly associated with an increased rate of cardiovascular events.

Moreover, lead investigator Dr. Daniel H. Solomon told Reuters Health, "Our findings suggest that the cardiovascular risk associated with rofecoxib begins immediately and persists throughout the period of use. No other agents were found to be associated with risk."

To shed further light on the cardiovascular risks that may be associated with use of coxibs and NSAIDS, Dr. Solomon of Brigham and Women's Hospital, Boston and colleagues studied data on about 100,000 Medicare beneficiaries. Almost 75% had started use of a coxib or NSAID after the beginning of 1999. The remaining subjects were comparable users of other drugs and acted as a reference group.

Reporting in the May issue of Arthritis and Rheumatism, the researchers found that there was a significant elevation in the rate of myocardial infarction or ischemic stroke in users of rofecoxib (relative risk 1.15). This was seen within 60 days and persisted throughout 3 years. The pattern appeared similar in patients at high and low baseline cardiovascular risk.

There was significant reduction in risk with use of naproxen (relative risk 0.75), but no other coxib or NSAID was associated with a significant increase or decrease in cardiovascular event rate.

"This study was undertaken to assess the time course of cardiovascular risk in patients who use an NSAID or coxib." Dr. Solomon pointed out.

"These results," he concluded, "should give patients and doctors confidence that at typical dosages used in practice, most of these agents are not associated with excess cardiovascular risk."

AMIODARONE

2006-05-19T16:05:00.000+04:00

AMIODARONE (Cordarone®, Pacerone®) is an antiarrhythmic agent and is used to help your heart to beat regularly. Because this drug can have significant side-effects, this is a medicine that is used when irregular heartbeats have not responded to other medicines. It is usually reserved for treating potentially life-threatening heartbeat problems. Generic amiodarone tablets are available.

Side effects that you should report to your prescriber or health care professional as soon as possible:•appetite increase or decrease•blue-gray coloring of the skin•blurred vision, seeing blue-green halos, increased sensitivity of the eyes to light•chest pain•cough, or difficulty breathing•difficulty walking•dry or puffy skin or eyes•feeling faint or light-headed•heart pounding or skipping a beat•heart beating very fast or very slow•intolerance to heat or cold•nervousness•numbness or tingling in hands or feet•pain and swelling of the scrotum•passing brown or dark-colored urine•skin rash•sleep difficulties•spitting up blood•sweating•trembling or shaking hands•unusual or uncontrolled movements of body•unusual tiredness or weakness•vomiting•weight gain or loss•yellowing of the eyes or skin
Side effects that usually do not require medical attention:•bitter or metallic taste in the mouth•constipation•decreased sexual ability or desire in men•dizziness•flushing of the face•headache•nausea

New study results:
Meta-analysis showed amiodarone to be associated with an increased risk of developing bradycardia and hypotension when used for the prophylaxis of postoperative atrial fibrillation. The greatest risk in the occurrence of these adverse events arose when using regimens containing i.v. amiodarone, initiating prophylaxis during the postoperative period, and using regimens with average daily doses exceeding 1 g.

Patients with wounds

2006-05-19T15:59:00.000+04:00

Patients with wounds often ask the pharmacist about care issues. These wounds include burns of all depths, cuts, abrasions, and skin tears (e.g., on the cuticles). The wound may have arisen due to an accident, self-mutilation, surgery, an animal bite or scratch, a sports injury, or an insect bite or sting. This column discusses issues related to the treatment of minor wounds.

Chronicity of Wounds
The pharmacist should ask about the duration of the wound. The FDA requires wound care antiseptics and antibiotics to be labeled with the warning that they should not be used beyond one week. Thus, a wound persisting longer than one week requires referral. This ensures that these products will be used only on minor wounds and not on those that are serious and chronic, such as pressure ulcers or wounds on the legs of a diabetic patient.
Moist Versus Dry Wound Healing
Recent medical wisdom states that a moist wound will heal more rapidly and favorably than one that is dry.[6] If the wound is allowed to fully dry during healing, cells on the leading edges may lose viability. Cells in lower tissues are left to heal the wound from the moist tissues on the bottom upward to dead tissues.[7] This is the reason for the proliferation of wound dressings that can keep the wound moist.

First Aid
One of the first matters to address with minor wounds is cleansing the wound.[3,8] Cleansing is important for incisions that are caused by sharp objects, such as knives or broken glass. However, it is even more critical in abrasion injuries, in which the skin's outer layers have been scraped away by abrasion against a rough object, such as when elbows and arms scrape against pavement during a skateboard fall. If the abrasion occurred on a surface that contains loose materials, the wound is likely to be contaminated with gravel, dirt, grass, and other foreign substances. Each foreign object remaining may serve as a source of infection and should be removed.
The wound can be washed with tap water under enough pressure to thoroughly cleanse the wound of foreign materials. Wound Wash Saline is a pressurized sterile 0.9% sodium chloride product that can accomplish this cleansing for minor wounds.

Antiseptics/Antibiotics
Application of an antiseptic/antibiotic can help prevent infection in a minor wound. (These products are not appropriate for an infected wound; self-treatment of any type of bacterial skin infection [e.g., boils, folliculitis, impetigo] is inappropriate and delays the patient from making a physician appointment.) The FDA requires the following labeling on these products: "Stop use and consult a doctor if the condition persists or gets worse. Do not use for longer than one week unless directed by a doctor."[9] Product labeling will also caution patients against use in the eyes or over large areas of the body. Safe and effective local antiseptics that are readily available include denatured ethyl alcohol 48% to 95%, isopropyl alcohol 50% to 91.3%, hydrogen peroxide 3% solution, tincture of iodine, povidone-iodine, and creams and ointments containing polymyxin and bacitracin (e.g., Polysporin). Products containing neomycin (e.g., Neosporin) should be avoided, as neomycin is a potential cause of allergic dermatitis.[10] Band-Aid Antiseptic Foam is a one-step product for cleaning and disinfecting; its antiseptic ingredient is 0.13% benzalkonium chloride. A note of caution is necessary for the ingredient triclosan. Its popularity is unparalleled among antimicrobial hand cleansers, but it can cause resistance in such organisms as Staphylococcus aureus.[11-13]
Local Anesthetics
Patients may request relief for the minor pain of scratches, scrapes, and minor burns. Some antibiotic ointments incorporate local anesthetics in neomycin-free formulas (e.g., Betadine Plus First Aid Antibiotics + Pain Reliever Ointment, with polymyxin, bacitracin, and pramoxine). Patients could also choose a polymyxin/bacitracin cream or ointment and use a separate local anesthetic product. An innovative method to prevent pain is the application of tissue adhesives. These "superadhesive" cyanoacrylate polymers have been used in surgical procedures since the late 1990s and are superior to sutures in closing wounds. A leading product is Band-Aid Liquid Bandage. The patient applies it to a minor laceration, abrasion, friction blister, hangnail, paper cut, or cracked finger using the activator provided. The product reduces the time of wound closure, provides instant hemostasis, and seals off damaged nerve endings, which reduces pain. The adhesive serves as a barrier to wound contamination during its five- to 10-day duration on the skin before it is shed along with the surface layer of skin cells.
Types of Wound Dressings
Nonadherent Dressings. An abrasion may have exudate issuing from it. If the patient applies most types of dressings directly over the area, exudate may become encrusted in the bandage. Subsequent removal can damage the healing wound. The pharmacist can recommend a nonadherent dressing over a minor wound with drainage. The nonadherent nature is achieved through impregnation with petrolatum or the use of a specially constructed rayon-polyethylene laminate. Such products as Adaptic Non-Adhering Dressing, Vaseline Gauze, Nexcare Non-Stick Pads, Release Non-Adhering Dressing, and Telfa Pads are easily removed when the dressing needs to be changed but do not absorb exudates from draining wounds.
Primary Dressings. Wounds can be covered with a primary dressing—a type of bandage with a small degree of absorbency for lightly draining wounds or those with no drainage. Their absorbency wicks drainage away from wounds to minimize the risk of exudate adherence. They also provide some protection for the wound and cover it for purposes of aesthetics. Primary dressings include the Kerlix Sponge, Sof-Wick Drain Sponge, Sof-Wick Dressing Sponge, Steri-Pad, and Topper Dressing Sponge. The set of products marketed under the Band-Aid trade name is a veritable cornucopia of primary dressings. A major advantage of Band-Aid products is that they are manufactured with the tape needed to secure them to the wound, while most other primary dressings require separate tape. Band-Aid products range from standard sizes (e.g., rectangular or round pads) to those with pads impregnated with polymyxin and bacitracin (Band-Aid Plus Antibiotic). Other products have waterproof seals to speed wound healing (Band-Aid Activ Flex).
Secondary Dressings. These dressings are advisable when a wound is producing moderate to heavy drainage. They are absorbent materials (e.g., gauze or cotton) and cannot be placed directly over a wound, since they will yield fibers that could hamper wound healing. However, when placed over a primary dressing, they provide added absorbency, increased compression, and enhanced protection from environmental contaminants.
Most minor wounds would not produce drainage heavy enough to require a secondary dressing; thus, secondary dressings are seldom necessary for accidental wounds for which self-care is appropriate. However, the trend to discharge surgical patients on the day of surgery, or very soon thereafter, has created a compelling need for them. The individual changing the postsurgical wound dressing may be a family member with no medical training or understanding of even the most basic principles of wound care. The pharmacist must stress the need to wash hands thoroughly before applying the dressing, to keep all dressings wrapped prior to application, and to not touch the side of any primary dressing that will face the wound before applying the secondary dressing.
Tapes
Dressings that do not have a self-contained adhesive will require tape to secure them to the skin. Patients should be advised against the use of old "adhesive" tapes, as they have a stiff backing that can damage skin during removal and are prone to be allergenic. Rather, the patient should choose any of several hypoallergenic tapes. These have light adhesives that are gentler on skin with repeated bouts of application and removal. An allergic reaction on broken skin may also retard healing.
Silver as an Antiseptic
Silver nitrate and other silver products, such as colloidal silver, have been traditionally used as antiseptics for many years. The FDA, in its sweeping review of nonprescription products, addressed the safety and efficacy of silver products for self-care in a final rule published in the Federal Register in 1999.[14] The agency stated that many products containing colloidal silver or silver salts were being marketed to treat numerous serious disease conditions, and the FDA was unaware of any evidence to support these therapeutic claims. It ruled that products containing silver would be subject to regulatory action after September 16, 1999. In addition, the agency explained that topical silver products cannot be marketed as dietary supplements under the Dietary Supplement Health and Education Act of 1994, since this law pertains only to orally ingested products. Yet, silver products continue to be marketed. Even now, in 2006, a Google search of the Internet using the term "colloidal silver" returns over two million hits, many directing the reader to sites still promoting unproven claims. Furthermore, a product known as Curad Silver Bandages is being promoted as an effective antibacterial for wound care. Until topical silver products are ruled to be safe and effective for wound care by the FDA, this product should not be recommended.

Aspirin May Reduce the Risk for Aminoglycoside-Related Hearing Loss

2006-05-03T21:46:00.000+04:00

Concurrent administration of aspirin therapy significantly reduces the risk for gentamycin-induced hearing loss, according to the results of a prospective, randomized, double-blind, placebo-controlled Chinese trial reported in a letter to the editor in the April 27 issue of the New England Journal of Medicine.

"The incidence of aminoglycoside-induced hearing loss averages 8% but the numbers may be higher in developing countries where aminoglycosides are frequently the only affordable antibiotics and are sold over the counter," lead author Su-Hua Cha, MD, associate laboratory director of the Kresge Hearing Research Institute's biochemistry laboratory at the University of Michigan (U-M) Medical School in Ann Arbor, says in a news release.

For the study, investigators randomized 195 adult patients at the Xijing Hospital and Airforce Chengdu Hospital scheduled for 5 to 7 days of intravenous gentamycin therapy to receive 2 weeks of supplementation with 1 g of aspirin 3 times daily (n = 89) or to placebo (n = 106).

Results at 5 to 7 weeks posttherapy showed that aspirin therapy significantly reduced the risk for ototoxicity, defined as a unilateral or bilateral shift from baseline of 15 dB or more at both 6 and 7 kHz (3% vs 13%; P = .013; relative risk, 0.26 [95% confidence interval, 0.08 - 0.86]). The efficacy of gentamycin was similar in both groups.

Potential drawbacks to use of aspirin in this setting include the off-label nature of the indication and the risk for gastric bleeding. In the study, gastrointestinal symptoms were more commonly reported among aspirin-treated patients and gastric bleeding led to discontinuation of treatment in 3 patients.

Nevertheless, aspirin is commonly available and inexpensive. "We would like to see the word get around to the medical community in the world that you can take some precautions to minimize the risk to your patients," senior author Jochen Shacht, PhD, professor of biological chemistry in otolaryngology at the U-M Medical School and director of the Kresge Hearing Research Institute, says in a news release.

Dr. Schacht notes that although gentamycin is not commonly used in the United States and its use has been declining in other industrialized countries, it is unlikely to be replaced in the near future due to the specificity of its applications and its widespread and inexpensive availability in poorer countries.

While aspirin shows promise for reducing the risk for aminoglycoside-induced ototoxicity, the authors conclude that further studies are needed to develop a prophylactic drug with fewer adverse effects and/or new and safer antibiotics.

Promethazine Products Contraindicated in Children Under 2 Years

2006-05-03T21:42:00.000+04:00

The US Food and Drug Administration (FDA) is warning healthcare professionals, parents, and caregivers against the use of promethazine HCl in children younger than 2 years due to the risk for fatal respiratory depression, according to an alert sent yesterday from MedWatch, the FDA's safety information and adverse event reporting program.

The FDA has received postmarketing reports of serious adverse events, including 7 deaths and 22 cases of respiratory depression, that were associated with use of promethazine in children younger than 2 years. As a result, all promethazine-containing syrups, tablets, suppositories, and injectables are contraindicated in this population.

Because these adverse events were not directly related to individualized weight-based dosing, promethazine should be administered with caution and at the lowest effective dose for pediatric patients aged 2 years and older. Concurrent administration of other drugs with the potential for respiratory depression should also be avoided.

Promethazine-containing products are marketed in the United States as brand name (Phenergan, made by Wyeth Pharmaceuticals, Inc) and generic formulations. They are indicated for use in treating hypersensitivity reactions and as an antiemetic and/or sedative in various settings.

The FDA notes that antiemetics are not recommended for the treatment of uncomplicated vomiting in pediatric patients; use of these agents should be limited to prolonged vomiting of known etiology.

Because the drug's extrapyramidal effects may be confused with central nervous system signs of undiagnosed primary disease, promethazine should not be used in pediatric patients with signs and symptoms suggestive of Reye's syndrome or other hepatic diseases.

Ziconotide Infusion for Severe Chronic Pain

2006-04-28T13:32:00.000+04:00

http://www.medscape.com/viewarticle/529172?src=mp

Ziconotide intrathecal infusion was recently approved by the United States Food and Drug Administration for the treatment of intractable severe chronic pain. Patients with neuropathic pain make up a significant population among those who experience chronic pain for which there are less than optimal pharmacotherapeutic options. Published clinical trials provide a global view of ziconotide efficacy and safety. A subset of patients in clinical trials obtained complete pain relief, a remarkable finding given the history of drug treatment for neuropathic pain. To provide more information regarding those who respond to ziconotide therapy, we discuss three patients with neuropathic pain who received ziconotide infusion. Two patients with longstanding neuropathic pain, one with complex regional pain syndrome (formerly known as reflex sympathetic dystrophy) of the leg and one with lumbar radiculitis, achieved temporary but complete pain relief from single 5- and 10-µg epidural test doses. In the third case, a patient with longstanding bilateral leg and foot neuropathic pain from acquired immunodeficiency syndrome and antiretroviral drug therapy achieved considerable pain relief from a long-term continuous intrathecal infusion. The patients who received a single dose had mild central nervous system adverse effects such as sedation, somnolence, nausea, headache, and lightheadedness. The patient who received the intrathecal infusion experienced mild-to-severe adverse effects depending on the rate of infusion; these effects included sedation, confusion, memory impairment, slurred speech, and double vision. This patient could sense impending adverse effects and made rate adjustments or suspended infusion to avert untoward symptoms. In all three cases, patients achieved considerable pain relief that was long-lasting and persisted well after dose administration or suspension of infusion.

The Role of Inhaled Insulin in Patient Care

2006-04-14T19:24:00.000+04:00

Response from Karen Shapiro, PharmD, BCPS Clinical Pharmacist, Rancho Los Amigos National Rehabilitation Center, Downey, California; Adjunct Assistant Professor, University of Southern California School of Pharmacy, Los Angeles, California

Exubera, an inhaled insulin product, is the first noninjectable insulin with efficacy comparable to that of regular insulin. It can be used as an alternative to rapid-acting (regular) insulin in combination with longer-acting insulin in patients with type 1 diabetes mellitus, and alone or in combination with longer-acting insulin and/or oral agents in patients with type 2 diabetes.
Exubera appears to be safe for use in nonsmoking patients with normal lung function. Of course, drugs can appear safe initially, only to be linked to serious health consequences once they are widely used. As part of the drug approval process, Pfizer is required to study pulmonary function in 5000 patients over a period of 5 years.
Patients may prefer noninjectable insulin. However, many patients do not object to the injection itself as much as they object to the association of insulin use with end-stage diabetes and related complications. In patients with type 2 diabetes, insulin is often started when poor health has developed, after many years (or decades) of poor control. Early in my clinical career, I had the privilege of working with an endocrinologist who had the majority of his patients controlled to goal. Patients were taught insulin injection by a group of peers, with a nurse diabetes educator facilitating the group. I cannot recall a graduate of this group having any problem with insulin injection. An injection itself can be seen as scary, but most patients associate injections with vaccinations, which are given with long and relatively thick intramuscular (IM) needles, very different from those used to inject insulin.
That being said, it still will be preferable for most patients starting on insulin to use a noninjectable form. However, most patients will require a longer-acting insulin, such as glargine, to lower around-the-clock glucose levels. That means that Exubera will not eliminate injections for the majority of patients.
Exubera is inhaled through a device about the size of a flashlight. Regular insulin is administered at mealtimes, so ambulatory patients may have to carry this device with them. This will be acceptable to some patients, but not all. Exubera will cost about $4 a day in the United States; this cost is much higher than that for injectable regular insulin.
I believe that noninjectable insulin will take off in a substantial manner when a baseline (longer-acting) insulin is available. Exubera is costly, short-acting, and delivered in a bulky container. Once these limitations are overcome, we will see a blockbuster drug that will substantially replace injectable insulin.

Abortion Drug Mifeprex

2006-04-05T23:08:00.000+04:00

Abortion Drug Mifeprex Linked to 2 More Deaths
Yael Waknine
http://www.medscape.com/viewarticle/527988

The US Food and Drug Administration (FDA) has notified healthcare professionals of 2 additional deaths after medical abortion with mifepristone (Mifeprex 200-mg tablets, made by Danco Laboratories, LLC), according to an alert sent today from MedWatch, the FDA's safety information and adverse event reporting program.After verbal notification of the deaths by the manufacturer, an FDA investigation was launched into their circumstances. Although use of mifepristone was previously linked to 4 deaths from Clostridium sordellii-associated sepsis, the causes of death for the present cases remain unconfirmed.Abortion providers and patients are reminded to consider the specific circumstances and directions for use of mifepristone prior to initiating therapy. Potential adverse events such as sepsis should also be discussed, and patients warned of early signs and symptoms that may require immediate medical evaluation, such as fever, abdominal pain, and heavy bleeding.The FDA notes that although a sustained fever of 100.4°F or higher, severe abdominal pain, or pelvic tenderness in the days after a medical abortion may be particularly indicative of infection, some infections may present atypically, with no fever, bacteremia, or significant findings on pelvic examination.Providers of medical abortion and emergency department care are advised to investigate the possibility of sepsis in afebrile patients presenting with symptoms of general malaise (nausea, vomiting, or diarrhea and weakness), with or without abdominal pain, more than 24 hours after taking misoprostol. A complete blood count may be needed to identify patients with hidden infection.Immediate treatment with an antibiotic regimen effective against anaerobes bacteria such as C sordellii should be considered in patients suspected of infection. The FDA does not recommend prophylactic therapy at this time because of the low risk for sepsis (approximately 1 in 100,000) and the risks inherent to antibiotic therapy, such as severe or fatal allergic reactions and the development of antimicrobial resistance. Furthermore, an appropriate antibiotic regimen for this purpose has not yet been determined.Mifepristone is indicated for the termination of intrauterine pregnancies that have progressed for 49 days or fewer, as determined by the first day of the last menstrual period. It is not indicated for use in terminating ectopic pregnancy. Unless a complete abortion is confirmed, 400 µg of misoprostol should be administered on day 3 after oral administration of 600 mg of mifepristone. Surgical termination is recommended if complete termination has not been confirmed after 2 weeks. The FDA notes that the safety and effectiveness of intravaginally administered oral tablets has not been established.

Incretin Mimetics: Clinical Use in Combination Therapy

2006-03-11T23:47:00.000+04:00

Anne Peters, MD
Medscape Diabetes & Endocrinology. 2005;7(2) ©2005 Medscape
http://www.medscape.com/viewarticle/519727

Incretin mimetics are a new class of antidiabetic agents. The first of this class is exenatide, which became available for use at the end of May 2005. Incretins are hormones produced from the gastrointestinal track that act to enhance the normal release of insulin after the oral ingestion of carbohydrates. They also slow the gastric absorption of nutrients and act to promote a feeling of satiety that can lead to weight loss in overweight individuals. Therefore, these agents work to lower glucose levels in a glucose-dependent fashion without causing hypoglycemia, but with a gradual weight loss due to a decrease in caloric intake.
Although these agents can work as monotherapy, the first indication for their use is in combination with oral agents. Specifically, they were approved for the treatment of type 2 diabetes in combination with a sulfonylurea agent, metformin, or metformin plus a sulfonylurea agent. The data from the registry trials demonstrating the effectiveness of exenatide in combination with these agents have been published.In the series of 3 trials (adding exenatide to a sulfonylurea agent, to metformin, or to metformin plus a sulfonylurea agent), patients were randomized to placebo or exenatide injection twice daily. The studies were conducted in a double-blind, randomized, placebo-controlled manner. Patients were eligible for inclusion in the study if they were at a maximal tolerated dose of an oral agent and had inadequate glucose control, defined as a glycosylated hemoglobin (A1C) level > 8%. Baseline demographic characteristics were very similar among the groups . The average age of patients entering the study was 55 years ± 10 years, and these patients had a body mass index of 34 kg/m2 ± 6 kg/m2 and duration of diabetes of 8 years ± 6 years.
Patients in all 3 groups had a decrease in A1C levels of approximately .9%, with a corresponding weight loss of 1.9 kg (Figure). The greatest weight loss was seen in patients who were on metformin monotherapy when the exenatide was started. The reduction in A1C level is fairly similar to the findings from other studies of combination therapy in patients with type 2 diabetes, although, as with all antidiabetes medications, the higher the initial blood glucose levels, the greater the fall.
The most common side effect was nausea, which in some participants was accompanied by vomiting. Nausea was noted in 44% of patients in the clinical trials on the higher dose of exenatide (10 mcg twice daily), but led to discontinuation of the drug in only 3%. A rarer side effect is vomiting, which occurred in 13% of patients on exenatide and 4% of those on placebo . Nausea and vomiting tended to diminish over time and were less frequent if patients started on a lower dose of exenatide. Therefore, to reduce the occurrence of nausea, a lower starting dose (5 mcg twice daily) is recommended for the first month, with an increase to 10 mcg twice daily (if tolerated) thereafter.
I always warn patients about the potential for nausea when starting exenatide. It always helps if patients are forewarned, so they know what to expect and understand that the nausea will usually improve over time. I also recommend that the patient contact me if the nausea and/or vomiting is severe or persistent. There is no known treatment for the nausea, other than time. If a patient is having a lot of difficulty with nausea, reducing the dose from twice daily (before breakfast and before dinner) to just once daily (before dinner for a week or 2) until the drug is tolerated has been helpful in reducing the symptoms.
In the longer-term extension studies, exenatide continued to maintain the same reduction in A1C level, but there was a slow, gradual weight loss that continued out to 104 weeks.Extension studies are limited by the fact that they are no longer placebo-controlled and not all patients opt to continue, and those who are not doing as well may choose not to stay in the study. However, those who stayed in the study continued to do well and even showed improvement over time. Patients were not counseled on lifestyle changes in any of the studies, such as weight reduction and physical activity.
In my practice, when starting a new antidiabetes medication, I use the change in therapy as an opportunity to readdress lifestyle modifications. I have found this particularly true with exenatide, which is a drug that enhances a patient's sense of satiety and makes it easier for a patient to eat less without the usual struggle against food craving. However, I have had occasional patients who start on exenatide; find themselves eating less; and then decide that, because they are eating smaller portions, they can eat more high-calorie foods, such as cake, cookies, candy, and potato chips. Unfortunately, fewer high-calorie foods are largely equivalent to more lower calorie foods, and these patients have little, if any, weight loss while on the exenatide. On the other hand, I have patients on exenatide who have worked hard on eating less overall, with an improvement in the composition of their diet and a reduction in caloric intake, such as eating a salad with light dressing for lunch instead of a roast beef sandwich, who have lost much more than the expected weight loss (20-30 lb in a few months). An important message for all patients with diabetes, no matter what treatment is used, is that the therapeutic response is always enhanced when lifestyle modifications are incorporated into the daily pattern of behavior.
Another effect of exenatide in the pivotal studies was an increase in rates of hypoglycemia when used in patients on a sulfonylurea agent. Exenatide, on its own, will not cause hypoglycemia -- and didn't when used in combination with metformin alone. However, when added to a sulfonylurea agent, it will lower blood sugar levels and make the patient more susceptible to sulfonylurea agent-induced hypoglycemia . Therefore, if a patient is taking a sulfonylurea agent, the dose should be reduced by 30% to 50% when exenatide is added. Clinically, because exenatide has a greater effect on postprandial blood glucose levels than on fasting levels, sometimes backing off too much on the sulfonylurea dose will cause an increase in fasting glucose levels while the exenatide improves postprandial levels. Therefore, it is a balance between preventing hypoglycemia with an anticipatory reduction in the sulfonylurea agent dose vs causing an increase in fasting blood sugar levels by cutting back too rapidly.
Although exenatide is only approved for use with metformin and/or a sulfonylurea agent, there is no pharmacologic reason to believe that it can't be used as monotherapy or in combination with all agents for treating diabetes, including thiazolidinediones and insulin. Studies have been completed assessing the combination of exenatide and a glitazone, and the data have been submitted to the US Food and Drug Administration. Anecdotally, I have used (off-label) glitazones in combination with exenatide essentially since the drug was released, and my patients have done well. The same is true for the combination with insulin, although there are yet no formal data on this approach to treatment. The rule of thumb for reducing the dose of any drug that can cause hypoglycemia when exenatide is added holds true when it is added to insulin. I generally keep the basal insulin dose the same, but reduce or eliminate the premeal insulin doses, using the exenatide to enhance endogenous premeal insulin secretion. Remember, however, that exenatide does not substitute for insulin in patients with type 1 diabetes; patients need to have functional beta cells to respond to exenatide. Patients with type 1 diabetes may benefit from the administration of pramlintide with their premeal insulin; pramlintide is neuroendocrine hormone secretion from pancreatic beta cells.
Other incretin mimetics that should be useful in combination therapy for the treatment of type 2 diabetes are under development.One is liraglutide, which is a human long-acting form of glucagon-like peptide (GLP)-1 that is similar in action to exenatide. A related class of medication, which increases endogenous GLP-1 levels, is the dipeptidyl peptidase IV inhibitors, such as vildagliptin. These oral agents increase GLP-1 levels by slowing its breakdown, which prolongs its half-life.
In summary, the incretin mimetics are extremely useful agents for the treatment of type 2 diabetes. The currently available drug exenatide is approved for use in combination with a sulfonylurea agent, metformin, or the combination of both. Exenatide is supplied in an easy-to-use predosed pen, and is generally well tolerated. However, patients should be warned that they may feel nauseated from the drug, a side effect that generally diminishes over time. Patients on sulfonylurea agents may need to have their dose reduced to avoid hypoglycemia. If used appropriately, exenatide can help improve A1C levels and aid in weight reduction, which helps both provider and patient achieve goals that were more difficult to reach in the past.

Future of Emergency Contraception Lies in Pharmacists' Hands

2006-03-11T23:43:00.000+04:00

Nicole Monastersky; Sharon Cohen Landau
J Am Pharm Assoc. 2006;46(1):84-88. ©2006 American Pharmacists Association
http://www.medscape.com/viewarticle/521833

Efforts have been made by reproductive health, advocacy, and pharmacy groups to educate patients, medical providers, and, in some instances, pharmacists about EC. But for EC to be widely known as the safe and effective backup birth control method to prevent pregnancy after sexual intercourse, and for pharmacists to be comfortable in providing an informed and valuable service, unified strategies for increasing educational opportunities about EC for pharmacists are essential.
Pharmacists can continue to take a leadership role in promoting EC and their own accessibility as a professional resource for information. In addition to stocking the product, pharmacists can participate in training programs, community outreach activities, conferences, legislative advocacy, and partnerships with other health care professionals to improve awareness and access. Considering pharmacists' changing role in the pharmacy, promoting increased access to EC is not only logical and important in meeting the contraceptive needs of their patients, it may also make sense from a business perspective.
Building the capacity of pharmacists while increasing the visibility of EC will contribute to the greater awareness and understanding that women can do something after unprotected intercourse to prevent an unintended pregnancy. Pharmacies are an ideal point of access to EC, with easy accessibility and open hours on evenings, weekends, and holidays. Pharmacists who are knowledgeable about EC are resourceful and educated members of the health care team available to increase access and effectively negate the reference to EC as the "nation's best kept secret."
An estimated 1.3 million unintended pregnancies could be avoided annually with pharmacy access to EC.[9] Pharmacists who are informed and educated about this method of birth control are not only more likely to stock EC, but are able to answer questions and provide appropriate information to women. FDA has reviewed the application to make EC available OTC for women aged 16 and older. Regardless of what FDA decides about nonprescription sales of Plan B, pharmacists remain key players in EC by providing access to needed products and by serving as professional and knowledgeable resources. Now more than ever is the time for pharmacists to reach out and take advantage of educational opportunities about EC.

Study Shows How Alcohol Damages the Bones

2005-12-29T12:13:00.000+04:00

NEW YORK (Reuters Health)

Bone loss is an often-overlooked consequence of heavy drinking, but recent research has illuminated how alcohol takes a toll on the bones, according to a new report.
In a review of cell, animal and human studies, Dr. Dennis A. Chakkalakal of the Omaha VA Medical Center in Nebraska describes how heavy drinking leads to bone loss, higher risk of fractures and slower healing of bone breaks.
The main problem appears to be that alcohol inhibits the normal formation of new bone, Chakkalakal reports in the journal Alcoholism: Clinical & Experimental Research.
Though excessive drinking has been shown to promote bone thinning and fractures, some studies have suggested that moderate drinking may actually help protect bone mass - possibly because small amounts of alcohol promote new bone formation.
The opposite appears true of high amounts of alcohol, according to Chakkalakal's review.
Throughout adulthood, bone undergoes a process of "remodeling," whereby cells called osteoclasts break down small portions of old bone, and cells called osteoblasts form new bone. In healthy, younger adults, this process is usually balanced, so that bone mass is maintained.
Too much alcohol, however, appears to inhibit osteoblasts from doing their job, and heavy drinkers may start to lose bone mass in just a few years, according to Chakkalakal. The potential for bone loss climbs in tandem with drinking, evidence shows, but it's not clear where the risk threshold lies.
Most studies on alcohol and bone loss have defined "heavy" drinking as roughly six or more drinks per day. But, the review points out, there's some evidence that bone loss is a risk for people who have closer to three or more drinks a day.
Though many people know about the damage heavy drinking can inflict on the liver, far fewer know about the effects on bone, according to Dr. Terrence M. Donohue Jr., also of the Omaha VA Medical Center.
In a statement, he recommended that anyone with a bone fracture avoid alcohol during the healing process.
"The review," he said, "underscores the importance of abstinence from alcohol consumption by patients - alcoholics or teetotalers - with fractures and who may want to drink during their convalescence."

Behavioral Therapies Aid Elderly with Insomnia

2005-12-29T12:03:00.000+04:00

NEW YORK (Reuters Health)

Therapies focused on changing sleep habits may be a good alternative to sleeping pills for older adults with insomnia, a research review suggests.
The review of 23 clinical trials found that behavioral therapies aimed at changing people's habits and attitudes regarding sleep were generally effective in helping older adults get a better night's sleep.
The findings, published in the journal Health Psychology, add to evidence supporting behavioral sleep therapies.
In a study published last year, for example, researchers found that a few sessions of counseling were more effective than a common sleep medication at bringing lasting relief to people with chronic insomnia.
Those researchers concluded that behavioral therapies should constitute the first line of therapy for chronic insomnia. Sleep medications, though often effective in the short run, carry the risk of dependence and side effects such as daytime drowsiness. Their effectiveness in the long run is also questionable, as people can suffer even worse sleep problems once they go off the drugs.
Behavioral therapies, on the other hand, may take several weeks to show effects, but these benefits are maintained longer than those of medications -- though the evidence for that is based on a limited number of studies, Dr. Michael Irwin, the lead author on the new study, told Reuters Health.
Of the 23 clinical trials included in the study, only eight focused on adults older than 55.
It's not clear why so few studies have been conducted in this age group, according to Irwin, who is a professor of psychiatry at the University of California Los Angeles Cousins Center for Psychoneuroimmunology.
One reason, he noted, may be that the prevalence of insomnia among older adults -- with up to 30 percent affected -- has only recently been documented in large-scale studies. In addition, he said, there may be a "bias" that insomnia is a normal part of aging, and that older adults will not respond as well to therapy as middle-aged adults.
For their study, Irwin and his colleagues reviewed the results of clinical trials that tested three broad types of behavioral therapy.
One was cognitive-behavioral therapy, which aims to change insomniacs' thoughts and feelings regarding sleep and to teach them practical ways to surmount their sleep problems - like getting in bed only when they're drowsy, or getting up and reading a book when they fail to fall asleep in 20 minutes or so.
In addition, some of the studies investigated relaxation-based therapies, while others tested "behavioral-only" approaches, which limit their focus to altering sleep habits.
All three forms of therapy, the review found, were similarly effective at improving older adults' sleep quality and their ability to fall asleep and stay asleep all night.
The findings, Irwin said, offer evidence that older adults, like younger ones, can benefit from behavioral therapies for insomnia.
Behavioral therapies for insomnia are based, in part, on therapies used for depression. So most mental health professionals -- and some general practitioners -- should be able to offer such treatment, according to Irwin.

Researchers Say Estrogen Can Kill Breast Cancer Cells Once Fueled By The Hormone

2005-12-08T07:29:00.000+04:00

Fox Chase Cancer Center
2005-12-07
http://www.sciencedaily.com/releases/2005/12/051207113139.htm

Fox Chase Cancer Center researchers say some breast cancer cells once fueled by estrogen can be killed by the same hormone. This raises the possibility that estrogen therapy after estrogen deprivation may overcome the cells' eventual resistance to hormone therapy. The finding by V. Craig Jordan, Ph.D., D. Sc., and his colleagues at Fox Chase is published in the December 7 issue of the Journal of the National Cancer Institute.
Many breast cancer cells (called estrogen receptor-positive breast cancers) require estrogen for survival. Women with these types of breast cancers are treated with drugs that that block estrogen, such as tamoxifen, fulvestrant, or aromatase inhibitors, causing the cells to die in a process called apoptosis. However, over time, these cancer cells learn to adapt and become resistant to this therapy.
"Tamoxifen and other estrogen inhibition drugs have been remarkably successful in the treatment of hormone-responsive breast cancers," said Jordan, vice president and scientific director for the medical science division at Fox Chase. "However, cancer cells are smart and they figure out how to survive these treatments. We believe we've become savvy to their art. Our laboratory study demonstrates that these same breast cancer cells die when we re-introduce them to estrogen." Jordan was the leader in the development of the use of tamoxifen to treat breast cancer. He holds the Alfred G. Knudson Jr., M.D., Ph.D., Chair in Cancer Research at Fox Chase.
The mechanism by which estrogen promotes apoptosis is not well understood. To understand this process, Jordan and his colleagues developed a line of breast cancer cells, called MCF-7:5C. These cells already are resistant to estrogen withdrawal. When the researchers treated MCF-7:5C cells with very small concentrations of estradiol they underwent apoptosis. The researchers also tested these cells in mice to see how this process might influence existing tumors. Again, the exposure to estradiol caused the cancer cells to die.
"These laboratory data have important clinical implications, particularly for the use of aromatase inhibitors as long-term therapy," write the authors, "and they suggest that, if and when resistance to aromatase inhibition occurs, a strategy of treatment with estrogen ... may be sufficient to kill the cancer and control disease progression."

###
Fox Chase Cancer Center was founded in 1904 in Philadelphia as the nation's first cancer hospital. In 1974, Fox Chase became one of the first institutions designated as a National Cancer Institute Comprehensive Cancer Center. Fox Chase conducts basic, clinical, population and translational research; programs of prevention, detection and treatment of cancer; and community outreach. For more information about Fox Chase activities, visit the Center's web site at http://www.fccc.edu/ or call 1-888-FOX CHASE.

UCSF Study Finds Nerve Regeneration Is Possible In Spinal Cord Injuries

2005-12-08T07:19:00.000+04:00

University of California - San Francisco
2005-12-07
http://www.sciencedaily.com/releases/2005/12/051207114205.htm

A team of scientists at UCSF has made a critical discovery that may help in the development of techniques to promote functional recovery after a spinal cord injury.

By stimulating nerve cells in laboratory rats at the time of the injury and then again one week later, the scientists were able to increase the growth capacity of nerve cells and to sustain that capacity. Both factors are critical for nerve regeneration.

The study, reported in the November 15 issue of the Proceedings of the National Academy of Sciences, builds on earlier findings in which the researchers were able to induce cell growth by manipulating the nervous system before a spinal cord injury, but not after.

Key to the research is an important difference in the properties of the nerve fibers of the central nervous system (CNS), which consists of the brain and spinal cord, and those of the peripheral nervous system (PNS), which is the network of nerve fibers that extends throughout the body.

Nerve cells normally grow when they are young and stop when they are mature. When an injury occurs in CNS cells, the cells are unable to regenerate on their own. In PNS cells, however, an injury can stimulate the cells to regrow. PNS nerve regeneration makes it possible for severed limbs to be surgically reattached to the body and continue to grow and regain function.

Regeneration occurs because PNS cell bodies are sensitive to damage to their nerve processes, and they react by sending out a signal that triggers the nerve fibers to regrow, explains Allan Basbaum, PhD, senior study author and chair of the UCSF Department of Anatomy. "Apparently this communication doesn't take place within the CNS."

Scientists do not yet know the biochemical cause for the difference, he adds.

The traditional scientific approach in efforts to enhance CNS regeneration is to manipulate the biochemical environment of the cells at the site of the spinal cord injury, according to Basbaum. Instead of this type of investigation, Basbaum's team used nervous system manipulation techniques to apply the principles of PNS cell growth capability to CNS cells.

The researchers took advantage of an unusual class of nerve fibers that has both a PNS and a CNS branch. Previously, the researchers had shown in animal studies that an injury made to the peripheral branch prior to a spinal cord injury provided the essential communication signal that enabled the CNS branch to grow. But this only worked if the PNS injury--which served as priming for CNS cell growth--was made at least a week before the CNS injury. "Clearly this would have no utility in clinical situations, where treatments cannot be made in anticipation of spinal cord injury," says Basbaum. Another challenge the researchers faced was stimulating CNS cells to grow beyond the injury site and into healthy tissue, which is essential to help regain function.

"A PNS injury at the time of spinal cord damage will only promote growth of nerve fibers into the spinal cord lesion, but not into the tissue beyond it. This is because growth capacity is enhanced, but it is not sustained," he explains. In the new study, researchers evaluated the effect of two peripheral nerve lesions (injuries) in animals with spinal cord injury. One lesion was made at the time of the cord injury and a second was made a week later. Both lesions were located in the animals' sciatic nerve, which is part of the PNS.

The researchers found that the two "priming lesions" not only promoted significant spinal cord regeneration within the area of the spinal cord injury, but more important, the regenerating axons grew back into normal areas of the spinal cord, where the hope is that functional connections can be reestablished. Axons are the long, fragile, fibers that conduct impulses between nerve cells in the brain, spinal cord and limbs.

"Getting the growth beyond the lesion is key. If we can get those axons to grow even a few centimeters past the lesion, they can start sending signals and developing new circuits throughout the body," says Basbaum. Basbaum adds that timing is critical for successful nerve regeneration. "There is a window of opportunity just after the injury when the potential for growth through and beyond the lesion is greatest. If we wait too long after an injury, the cells revert back to their normal, no-growth state. Plus, scar tissue begins to form, making growth difficult." "These findings give us hope. The nervous system is capable of being modified to a level where we can achieve nerve fiber growth. Ultimately, the goal is to promote growth and sustain it long enough for recovery of movement to occur in spinal cord injury patients," he concludes. Study co-authors include first-author Simona Neumann, PhD, and Kate Skinner, MD, both of UCSF. The research was funded by the Roman Reed Spinal Cord Injury Research Fund of California and the National Institutes of Health.

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UCSF is a leading university that consistently defines health care worldwide by conducting advanced biomedical research, educating graduate students in the life sciences, and providing complex patient care.

Omalizumab Improves Quality of Life for Asthma and Rhinitis Patients

2005-11-26T13:22:00.000+04:00

Omalizumab (Xolair), a monoclonal anti-IgE antibody, provided symptomatic relief and a better quality of life for patients who suffer from both allergic asthma and persistent allergic rhinitis, according to two studies presented here at the annual meeting of the American Academy of Allergy, Asthma & Immunology. Omalizumab received U.S. Food and Drug Administration approval in June 2003."For patients with concomitant allergic asthma and persistent allergic rhinitis, omalizumab is effective," said Ulf Harnest, MD, from ClinGuard GmbH Institute for Medical Treatment Strategies in Munich, Germany, during his presentation of the first study. "It is rated effective by patients, and most important, it is well-tolerated."The researchers conducted a 28-week double-blind, placebo-controlled trial of 405 patients with both moderate to severe allergic asthma and persistent allergic rhinitis. The patients were between the ages of 12 and 74 years.Patients were randomized to receive either treatment or placebo, in addition to conventional therapies of inhaled budesonide plus the option of a long-acting beta2-agonist and nasal steroids.In the omalizumab group, 209 patients were given 0.016 mg/kg/IgE (IU/mL) every four weeks, while 196 patients received placebo.The first study's primary end points were the exacerbation of asthma, which was defined as having worsening symptoms requiring oral or intravenous steroids or a doubling of the budesonide dose, as well as worsening quality of life.Secondary end points included clinical symptoms, patients' self-evaluation, and drug safety and tolerability.The researchers used the Juniper asthma scale and rhinitis questionnaires to measure quality of life. Responders were considered those who showed improvement of more than 1 point on both scales.Before treatment, there was no difference between the two groups' scores on their quality-of-life questionnaires. After treatment, 57.7% of those treated with omalizumab were responders compared with 40.6% of those who received placebo. Similarly, 65.6% of the omalizumab-treated patients rated control of their asthma symptoms as excellent/good compared with 53.1% of placebo-treated patients.Nearly 17% of the patients receiving omalizumab experienced adverse events compared with 12% of those in the placebo group. Serious adverse effects were seen in 1.4% of the omalizumab group and 1.5% of the placebo group.In the second study, researchers looked at efficacy as measured by number of exacerbations, a combined asthma and rhinitis clinical symptom score, and pulmonary function.They found fewer exacerbations in patients treated with omalizumab, as well as a significant difference in mean morning pulmonary function at all assessments during treatment. The combined symptom score decreased by an adjusted average of 17.8 points for patients in the omalizumab groups compared with a 12.4 decrease for those receiving placebo.Sami L. Bahna, MD, DrPH, professor of pediatrics and medicine and chief of allergy and immunology at the Louisiana State University Health Sciences Center in Shreveport, found the difference of 15% vs. 10% on FEV1 not a robust finding. He was not involved in the studies."I was surprised that the study did not show a more favorable effect, as previous studies in asthma did," Dr. Bahna told Medscape, noting that less-expensive and easier-to-use drugs may have an equivalent effect.

Dosage and Administration

Omalizumab is supplied as a lyophilized, sterile powder in a single-use, 5-mL vial designed to deliver 150 mg of drug after reconstitution.The recommended starting dosage is 150-375 mg administered subcutaneously every two or four weeks. More than one injection site should be used if the dosage exceeds 150 mg. Body weight and serum total IgE levels, measured before the start of treatment, are used to determine the dosage and frequency of administration .Patients with baseline serum IgE concentrations of <30>700 IU/mL and a body weight of >150 kg were excluded from pivotal clinical trials that established the safety and efficacy of omalizumab.[23,26] Protocol violations did lead to the treatment of patients outside of the recommended dosing range; however, the number was too small for a subgroup analysis.Thus, the safety and efficacy of dosages of <150>750 mg per four-week interval have not been established for patients with a body weight or baseline serum IgE outside the recommended range.The maximum dosage is 750 mg administered subcutaneously every four weeks.Safe and effective use has not been established for children under 12 years of age.During treatment, total IgE levels are elevated and remain elevated for up to one year after discontinuation of treatment; therefore, IgE levels cannot be used as a guide for dosing omalizumab. Dosage determination should be based on the initial serum IgE level if treatment interruption occurs and lasts less than one year, but total serum IgE levels may be retested for dosage determination if treatment with omalizumab has been interrupted for one year or more. Dosage should be adjusted for significant changes in body weight.There are no data to support the need for dosage adjustments in patients with hepatic or renal impairment.For subcutaneous administration, omalizumab should be prepared using only sterile water for injection USP. The lyophilized product takes approximately 15-20 minutes to dissolve. The product will appear slightly opalescent or clear and may form small bubbles or foam around the edge of the vial. To obtain a 1.2-mL dose, all of the product must be withdrawn from the vial before ejecting any air or surplus solution from the syringe. The solution should be used within eight hours of reconstitution when stored in the vial at 2-8 °C (36-46 °F) or within four hours of reconstitution when stored at room temperature. A vial delivers 1.2 mL (150 mg) of omalizumab. The reconstituted product is somewhat viscous and may require 5-10 seconds to administer. Reconstituted omalizumab can be used only once, as it does not contain preservatives.

Resources:

http://www.medscape.com/viewarticle/483809_1

http://www.medscape.com/viewarticle/472390

Hypertension|Full File

2005-11-19T15:35:00.000+04:00

HYPERTENSION

Hypertension (high blood pressure) is a common condition that can lead to serious complications if left untreated. Studies suggest that a person's diet and weight play an important role in the onset and persistence of hypertension, and that simple dietary changes and weight loss are effective measures for reducing blood pressure.
Dietary changes and weight loss are called nonpharmacologic measures, that is, measures that do not involve drugs. Other nonpharmacologic measures for controlling blood pressure and its associated risks include smoking cessation, stress reduction, and regular exercise. These different types of nonpharmacologic measures are effective individually, but often have the greatest benefit when used together.
Nonpharmacologic measures can improve the effectiveness of antihypertensive drugs and may even eliminate the need for drugs. These measures also have other benefits: they have few or no side effects, they reduce a person's overall risk of cardiovascular disease, and, if started early, they may even prevent hypertension in people who are at risk for this condition.
It is important to work with your doctor to develop a reasonable, well-rounded treatment plan for hypertension. Nonpharmacologic measures entail lifestyle adjustments that can be difficult to initiate and maintain, but your doctor can provide guidelines to ease these adjustments and can help you track your progress over time.
DIETARY CHANGES AND BLOOD PRESSURE — Research has shown that dietary factors affect blood pressure and that dietary changes are an effective approach for controlling hypertension and possibly even preventing this condition.
Dietary changes usually begin with an evaluation of a person's current diet, cooking habits, and eating habits. After specific dietary patterns are identified, a person can learn strategies for altering the amounts of specific nutrients in his or her diet.
Reducing sodium intake — Sodium makes up 40 percent of table salt so that 3000 mg of salt (about one level teaspoon or three packets of salt) contain 1200 mg of sodium, which is the ingredient listed on the label of all processed food. Most fresh foods have a low sodium content, but sodium is often added during food and beverage processing. In the American diet, this added sodium accounts for about 80 percent of a person's total sodium intake.
Several lines of evidence strongly link a high sodium intake to hypertension. As an example, hypertension rarely occurs in countries in which people consume less than 1000 mg per day of sodium; it primarily occurs in countries in which people consume more than 2000 mg of sodium per day. Most Americans consume about 4000 milligrams of sodium per day.
One study found that, compared to adolescents who were fed a standard diet in infancy, adolescents who were fed a low-salt diet in infancy had a lower blood pressure. Other studies have shown that reducing sodium intake lowers blood pressure both in people with hypertension and in people with borderline high blood pressure. Reducing sodium intake has also decreases the likelihood that hypertension will return in people who stop taking antihypertensive drugs.
Switching from a higher sodium diet to a lower sodium diet has also been associated with a slight reduction in blood pressure in people with normal blood pressure. When people with normal blood pressure reduce their sodium intake from 4000 mg to 2000 mg per day, their blood pressure falls by 2 to 3 mmHg; over several years, the reduction may be as great as 10 mmHg. The benefit of this reduction may be a substantially lower risk of cardiovascular disease.
Added benefits of reducing sodium intake — In addition to directly reducing blood pressure, a lower sodium intake may also enhance the effectiveness of antihypertensive drugs and the effectiveness of other nonpharmacologic measures such as weight loss. A lower sodium intake has also been associated with other health benefits, including a reduced risk of dying from a stroke, a reversal of heart enlargement, and a reduced risk of kidney stones and osteoporosis.
Guidelines for reducing sodium intake — Several professional organizations have issued guidelines for reducing sodium intakes. The guidelines recommend that people with an elevated blood pressure consume no more than 2400 milligrams of sodium or 6 grams of salt per day. The sodium content of packaged, processed, and prepared foods can usually be determined by reading food labels. However, it is important to remember that the amounts listed are for a "serving size" which may be only a small portion of the total content.
It is difficult to abruptly cut back on the amount of sodium in the diet, but most people find that they do not miss the sodium if they cut back gradually. The full benefits of a lower sodium diet on blood pressure may not be evident for at least six weeks.
Reducing alcohol intake — There is a clear association between excess alcohol intake and the development of hypertension. People who have more than two drinks per day have a one- to two-fold increase in the incidence of hypertension compared to nondrinkers; this effect is dose-related and is most prominent when intake exceeds five drinks per day. On the other hand, alcohol intake below two drinks per day appears to have a cardioprotective effect (benefits the heart), even in patients with preexisting hypertension.
Maintaining a vegetarian diet — Maintaining a vegetarian diet may reduce elevated blood pressure and protect against the onset of hypertension. One study found that people with mild hypertension have a lower systolic blood pressure (the top number of the blood pressure reading) when they ate a vegetarian diet than when they ate a standard diet.
A strict vegetarian diet may not be necessary to obtain the associated health benefits: one study showed that increased consumption of fruits and vegetables, low-fat dairy products, and a low saturated and total fat intake lower blood pressure when incorporated into a non-vegetarian diet.
Moreover, high-fiber diets may have other health benefits, including lower total cholesterol levels and lower insulin levels. A strict vegetarian diet may not be necessary to obtain the associated health benefits: one study suggested that some components of a vegetarian diet, such as fruits and vegetables, as well as low-fat dairy products, and a low saturated and total fat intake lower blood pressure when incorporated into a non-vegetarian diet.
Reducing caffeine intake — Caffeine may cause a rise in blood pressure and can worsen the rise in blood pressure triggered by stress. However, this rise in blood pressure is transient because the body compensates for the effects of caffeine. Moderate caffeine consumption has not been associated with an increased risk of hypertension in most people.
WEIGHT LOSS AND BLOOD PRESSURE — Excess body weight is associated with a higher risk of hypertension and adds to the risk of cardiovascular disease associated with hypertension. Gradual weight gain throughout life appears to contribute to the increase in blood pressure associated with aging.
Weight loss can be achieved by a sensible program that entails reducing the number of calories in a diet, increasing physical activity, or best of all, a combination of these measures.
Benefits of weight loss on blood pressure — Obesity raises blood pressure and makes hypertension more difficult to control; in contrast, weight loss reduces blood pressure. Blood pressure falls by about 1 mmHg for every 2.2 pounds (1.0 kg) of weight lost, an effect that is consistent for both men and women and for people of different ethnicities. The beneficial effects of weight loss on blood pressure add to those of drug therapy and other nonpharmacologic measures, including reducing sodium intake, reducing alcohol intake, and exercise.
Added benefits of weight loss — In addition to reducing blood pressure, weight loss has several other benefits, including a reduction of blood levels of lipids (cholesterol and related substances), a partial reversal of heart enlargement, a reduced risk of diabetes, and an improved sense of well-being and quality of life.
Maintaining weight loss — Weight loss is difficult to maintain because of enticements of large portions of fast foods, particularly for young children, and the lack of physical activity so common in our society. In people with severe obesity, drug therapy or gastric surgery may be necessary to achieve and maintain weight loss. STUDIES OF NONPHARMACOLOGIC MEASURES FOR THE TREATMENT AND PREVENTION OF HYPERTENSION — Several studies have evaluated the benefits of nonpharmacologic measures in people with hypertension and in people at risk for hypertension.
Treatment of hypertension — Three large studies have assessed the role of nonpharmacologic measures in the treatment of hypertension.
Standard diet versus modified diet plus weight loss — In one study, people who had well-controlled blood pressure when taking antihypertensive drugs discontinued these drugs. Half of the people ate a standard diet while the other half ate a lower salt diet, moderated alcohol intake, and followed a plan for weight loss. After four years, hypertension had returned in 95 percent of the people who ate the standard diet but in only 61 percent of the people who ate the modified diet and followed measures to lose weight.
Treatment of Mild Hypertension Study (TOMHS) — In the TOMHS, a group of people with mild hypertension followed a program that entailed weight loss, reductions of dietary sodium and alcohol, and increased physical activity; this program was associated with a fall in blood pressure. Some of the people were then assigned to antihypertensive drugs, and some were assigned to a placebo. Four years later, the reductions in blood pressure were still present in the placebo group, although the reductions in blood pressure were greater in the group that took antihypertensive drugs. The results of the study also suggested that, although people were less likely to follow the initial program over time, the program still had measurable benefits four years later.
Dietary Approaches to Stop Hypertension (DASH) Trial — In the DASH trial, people with normal or high blood pressure were assigned to one of three diets: a standard diet (a diet low in fruits and vegetables), a diet rich in fruits and vegetables, or a combination diet (a diet rich in fruits, vegetables, and low-fat dairy products, and low in saturated and total fat). Compared to the people who ate the standard diet, the people who ate the fruits and vegetables and combination diets had significant reductions in blood pressure. Blood pressure reductions were greater in the people who ate the combination diet than in the people who ate the extra fruit and vegetable diet; this difference was more pronounced in people with hypertension than in people without hypertension. The effects of the diets on blood pressure were maximal after only two weeks and were still present at eight weeks.
In a separate study, restricting dietary sodium in combination with the DASH diet produced a further reduction in blood pressure.
Prevention of hypertension — Three large studies have assessed the role of nonpharmacologic measures in the prevention of hypertension.
Standard diet versus modified diet plus weight loss — One study, the Trials of Hypertension Prevention, Phase I, evaluated the effects of dietary changes and weight loss in people with borderline high blood pressure. Half of the people ate a standard diet, and half of the people followed a program that included a lower sodium diet, lower alcohol intake, and measures to lose weight. After five years, 19.2 percent of the people who ate the standard diet had developed hypertension compared to only 8.8 percent of the people who followed the program.
Trials of Hypertension Prevention, Phase II — The Trial of Hypertension Prevention, Phase II, included overweight, middle-age adults with normal blood pressure who were assigned to one of four treatments: usual medical care, a lower salt diet, a weight loss program, or combined treatment (both a lower salt diet and weight loss). After six months, the people assigned to the weight loss group and the combined treatment group had the greatest reductions of blood pressure. Although the effectiveness of these treatments decreased over time, individuals in the treatment groups were still less likely than individuals in the usual care group to have hypertension four years later.
Trial of Nonpharmacologic Interventions in the Elderly (TONE) — The TONE study included older adults who took only one antihypertensive drug to control their blood pressure. The people were assigned to one of four treatments: usual medical care, a weight loss program, a lower sodium diet, or combined treatment (both weight loss and a lower sodium diet). All of the groups had reductions of blood pressure, but reductions were greatest in the people assigned to the combined treatment group. After 30 months, the people assigned to the treatments were less likely to have a return of hypertension, to need antihypertensive drugs, and to experience cardiovascular events.
WHERE TO GET MORE INFORMATION — Your doctor is the best resource for finding out important information related to your particular case. Not all patients with hypertension are alike, and it is important that your situation is evaluated by someone who knows you as a whole person.

Cola Not Coffee May Raise Risk of High BP

Habitual coffee drinking does not increase the risk of hypertension (high blood pressure) in women, but consuming cola beverages might, according to the results of a study looking at the effects of various caffeine-containing products.
"The findings should give peace of mind to women who drink a lot of coffee that their habit is not putting them at risk for high blood pressure," lead author Dr. Wolfgang C. Winkelmayer, from Brigham and Women's Hospital in Boston, told Reuters Health. Further studies are needed to determine if this is also the case in men, he added.
"The association between cola beverage use and hypertension was a big surprise to us, especially since we were careful to control for other factors known to increase the risk of hypertension, such as BMI," Winkelmayer said. "This was a surprise because this association has never been reported before and because there are no ingredients in colas that we're aware of that should have this effect."
Approximately 50 million Americans have hypertension, the researchers note in the Journal of the American Medical Association this week. Previous reports had tied caffeine intake with acute elevations in blood pressure, but the long-term effects were unclear.
The current findings stem from a study of 155,594 women who participated in the Nurses' Health Studies (NHS) I and II. The subjects were free of high blood pressure when the studies began in the early 1990s and were followed over 12 years.
During follow-up, a total of 19,541 and 13,536 cases of hypertension were observed in the NHS I and II cohorts, respectively. In both cohorts, caffeine intake was not directly linked to incident hypertension.
When an analysis by beverage type was performed, habitual coffee intake was not linked to an elevated risk of high blood pressure. By contrast, drinking cola beverages, either sugared or diet, seemed to increase the risk of hypertension significantly.
While the findings should provide reassurance to coffee drinkers, further research is needed to shed light on the association between cola beverages and hypertension, Winkelmayer said.

Medication for High Blood Pressure

What is the aim of treatment?
The usual target is to reduce blood pressure to below 140/90. (This figure is controversial as some experts say the target for treatment should be to below 140/85 mmHg.)
In some cases, your doctor is likely to advise an even lower target. For example, if you have diabetes or certain other conditions.
Which medicines are used to lower blood pressure?
There are five main classes of medicines which are used to lower blood pressure. There are various types and brands of medicine in each class. The following gives a brief overview of each of the classes. However, for detailed information about your own medication you should read the leaflet that comes inside the medicine packet.
Diuretics ('water tablets')The most commonly used diuretic to treat high blood pressure in the UK is called bendroflumethiazide (bendrofluazide) - but there are others. For example, chlorothiazide, chlorthalidone, cyclopenthiazide, hydrochlorothiazide, and indapamide. Diuretics work by:
increasing the amount of salt and fluid that you pass out in your urine. This has some effect on reducing the fluid in the circulation which reduces blood pressure, and
they may also have a 'relaxing' effect on the blood vessels which reduces the pressure within the blood vessels.
Only a low dose of a diuretic is needed to treat high blood pressure. Therefore, you will not notice much diuretic effect (you will not pass much extra urine).
Beta-blockersThere are various types and brands. For example, acebutolol, atenolol, bisoprolol, metoprolol, oxprenolol, pindolol, propanaolol, sotalol, and timolol. They work by slowing the heart rate, and reducing the force of the heart. These actions lower the blood pressure. Beta-blockers are also commonly used to treat angina, and some other conditions. You should not take a beta-blocker if you have asthma, chronic obstructive pulmonary disease, or certain types of heart or blood vessel problems.
Angiotensin-converting enzyme (ACE) inhibitorsThese medicines work by reducing the amount of a chemical that you make in your bloodstream called angiotensin II. This chemical tends to constrict (narrow) blood vessels. Therefore, less of this chemical causes the blood vessels to relax and widen, and so the pressure of blood within the blood vessels is reduced.
Again, there are various types and brands. For example, captopril, cilazapril, enalapril, fisinopril, lisinopril, perindopril, quinapril, ramipril, and trandolapril. An ACE inhibitor is particularly useful if you also have heart failure or diabetes. ACE inhibitors should not be taken by people with certain types of kidney problems, people with some types of artery problems, and if you are pregnant. You will need a blood test before starting an ACE inhibitor, and within a week after starting it, and one week after any increase in dose. Then, a yearly blood test is usual.
Angiotensin Receptor Blockers These medicines are sometimes called angiotension II receptor antagonists. There are various types and brands. For example, candesartan, eprosartan, irbesartan, losartan, olmesartan, telmisartan and valsartan. They work by blocking the effect of angiotensin II on the blood vessel walls. So, they have a simialar effect to ACE inhibitors (described above).
Calcium-channel blockersThese medicines affect the way calcium is used in the blood vessels and heart muscle. This has a relaxing effect on the blood vessels. Again, there are various types and brands. For example, amlodipine, diltiazem, felodipine, isradipine, lacidipine, lercanidipine, nicardipine, nifedipine, nisoldipine, and verapamil. Calcium-channel blockers can also be used to treat angina.
What about side-effects?
All medicines have possible side-effects, and no medicine is without risk. However, most people who take medicines to lower blood pressure do not develop any, or only have mild, side-effects. A full list of cautions and possible side-effects is listed on the leaflet inside the medicine packet. The most common are:
Diuretics - can cause gout attacks in a small number of users, or can make gout worse if you already have gout.
Beta-blockers - can cause cool hands and feet, poor sleep, tiredness, and impotence in some users.
ACE inhibitors - sometimes cause an irritating cough.
Angiotensin Receptor Blockers - sometimes cause dizziness.
Calcium channel blockers - sometimes cause dizziness, facial flushing, swollen ankles, and constipation.
If you do develop a side-effect, a different medicine may suit you better. There is a lot of choice so one can usually be found to suit. See your doctor if you develop any problem which you think is due to your medication.
So, which is the best medicine for high blood pressure?
Research trials seem to show that the five classes of medicines discussed above, on average, are just as good as each other at lowering blood pressure. Therefore, the one chosen depends on such things as: if you have other medical problems; your ethnic orignin; if you take other medication; possible side-effects; your age; etc.
For example: beta-blockers and calcium channel blockers can also treat angina; ACE inhibitors also treat heart failure; some medicines are not suitable if you are pregnant; some are thought to be better if you have diabetes; some tend to work better in people of Afro-Caribbean origin than others; etc.
However, individuals can vary. Sometimes, if one medicine does not work so well or causes side-effects, a switch to a different class of medicine may work fine.
Other medicines for high blood pressure
Apart from the five main classes of medicines listed above, sometimes other medicines are used to lower blood pressure. For example, methyldopa or alpha blockers are sometimes used if there are problems with the more commonly used medicines.
Combinations of medicines
One medicine can reduce high blood pressure to the target level in less than half of cases. It is common to need two or more different medicines to reduce high blood pressure to a target level. In about a third of cases, three medicines or more are needed to get blood pressure to the target level. So, for example, you may need an ACE inhibitor plus a diuretic (and sometimes also another medicine) to control your blood pressure. This is just an example, and various combinations of medicines can be used.
In some cases, despite treatment, the target level is not reached. However, although to reach a target level is ideal, if you have high blood pressure you will benefit from any reduction in blood pressure.
How long is medication for high blood pressure needed for?
In most cases, medication is needed for life. However, in some people whose blood pressure has been well controlled for three years or more, medication may be able to be stopped. In particular, in people who have made significant changes to lifestyle which can affect blood pressure (such as lost a lot of weight, or stopped heavy drinking, etc). Your doctor can advise. If you stop medication, you need regular blood pressure checks. In some cases the blood pressure remains normal. However, in others it starts to rise again. Medication can then be started again.

Possible Side Effects of Drugs That Lower Blood Pressure

Some of the drugs listed below can affect certain functions of the body, resulting in bad side effects. However, drugs that lower blood pressure have proven effective over the years. The benefits of using them far outweigh the risk of side effects. Most people who’ve taken these drugs haven’t had any problems.
Diuretics — Some of these drugs may decrease your body's supply of a mineral called potassium. Symptoms such as weakness, leg cramps or being tired may result. Eating foods containing potassium may help prevent significant potassium loss. You can prevent potassium loss by taking a liquid or tablet that has potassium along with the diuretic, if your doctor recommends it. Diuretics such as amiloride (Midamar), spironolactone (Aldactone) or triamterene (Dyrenium) are called "potassium sparing" agents. They don’t cause the body to lose potassium. They might be prescribed alone but are usually used with another diuretic. Some of these combinations are Aldactazide, Dyazide, Maxzide or Moduretic.
Some people suffer from attacks of gout after prolonged treatment with diuretics. This side effect isn't common and can be managed by other treatment.
In people with diabetes, diuretic drugs may increase the blood sugar level. A change in drug, diet, insulin or oral antidiabetic dosage corrects this in most cases. Your doctor can change your treatment. Most of the time the degree of increase in blood sugar isn't much. Impotence may also occur in a small percentage of people.
Beta-blockers — Acebutolol (Sectral), atenolol (Tenormin), metoprolol (Lopressor), nadolol (Corgard), pindolol (Visken), propranolol (Inderal) or timolol (Blocadren) may cause insomnia, cold hands and feet, tiredness or depression, a slow heartbeat or symptoms of asthma. Impotence may occur. If you have diabetes and you’re taking insulin, have your responses to therapy monitored closely.
ACE inhibitors — These drugs, such as captopril (Capoten), enalapril (Vasotec), lisinopril (Zestril or Prinivil), may cause a skin rash; loss of taste; a chronic dry, hacking cough; and in rare instances, kidney damage.
Angiotensin II receptor blockers — These drugs may cause occasional dizziness.
Calcium channel blockers — Diltiazem (Cardizem), nicardipine (Cardene), Nifedipine (Procardia) and verapamil (Calan or Isoptin) may cause palpitations, swollen ankles, constipation, headache or dizziness. Side effects with each of these drugs differ a great deal.
Alpha blockers — These drugs may cause fast heart rate, dizziness or a drop in blood pressure when you stand up.
Combined alpha and beta blockers — People taking these drugs may experience a drop in blood pressure when they stand up.
Central agonists — Alpha methyldopa (Aldomet) may produce a greater drop in blood pressure when you're in an upright position (standing or walking) and may make you feel weak or faint if the pressure has been lowered too far. This drug may also cause drowsiness or sluggishness, dryness of the mouth, fever or anemia. Male patients may experience impotence. If this side effect persists, your doctor may have to change the drug dosage or use another medication.
Clonidine (Catapres), guanabenz (Wytensin) or guanfacine (Tenex) may produce severe dryness of the mouth, constipation or drowsiness. If you're taking any of these drugs, don’t stop suddenly, because your blood pressure may rise quickly to dangerously high levels.
Peripheral adrenergic inhibitors — Reserpine may cause a stuffy nose, diarrhea or heartburn. These effects aren't severe and no treatment is required other than to change the amount of drugs taken. If you have nightmares or insomnia or get depressed, tell your doctor. You should stop using the drugs.
Guanadrel (Hylorel) or guanethidine (Ismelin) may cause some diarrhea, which may persist in some people. This side effect usually becomes less of a problem if you continue treatment.
These drugs reduce blood pressure more when you stand. Consequently, you may get dizzy and lightheaded and feel weak when you get out of bed in the morning or stand up suddenly. If you notice any of these reactions — and if they persist for more than a minute or two — sit or lie down and either reduce or omit the next dose of the drug. If symptoms continue, contact your doctor.
When you're taking guanethidine, don't keep standing in the hot sun or at a social gathering if you begin to feel faint or weak. These activities cause low blood pressure. Male patients may experience impotence. Contact your doctor if this occurs. These drugs are rarely used unless other medications don’t help.
Blood vessel dilators — Hydralzine (Apresoline) may cause headaches, swelling around the eyes, heart palpitations or aches and pains in the joints. Usually none of these symptoms are severe, and most will go away after a few weeks of treatment. This drug isn't usually used by itself. Minoxidil (Loniten) is a potent drug that's usually used only in resistant cases of severe high blood pressure. It may cause fluid retention (marked weight gain) or excessive hair growth.

Acute Cardiac Toxicity Associated With High-Dose Intravenous Methotrexate Therapy

2005-11-17T13:44:00.000+04:00

Read the full study

Here is only the conclusion with a identification introduction

Methotrexate is frequently used for cancer treatment and for management of inflammatory diseases, such as rheumatoid arthritis. By inhibiting folic acid reduction, it impairs DNA synthesis and stops cell proliferation. However, clinical studies have also demonstrated direct cellular toxicity independent of its antiproliferative effects. These reports principally describe central nervous system toxicity and suggest metabolic pathways that could cause this toxicity.

Cases reviews demonstrate an association between methotrexate therapy and development of myocardial arrhythmias that could lead to a potentially lethal arrhythmia. Therefore, we would encourage frequent clinical monitoring for patients treated with high-dose intravenous methotrexate. Those known to have cardiac disease or cardiac symptoms while receiving methotrexate therapy probably should have continuous electrocardiographic monitoring during drug infusion. Greater awareness of this potential complication associated with methotrexate therapy may lead to more reports of its occurrence, which would facilitate our understanding of its true incidence and pathophysiologic mechanism. Finally, the metabolic alterations associated with high-dose methotrexate therapy offer therapeutic approaches for both prevention and treatment.

Impotence drugs and possibilities of blindness(a news with scientifical review)

2005-11-15T14:51:00.000+04:00

Impotence Drugs Need Stronger Warning - US Group
By Susan Heavey
WASHINGTON (Reuters) Oct 20 - Drugs to treat erectile dysfunction need stronger warnings on their packaging about the risk of blindness, U.S. consumer group Public Citizen said on Thursday in a petition filed with health regulators.
The U.S. Food and Drug Administration should "immediately add a black box warning regarding the risks of drug-induced blindness for the three phosphodiesterase 5 (PDE5) inhibitors that are prescribed for the treatment of erectile dysfunction," Public Citizen's Health Research Group wrote.
Pfizer Inc.'s pulmonary hypertension drug Revatio, which has the same active ingredient as its impotence drug Viagra, should also carry a similar black box warning -- the strongest warning the agency can require, the advocacy group said.
Earlier this year drugmakers agreed to put information on their impotence drug labels about the possible vision loss, called non-arteritic anterior ischemic optic neuropathy.
Viagra, Cialis, sold by Eli Lily & Co. and Icos Corp., and Levitra, sold by GlaxoSmithKline , Bayer AG and Schering-Plough Corp., now carry the new labels, which say the condition "has been reported rarely."
Both the companies and the FDA have said the cause of the blindness is not known.
But Public Citizen said 19% of all cases of the vision disorder reported to the FDA since 1998 were among users of Viagra.
"The fact that Viagra's large numbers of adverse reaction reports occurred without any warnings to the medical profession strongly suggests that Viagra is an important factor in causing (ischemic optic neuropathy)," the petition said.
The current label warnings are inadequate, the group said. "The wording is ambiguous and the location of this information is buried," the petition said.
Public Citizen also called on the FDA to start a registry of all patients who are diagnosed with the vision disorder. The agency should also require manufacturers to send all U.S. physicians a letter about the risk and call for pharmacists to give FDA-approved leaflets with prescriptions.
FDA's handling of the blindness reports has been questioned. In June, Senate Finance Committee Chairman Charles Grassley, an Iowa Republican, requested internal FDA documents and other information about why it took "so long" for the agency to call for the label changes and notify the public.
Men most at risk for the vision loss are those older than 50 who have diabetes, heart disease, high blood pressure and high cholesterol, among other ailments.

PDE-5 Inhibitors and NAION
Wayne J.G. Hellstrom, MD, FACS; Muammer Kendirci, MD
Background
In response to a small number of postmarketing reports of vision loss in men taking type 5 phosphodiesterase (PDE-5) inhibitors, the US Food and Drug Administration (FDA) has issued a news release to advise healthcare providers of the potential risk. FDA has received 43 reports of varying degrees of vision loss, including blindness, among users of these drugs -- 38 cases in men using sildenafil, 4 in men using tadalafil, and 1 case in a man using vardenafil. Most of these cases of vision loss were due to nonarteritic anterior ischemic optic neuropathy (NAION). The loss of vision in some cases has been irreversible.
What Is NAION?
NAION is a vascular event that is presumed to occur due to a decrease in blood flow to the small arteries that supply the optic nerve. A disruption in the blood supply to the optic nerve causes damage to the nerve. Injury to the nerve may result in permanent visual loss in 1 or both eyes. There are 2 types: arteritic and nonarteritic. Arteritic anterior ischemic optic neuropathy (AAION) is an inflammatory vasculitis, and nonarteritic (NAION) is a diagnosis of exclusion, which is made in the absence of provable arteritis. NAION is 6 times more common than AAION due to temporal arteritis. NAION is the most common acute optic neuropathy and one of the most common causes of sudden vision loss in the elderly. The annual incidence in white persons is 2.3 to 10.2 per 100,000 for persons over the age of 50. There are 1500 to 6000 new cases every year in the United States.
NAION is characterized clinically by the acute onset of unilateral visual loss. Patients are typically older than 50 years of age; clinical examination reveals unilateral visual acuity and visual field loss, a relative afferent pupillary defect (RAPD), and optic disk edema. Despite the frequency with which this condition occurs, its exact cause is not known. Numerous risk factors have been proposed, including a small cup-to-disk ratio, hypertension, diabetes mellitus, arteriosclerosis, hypercholesterolemia, and after intraocular surgery. A recent study reports a high prevalence of sleep apnea syndrome in patients with NAION.
NAION in Men Using PDE-5 Inhibitors
Recently, Pomeranz and colleagues reported 7 cases of NAION in men who had recently taken sildenafil. These patients, aged between 50 and 69 years, had typical features of NAION within 36 hours after ingestion of sildenafil citrate for erectile dysfunction (ED). Both eyes were affected in one man. All affected men had preexisting hypertension, diabetes, elevated cholesterol, or hyperlipidemia. Sildenafil may provoke NAION in individuals with an arteriosclerotic risk profile.
The onset of NAION in these 7 patients within hours after ingestion of sildenafil may support an association between use of this agent and NAION.As patients with ED are more likely to have the microvascular risk factors typically associated with spontaneous NAION, an ischemic effect by sildenafil on the optic nerve is plausible, but unlikely. In normal adults, sildenafil increased pulsatile ocular blood flow, a result of filling the choroidal circulation. Grunwald and coworkers did not find any significant change in the optic nerve rim, foveolar choroidal blood flow, or retinal vessel caliber after treatment with sildenafil. However, Pache and colleagues found that sildenafil caused significant dilation of retinal arteries and veins in healthy individuals. One healthy young woman in another study had severe flushing, headache, and visual field defects after ingestion of 200 mg of sildenafil, suggesting that the effect on the optic nerve is acutely and temporally related to ingestion of the medication. Morgan and colleagues reported the occurrence of a transient ischemic attack in a 50-year-old man 2 hours after he had ingested 50 mg of sildenafil. When the same patient took 100 mg of sildenafil 6 days later, permanent neurologic deficits from an ischemic stroke developed.
Because of the lack of a model to test for a possible relationship between PDE-5 inhibitors and NAION, a definite causal relationship cannot be established at this time. An animal model for NAION has been developed and may provide an experimental paradigm. Based on the fact that 43 cases of NAION have now been reported soon after use of PDE-5 inhibitors, doctors should warn their ED patients about the possible relationship between NAION and PDE-5 inhibitor use.
Despite the differences in the number of cases of NAION among men taking the various PDE-5 inhibitors, there is no evidence that one drug presents a higher risk than another. Sildenafil has been used by more than 23 million men worldwide, tadalafil by more than 4.5 million, and vardenafil by more than 1.8 million. The difference in the number of NAION cases among all 3 PDE-5 inhibitors reflects the number of each drug used worldwide rather than real differences in risk among drugs.
What to Tell Patients
As we mentioned, a number of risk factors have been proposed, including a small cup-to-disk ratio, hypertension, diabetes mellitus, arteriosclerosis, hypercholesterolemia, and intraocular surgery. In a recent study, Nagy and colleagues investigated predictive factors for the development of NAION and reported that high lipoprotein (odds ratio, 16.88), diabetes mellitus (odds ratio, 5.78), and factor V Leiden mutation (odds ratio, 4.44) were the main predictive components.
It can be recommended that patients with a history of monocular NAION be cautioned that PDE-5 inhibitors may increase the risk of NAION in the fellow eye. Patients who have risk factors for the development of NAION should be referred to an ophthalmologist before being prescribed PDE-5 inhibitors. Any man taking a PDE-5 inhibitor who develops visual problems should stop taking the PDE-5 inhibitor and be seen by an ophthalmologist. Also, ophthalmologists should ask all men with NAION about the use of PDE-5 inhibitors.
Questions of Causation
NAION is thought to be an ischemic phenomenon due to constriction of arterioles in the optic nerve. PDE-5 inhibitors, however, are well known to cause vasodilation, not vasoconstriction. Vascular damage leading to NAION is due to the presence of cardiovascular risk factors, including age over 50 years, diabetes, hypercholesterolemia, and hypertension. NAION shares common risk factors with cardiovascular diseases and ED. NAION has been reported in patients taking several other medications, specifically sumatriptan (a migraine drug), amiodarone, and nasal decongestants.
There have also been multiple clinical studies on the effects of PDE-5 inhibitors on the ocular circulation. None of those studies indicated that PDE-5 inhibitor treatment causes a decrease in optic nerve head or choroidal blood flow; on the contrary, some studies actually suggested that the drug causes small increases in ocular blood flow. A review of 103 clinical trials of sildenafil involving 13,000 patients found no reports of NAION. NAION has been reported rarely through postmarketing surveillance with short- and long-acting PDE-5 inhibitors. These cases have, for the most part, been in patients who had underlying anatomic or vascular risk factors for the development of NAION. For the time being, there is no evidence that NAION occurred more frequently in men taking sildenafil, tadalafil, or vardenafil than in men of similar age and health who did not take these medications.
Other Visual Side Effects of PDE-5 Inhibitors
The selectivity of the PDE-5 inhibitors for PDE-6 is 11-fold less for sildenafil, 25-fold less for vardenafil, and 187-fold less for tadalafil when compared with PDE-5. The available clinical trial data indicate that sildenafil, at the higher doses, can cause dose-related, mild, and readily reversible changes in color discrimination (generally only apparent with sophisticated visual function testing); these occur mostly in the blue-green spectrum and have little, if any, effect on visual function. These side effects are believed to be secondary to transient inhibition of PDE-6 when higher doses are used. PDE-5 inhibitors should be prescribed with caution in patients with retinitis pigmentosa due to a lack of efficacy and safety data in this patient population, a small percentage of whom have genetic abnormalities in PDE-6 production. Because NAION is a vascular event presumed to occur due to a decrease in blood flow to the small arteries that supply the optic nerve, and because PDE-5 inhibitors potentially increase ocular blood flow due to vasodilation, it is difficult to make a connection between NAION and the visual side effects of the PDE-5 inhibitors.

Insomnia and the increased risk of Diabetes in men

2005-11-14T15:36:00.000+04:00

NEW YORK (Reuters Health) - Sleep disturbances appear to increase the risk of developing diabetes in men but not in women, according to a Swedish study.
Dr. Lena Mallon, from University Hospital in Uppsala and her associates sent questionnaires regarding sleep complaints and other possible risk factors for diabetes to a random sample of subjects who were 45 to 65 years old in 1983, and again in 1995. A total of 1187 subjects completed both questionnaires.
During that interval, diabetes developed in 6 percent of women and 9 percent of men, according to a report in the medical journal Diabetes Care.
After adjusting for age and other risk factors, including high blood pressure, snoring, weight and depression, the team found that the risk of diabetes was nearly three-fold higher for men who got no more than 5 hours of uninterrupted sleep a night, and nearly five times higher for men with difficulties maintaining sleep.
However, sleep variables were not tied to diabetes in women in the study.
The researchers say there are several ways that lack of sleep might lead to diabetes. One possibility is that poor sleep is related to activation of the stress system, another is that sleep debt may impact carbohydrate metabolism.

My comment:

Insomnia in general effects the metabolic and endocrine functions. while Beta cells are the main part in pancreas which is a part of endocrine system which controls the Glucose level in the body we can easily understand that this part which works mainly on metabolic process may be effected by increasing or decreasing in hours of sleeping .More than 9 hours daily sleeping maybe turned to be a factor to inrease the risk of Diabetes mainly as a study said in men and also less than 6 hours or some said 4 hours will also be a factor to inrease the risk of diabetes ones again in men. (Mustafa Hamido)

Statins studied for heart failure therapy|Statin's full file

2005-11-13T14:28:00.000+04:00

NEW HAVEN, Conn., Nov 10, 2005 (UPI via COMTEX) -- Yale University scientists are evaluating the role of statin therapy in patients with heart failure -- a leading cause of hospitalization in older people.
Researchers say while statins are used primarily to lower cholesterol levels, there is evidence the drugs might also have beneficial effects on blood vessel function independent of cholesterol levels.
The Yale School of Medicine study will assess vascular function before and after a short course of statin therapy in heart failure patients with normal cholesterol levels. The randomized trial will include 30 patients with mild to moderate chronic heart failure.
The researchers -- led by Dr. Stuart Katz, associate professor of internal medicine/cardiovascular medicine -- will use a method called the Cholestech LDX System to check cholesterol-LDL levels in blood at the beginning and the end of the study. The method enhances physicians' ability to quickly identify patients with high risk of heart disease and offer treatment or counseling during the same office visit.

Statin's Full File:
Cholesterol is a soft, waxy substance found among the lipids (fats) in the bloodstream and in all your body's cells. It's an important part of a healthy body because it's used to form cell membranes, some hormones and is needed for other functions. But a high level of cholesterol in the blood — hypercholesterolemia — is a major risk factor for coronary heart disease, which leads to heart attack.
Cholesterol and other fats can't dissolve in the blood. They have to be transported to and from the cells by special carriers called lipoproteins. There are several kinds, but the ones to focus on are low-density lipoprotein (LDL) and high-density lipoprotein (HDL).
What is LDL cholesterol?
Low-density lipoprotein is the major cholesterol carrier in the blood. If too much LDL cholesterol circulates in the blood, it can slowly build up in the walls of the arteries feeding the heart and brain. Together with other substances it can form plaque, a thick, hard deposit that can clog those arteries. This condition is known as atherosclerosis. A clot (thrombus) that forms near this plaque can block the blood flow to part of the heart muscle and cause a heart attack. If a clot blocks the blood flow to part of the brain, a stroke results. A high level of LDL cholesterol (160 mg/dL and above) reflects an increased risk of heart disease. If you have heart disease, your LDL cholesterol should be less than 100 mg/dL. That's why LDL cholesterol is called "bad" cholesterol. Lower levels of LDL cholesterol reflect a lower risk of heart disease.
What is HDL cholesterol?
About one-third to one-fourth of blood cholesterol is carried by HDL. Medical experts think HDL tends to carry cholesterol away from the arteries and back to the liver, where it's passed from the body. Some experts believe HDL removes excess cholesterol from plaques and thus slows their growth. HDL cholesterol is known as "good" cholesterol because a high HDL level seems to protect against heart attack. The opposite is also true: a low HDL level (less than 40 mg/dL in men; less than 50 mg/dL in women) indicates a greater risk. A low HDL cholesterol level also may raise stroke risk.
What is Lp(a) cholesterol?
Lp(a) is a genetic variation of plasma LDL. A high level of Lp(a) is an important risk factor for developing atherosclerosis prematurely. How an increased Lp(a) contributes to heart disease isn't clear. The lesions in artery walls contain substances that may interact with Lp(a), leading to the buildup of fatty deposits.
What about cholesterol and diet?
People get cholesterol in two ways. The body — mainly the liver — produces varying amounts, usually about 1,000 milligrams a day. Foods also can contain cholesterol. Foods from animals (especially egg yolks, meat, poultry, fish, seafood and whole-milk dairy products) contain it. Foods from plants (fruits, vegetables, grains, nuts and seeds) don't contain cholesterol.
Typically the body makes all the cholesterol it needs, so people don't need to consume it. Saturated fatty acids are the main culprit in raising blood cholesterol, which increases your risk of heart disease. Trans fats also raise blood cholesterol. But dietary cholesterol also plays a part. The average American man consumes about 337 milligrams of cholesterol a day; the average woman, 217 milligrams.
Some of the excess dietary cholesterol is removed from the body through the liver. Still, the American Heart Association recommends that you limit your average daily cholesterol intake to less than 300 milligrams. If you have heart disease, limit your daily intake to less than 200 milligrams. Still, everyone should remember that by keeping their dietary intake of saturated fats low, they can significantly lower their dietary cholesterol intake. Foods high in saturated fat generally contain substantial amounts of dietary cholesterol.
People with severe high blood cholesterol levels may need an even greater reduction. Since cholesterol is in all foods from animal sources, care must be taken to eat no more than six ounces of lean meat, fish and poultry per day and to use fat-free and low-fat dairy products. High-quality proteins from vegetable sources such as beans are good substitutes for animal sources of protein.
How does physical activity affect cholesterol?
Regular physical activity increases HDL cholesterol in some people. A higher HDL cholesterol is linked with a lower risk of heart disease. Physical activity can also help control weight, diabetes and high blood pressure. Aerobic physical activity raises your heart and breathing rates. Regular moderate to intense physical activity such as brisk walking, jogging and swimming also condition your heart and lungs.
Physical inactivity is a major risk factor for heart disease. Even moderate-intensity activities, if done daily, help reduce your risk. Examples are walking for pleasure, gardening, yard work, housework, dancing and prescribed home exercise.
How does tobacco smoke affect cholesterol?
Tobacco smoke is one of the six major risk factors of heart disease that you can change or treat. Smoking lowers HDL cholesterol levels and increases the tendency for blood to clot.
How does alcohol affect cholesterol?
In some studies, moderate use of alcohol is linked with higher HDL cholesterol levels. However, because of other risks, the benefit isn't great enough to recommend drinking alcohol if you don't do so already.
If you drink, do so in moderation. People who consume moderate amounts of alcohol (an average of one to two drinks per day for men and one drink per day for women) have a lower risk of heart disease than nondrinkers. However, increased consumption of alcohol brings other health dangers, such as alcoholism, high blood pressure, obesity, stroke, cancer, suicide, etc. Given these and other risks, the American Heart Association cautions people against increasing their alcohol intake or starting to drink if they don't already do so. Consult your doctor for advice on consuming alcohol in moderation.

Cholesterol-Lowering Medications and You
If following a low-saturated-fat, low-cholesterol diet, increasing your physical activity, and losing weight have not lowered your risk for developing CHD after about 3 months, your doctor may consider prescribing a cholesterol-lowering medication. If your doctor prescribes medicine, you also will need to:
Continue to follow your cholesterol-lowering diet
Be more physically active
Lose weight if overweight
Control all of your other heart disease risk factors, including smoking, high blood pressure, and diabetes
Taking all these steps together may lessen the amount of medicine you need or make the medicine work better--and that reduces your risk for developing heart disease. The following is a description of cholesterol-lowering medicines:
Statins
Bile Acid Sequestrants
Nicotinic Acid
Fibrates

Statins

There are currently five statin drugs on the market in the United States: lovastatin, simvastatin, pravastatin, fluvastatin, and atorvastatin (cerivastatin was withdrawn from the market by the manufacturer in August 2001). The major effect of the statins is to lower LDL-cholesterol levels, and they lower LDL-cholesterol more than other types of drugs. Statins inhibit an enzyme, HMG-CoA reductase, that controls the rate of cholesterol production in the body. These drugs lower cholesterol by slowing down the production of cholesterol and by increasing the liver's ability to remove the LDL-cholesterol already in the blood. Statins were used to lower cholesterol levels in both the West of Scotland and AFCAPS/TexCAPS studies. The large reductions in total and LDL-cholesterol produced by these drugs resulted in large reductions in heart attacks and heart disease deaths. Thanks to their track record in these studies and their ability to lower LDL-cholesterol, statins have become the drugs most often prescribed when a person needs a cholesterol-lowering medicine.
Studies using statins have reported 20 to 60 percent lower LDL-cholesterol levels in patients on these drugs. Statins also reduce elevated triglyceride levels and produce a modest increase in HDL-cholesterol.
The statins are usually given in a single dose at the evening meal or at bedtime. It is important that these medications be given in the evening to take advantage of the fact that the body makes more cholesterol at night than during the day.
You should begin to see results from the statins after several weeks, with a maximum effect in 4 to 6 weeks. After about 6 to 8 weeks, your doctor can do the first check of your LDL-cholesterol while on the medication. A second measurement of your LDL-cholesterol level will have to be averaged with the first for your doctor to decide whether your dose of medicine should be changed to help you meet your goal.
The statins are well tolerated by most patients, and serious side effects are rare. A few patients will experience an upset stomach, gas, constipation, and abdominal pain or cramps. These symptoms usually are mild to moderate in severity and generally go away as your body adjusts. Rarely a patient will develop abnormalities in blood tests of the liver. Also rare is the side effect of muscle problems. The symptoms are muscle soreness, pain, and weakness. If this happens, or you have brown urine, contact your doctor right away to get blood tests for possible muscle problems.

Acne |A Full File

2005-11-12T16:33:00.000+04:00

What Is Acne?
Acne is a disease that affects the skin's oil glands. The small holes in your skin (pores) connect to oil glands under the skin. These glands make an oily substance called sebum. The pores connect to the glands by a canal called a follicle. Inside the follicles, oil carries dead skin cells to the surface of the skin. A thin hair also grows through the follicle and out to the skin. When the follicle of a skin gland clogs up, a pimple grows.
Most pimples are found on the face, neck, back, chest, and shoulders. Acne is not a serious health threat but, it can cause scars.
How Does Acne Develop?
Sometimes, the hair, sebum, and skin cells clump together into a plug. The bacteria in the plug causes swelling. Then when the plug starts to break down, a pimple grows.
There are many types of pimples. The most common types are:
Whiteheads. These are pimples that stay under the surface of the skin.
Blackheads. These pimples rise to the skin's surface and look black. The black color is not from dirt.
Papules. These are small pink bumps that can be tender.
Pustules. These pimples are red at the bottom and have pus on top.
Nodules. These are large, painful, solid pimples that are deep in the skin.
Cysts. These deep, painful, pus-filled pimples can cause scars.

Over-the-Counter Products
Used to treat mild, moderate and severe acne, the effectiveness of over-the-counter medications lies in the product’s active ingredient(s). Not all active ingredients work the same way. The active ingredient benzoyl peroxide reduces P. acnes; whereas, salicylic acid helps correct abnormal skin shedding. For lesions to clear, the product(s) must be effective against the factor(s) causing the acne. The following describes common active ingredients used in over-the-counter acne medications sold in the United States. Check with your dermatologist or pharmacist before combining acne products.
Alcohol and acetoneFound together in some over-the-counter medications used to treat acne, acetone works as a degreasing agent and alcohol has mild antimicrobial properties. When used alone, acetone tends to have no effect.
Benzoyl peroxideThe mainstay of over-the-counter acne treatment, benzoyl peroxide works to clear up acne by reducing P. acnes and removing dead cells from the skin to prevent comedones. It was one of the first agents found to be effective in treating mild acne and has been used in acne treatment for decades. The principal side effect is excessive dryness of the skin, so be sure to follow directions and not use more than stated unless otherwise instructed by a physician. Care should also be taken when applying it to avoid the bleaching effect. Benzoyl peroxide has been known to bleach hair, sheets, towels and clothing. For this reason, an old shirt should be worn after applying benzoyl peroxide to acne on the back or chest. Benzoyl peroxide is available over-the-counter as a lotion or gel. Use of benzoyl peroxide should be continued after acne clears to prevent new lesions from forming.
“Herbal,” “organic” and "natural" productsOver-the-counter products labeled “herbal,” "organic" or "natural" are marketed as acne treatments but their effectiveness has rarely been tested in clinical trials. The value of such treatments is generally unknown.
ResorcinolA popular ingredient in over-the-counter acne medications, resorcinol controls small acne lesions and is frequently combined with sulfur in over-the-counter products.
Salicylic acidEffective in treating non-inflammatory acne lesions, salicylic acid helps correct the abnormal shedding of skin cells and unclog pores to resolve and prevent lesions. Salicylic acid does not have any effect on sebum production or P. acnes. Like benzoyl peroxide, salicylic acid must be used continuously. Once stopped, pores clog and acne returns. Salicylic acid is found in many over-the-counter acne products, including lotions, creams and pads. It may be irritating to the skin.
SulfurSulfur has been used for more than 50 years in combination with other agents, such as alcohol, salicylic acid and resorcinol and is found in many over-the-counter acne medications. While long used to treat acne, it is not known how sulfur works to clear acne. Due to its unpleasant odor, sulfur is not frequently used alone as an acne treatment.

Prescription Medications for Treating Acne
A variety of prescription medications are used today to clear acne. Topical (applied to the skin) medications may be prescribed for mild to severe acne. Systemic (works internally) therapy is needed to treat severe acne and may be used for moderate cases. These medications, which play an important role in acne treatment, attack the different factors that lead to acne. To achieve long-term control and resolution, dermatologists may combine therapies. The following describes the prescription medications used in the United States to treat acne:
Interlesional Corticosteroid InjectionWhen an acne cyst becomes severely inflamed, there is a good chance that it will rupture and scarring may result. To treat these severely inflamed cysts and prevent scarring, dermatologists may inject such cysts with a much-diluted corticosteroid. This lessens the inflammation and promotes healing. An interlesional corticosteroid injection works by "melting" the cyst over a period of 3 to 5 days.
IsotretinoinIsotretinoin is a potent oral retinoid that is reserved for treatment of very severe cystic acne and severe acne that has proven itself resistant to other medications. For more information about isotretinoin, see Treating Severe Acne.
Oral AntibioticsFor patients with moderate to severe and persistent acne, oral antibiotics have been a mainstay of therapy for years. Like topical antimicrobials, oral antibiotics work to reduce the P. acnes population (a contributing factor in acne), which, in turn, decreases inflammation. Treatment with oral antibiotics usually begins with a higher dosage, which is reduced as acne resolves. Generally, antibiotics are prescribed for six months or less.
Over time, the P. acnes bacteria can become resistant to the antibiotic being used to treat it. When resistance occurs, acne is no longer controlled. Another antibiotic or alternative treatment can be prescribed. Numerous studies support the effectiveness of the following oral broad-spectrum antibiotics, which are used to treat acne in the United States:
Erythromycin. It is effective against a broad spectrum of bacteria, including P. acnes. The most common side effect is irritation of the gastrointestinal tract.
Tetracycline and derivatives. Tetracyclines reduce the papules and pustules (inflammatory lesions) of acne. These medications should not be taken by children younger than 8 years of age because they can affect growth and stain teeth. They should also not be taken by a woman who is pregnant or breast feeding. During pregnancy and breastfeeding, tetracyclines can affect the development of the child’s bones and teeth, leading to skeletal defects.
A typical tetracycline regimen for treating moderate to severe acne starts with a dose of 500 to 1000 milligrams a day, which is decreased as improvement occurs. Long-term, low-dose tetracycline therapy may be continued for many months to suppress acne. Higher doses may be prescribed for very severe acne.
Two synthetic derivatives of tetracycline used to treat acne are doxycycline and minocycline. Doxycycline proves especially effective in treating inflammatory acne. It can cause sun sensitivity in some patients. Minocyline has a long history of use in treating acne. It is often effective in treating acne that has not responded to other oral antibiotics. Minocycline also seems to produce fewer incidents of antibiotic resistance.
Oral ContraceptivesOral contraceptives have been shown to effectively clear acne in women by suppressing the overactive sebaceous glands and can be used as long-term acne therapy. However, oral contraceptives should not be prescribed to women who smoke, have a blood-clotting disorder, are older than 35 or have a history of migraine headaches—without the advice of a gynecologist.
Topical AntimicrobialsTopical antimicrobials work to inhibit the P. acnes populations and are used to treat patients with mild to moderately severe inflammatory acne. They may be used alone or combined with a medication that works on another factor that leads to acne aside from P. acnes. A dermatologist can determine whether a topical antimicrobial is appropriate for a patient and if so which topical antimicrobial should be prescribed. Prescription topical antimicrobials used to treat acne vulgaris in the United States include:
Azelaic acid. Naturally occurring in the skin, azelaic acid is used to treat mild to moderate inflammatory and non-inflammatory acne. It is believed that azelaic acid clears acne by reducing the populations of P. acnes, decreasing the abnormal shedding of skin cells and reducing inflammation. This medication has also proven effective in treating the dark spots that develop in some acne patients with skin of color. Azaleic acid is well tolerated by most people and can be safely used for years. Side effects may include skin dryness and lightening of the skin where applied.
Benzoyl peroxide. Benzoyl peroxide works by killing P. acnes. However, it does not have anti-inflammatory abilities. It is available in a wide range of strengths and can be found as a gel, lotion, cleanser, cream and wash. Many acne preparations include benzoyl peroxide because research shows that benzoyl peroxide increases the effectiveness of some medicines, such as erythromycin and clindamycin. When used in combination with antibiotics, benzoyl peroxide also reduces the likelihood of a patient developing resistance to the antibiotic. The most common side effects are skin irritation, the potential to bleach hair and fabrics as well as possible allergic reaction.
Clindamycin. A semi-synthetic antibiotic, topical clindamycin has a long history of successfully treating acne. It works by reducing P. acnes and decreasing inflammation. In topical form, clindamycin has proven safe and is well tolerated. Skin dryness and irritation are possible side effects. It is important to use as directed to decrease bacterial resistance that can occur with antibiotic use.
Erythromycin. This topical antibiotic is active against a broad spectrum of bacteria, including P. acnes. Topical erythromycin, which is an antimicrobial and anti-inflammatory, is used primarily to treat acne. When topical erthyromycin is combined with benzoyl peroxide, the combination proves to be quite effective as the patient gets the effects of two antimicrobial agents. Like topical clindamycin, erythromycin may cause skin dryness and possible irritation. It is important to use as directed to decrease bacterial resistance that can occur with antibiotic use.
Sodium sulfacetamide. A topical antibiotic that inhibits P. acnes and opens clogged pores, sodium sulfacetamide is effective in treating inflammatory acne. Many products containing sodium sulfacetamide include sulfur. Some patients do not like the smell of the sulfur or its grittiness. Usually, the newer products that contain sulfur do not have these problems.
Topical RetinoidsPrescribed to treat acne ranging from mild to moderately severe, topical retinoids are a derivative of vitamin A and considered a cornerstone in acne treatment. Retinoids work to unclog pores and prevent whiteheads and blackheads from forming. Topical retinoids can irritate the skin and increase sun sensitivity so it is important to use sun protection and follow the dermatologist’s directions to maximize effectiveness. An added benefit in using topical retinoids is that they may help diminish the signs of aging, such as fine lines and wrinkles. Topical retinoids currently prescribed for acne treatment in the United States include:
Adapalene. A synthetic retinoid applied as a gel or cream, adapalene unclogs pores and possesses moderate to potent anti-inflammatory abilities. Improvement is usually seen in 8 to 12 weeks. Side effects include minor skin irritation and dryness.
Tazarotene. A synthetic retinoid available as a gel or cream, it works to keep the skin’s pores clear and has proven effective in treating acne. This medication should not be used by women who are pregnant, and effective contraception is needed while taking tazarotene because the medication has produced birth defects in animals. Skin irritation is a possible side effect.
Tretinoin. The first retinoid developed for topical use, tretinoin is a natural retinoid. It works to gradually unclog pores and keep them unplugged. In the past, many patients found tretinoin too harsh for their skin; however, the newer forms are proving less irritating. Side effects include redness, scaling, dryness, itching and burning. If these occur, talk with the dermatologist who prescribed tretinoin as these side effects can be managed by adjusting the amount applied and when it is applied.

What Things Can Make Acne Worse?
Some things can make acne worse:
Changing hormone levels in teenage girls and adult women 2 to 7 days before their period starts
Leaning on or rubbing the skin
Pressure from bike helmets, backpacks, or tight collars
Pollution and high humidity
Squeezing or picking at pimples
Hard scrubbing of the skin.

What Are Some Myths About the Causes of Acne?
There are many myths about what causes acne. Dirty skin and stress do not cause acne. Also, chocolate and greasy foods do not cause acne in most people.

Refferences:

http://www.niams.nih.gov/hi/topics/acne/ffacne.htm

http://www.skincarephysicians.com/acnenet/prescriptmeds.html

http://www.skincarephysicians.com/acnenet/treatotc.html

Studies Suggest Aspirin Resistance is More Common Than Once Believed

2005-11-12T16:10:00.000+04:00

Two studies presented at the European Society of Cardiology Congress 2003 suggest that aspirin resistance is not only real, but also likely to be more common that once believed.
Robert Gabor Kiss, MD, PhD, from the National Center for Health Services in Budapest, Hungary, presented the finding that in Hungary "26.9% of the population is at risk for aspirin resistance." Thus, he said, it is shortsighted to rely on aspirin for secondary prevention.
This message was reiterated by Tina Poulsen, MD, PhD, a research fellow at Odense University Hospital in Denmark. Dr. Poulsen and colleagues took blood samples from patients admitted to her hospital with a suspected diagnosis of myocardial infarction (MI) and who were receiving aspirin therapy (150 mg/day) prior to admission. Blood from 298 patients was analyzed for "biochemical evidence of aspirin activity, that is, we measured platelet aggregation," she told Medscape.
Although all the patients were taking aspirin, "we could not find any evidence of aspirin biochemical activity in 36% of the patients with confirmed MI." And in patients who did not have an acute event, "19% had no evidence of aspirin activity," she said.
Dr. Kiss and colleagues also used a blood test to measure platelet aggregation and found similar results. They measured platelet reactivity in 2,275 patients — 2,215 patients receiving aspirin therapy, 100 to 325 mg/day, and 60 patients receiving ticlopidine 500 mg — and compared those results with platelet activity in blood samples taken from 150 MI or stroke survivors who were not receiving blood-thinning therapy. The patients were recruited at 10 participating centers.
Platelet activity was measured on a computerized Carat TX4 platelet aggregometer using fixed doses of different inductors (ADP 5 µM, collagen 2 µg/mL, epinephrine 10 µM, arachidonic acid 0.5 mM). The threshold of the measurable inhibition was defined as the mean of maximal aggregation percentage minus 2 standard deviations of the maximal values in the untreated controls. The patients were considered resistant if the results of their maximal aggregation were higher than the predetermined threshold.
Of 2,215 patients with cardiovascular disease taking aspirin alone for secondary prevention, 596 (26.9%) showed resistance compared with 4 of 60 ticlopidine patients, Dr. Kiss said.
Although both Drs. Kiss and Poulsen said they were convinced that aspirin resistance is real, both believe it is too soon to recommend universal testing to determine aspirin resistance. Moreover, Dr. Poulsen said that even if a patient is aspirin resistant by platelet aggregation measures, she "would not stop the aspirin because we really don't know if other activity of aspirin — for example, anti-inflammatory activity — could provide protection."
Freek W. A. Verheugt, MD, PhD, professor of cardiology at University Medical Center in Nijmegen, the Netherlands, told Medscape that there is a certain logic to the concept of aspirin resistance since "we have patients on aspirin and yet they have a second event. That suggests some resistance or some reason that aspirin is not enough to stop the thrombotic activity."
But Dr. Verheugt, who was not involved in the study, agreed that it would be premature to order lab tests for all aspirin patients, because "we don't have enough information. For example, perhaps something else is interfering with the aspirin." He noted that there are data to suggest that nonsteroidal anti-inflammatory drugs can interfere with aspirin's antiplatelet action and "smoking also blunts the effect of aspirin."
Nonetheless, he said that if patients have "recurrent events while on aspirin, it would be prudent to consider tailoring the therapy to add another antiplatelet."