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Researchers resolve how COX inhibitors cause heart hazards, and offer alternative treatment strategy
April 14, 2006Inhibitors of cyclooxygenase-2 (COX-2) were developed to relieve inflammatory pain as effectively as nonsteroidal anti-inflammatory drugs (NSAIDS), but without one of their major side effects, gastrointestinal bleeding. However, an unexpected adverse cardiovascular effect - a higher incidence of myocardial infarction - was subsequently detected, causing the highly publicized withdrawal of COX-2 inhibitors from the market in late 2004. A number of large, randomized, controlled trials designed to test the efficacy of different COX-2 inhibitors for a variety of indications have confirmed the cardiovascular toxicity, suggesting that this is an effect of all drugs in this class. However, just how this class of drug causes this heart hazard has remained controversial. Now, in a study appearing online on April 13 in advance of print publication in the May issue of the Journal of Clinical Investigation, Garret FitzGerald and colleagues from the University of Pennsylvania School of Medicine report how COX-2 inhibitors increase the incidence of myocardial infarction and stroke. In addition, they propose a new therapeutic approach that retains the beneficial anti-inflammatory effects of NSAIDS and COX-2 inhibitors, while avoiding their adverse cardiovascular consequences.
COX-2 inhibitors are believed to exert both their beneficial and their adverse effects by suppression of COX-2-derived prostacyclin (PGI2) and prostaglandin E2 (PGE2). These substances help prevent platelet clumping in blood vessels and vessel relaxation and/or constriction, respectively. Therefore, the challenge has been to identify a mechanism whereby PGI2 and PGE2 expression can be suppressed while avoiding adverse cardiovascular events. FitzGerald and colleagues now show that selective inhibition, knockout, or mutation of COX-2, or deletion of the receptor for COX-2-derived PGI2, accelerates the formation of blood clots and elevates blood pressure in mice. These responses were attenuated by COX-1 knock down, which mimics the beneficial effects of low-dose aspirin.
PGE2 biosynthesis is catalyzed by the coordinate actions of COX enzymes and microsomal PGE synthase-1 (mPGES-1). In the effort to propose an alternative therapeutic option to COX-2 inhibitors, FitzGerald et al. showed that deletion of mPGES-1 suppressed PGE2 expression, augmented PGI2 expression, but most importantly, affected neither blood clotting nor blood pressure. These results suggest that inhibitors of mPGES-1 may offer anti-inflammatory efficacy by depressing PGE2, while avoiding the adverse cardiovascular consequences associated with COX-2-mediated PGI2 suppression.
Journal of Clinical Investigation
Journal of Clinical Investigation
Nasal polyps from analgesics
If a patient develops respiratory problems after taking analgesics, this indicates that the active substances are poorly tolerated.
Fighting cancer with aspirin?
When looking for new weapons in the war on cancer, scientists should turn to their medicine cabinets for an age-old remedy-aspirin. According to scientists at the University of Newcastle (UK), aspirin has cancer-fighting effects that extend beyond already understood Cox inhibitors.
Pick your COX partners
Researchers at the University of Pennsylvania School of Medicine and Queen's University, Ontario, Canada report in the online edition of Nature Medicine this week that the COX enzymes — well-known for their contrasting role in cardiovascular biology — interact physically to form a previously unrecognized biochemical partnership and function in the development of blood vessels in a mouse model.
Blocking the nerve receptor EP1 in mouse models reduces brain damage caused by stroke
Researchers at Johns Hopkins have discovered how to block a molecular switch that triggers brain damage caused by the lack of oxygen during a stroke.
New arthritis drugs less likely to cause side effects
A new group of arthritis drugs recommended by NICE for patients at risk of gastrointestinal complications may be safer than traditional drugs, research in this week's BMJ suggests. Claims that the drugs, known as selective COX2 inhibitors, caused fewer gastrointestinal problems than traditional arthritis drugs led to an increase in their use, but the research on which they were based was criticised. Two studies in this week's BMJ, however, show that the risk of gastrointestinal complications associated with selective COX 2 inhibitors is lower than that associated with conventional non-steroidal anti-inflammatory drugs (NSAIDs). In the first study researchers in Oxford reviewed all trials of
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Understanding Osteoarthritis and its Treatments Musculoskeletal disorders are the most common cause of severe long-term pain and physical disability, affecting hundreds of millions of people worldwide. Diseases of the joints are the leading chronic condition in the elderly; almost one of every 8 Americans and almost 50% of people over 65 years of age have osteoarthritis, also known as degenerative joint disease. Doctors Genovese, Andriacchi, Smith and Goodman join together to describe the wide variety of Stanford's cutting edge basic and applied research to elucidate the causes and progression of arthritis and formulate new treatments for earlier diagnosis and treatment. They present a vision of the future where people with arthritis will experience decreased pain and improved mobility and function as a result of this work. |
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COX-2 inhibitors intensify aspirin's gastric effects: even at low doses. (Gastroenterology).: An article from: Internal Medicine News by Robert Finn (Author) This digital document is an article from Internal Medicine News, published by International Medical News Group on April 1, 2003. The length of the article is 374 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser. Citation Details Title: COX-2 inhibitors intensify aspirin's gastric effects: even at low doses. (Gastroenterology). Author: Robert Finn Publication: Internal Medicine News (Magazine/Journal) Date: April 1, 2003 Publisher: International Medical News Group Volume: 36 Issue: 7 Page: 55(1) Distributed by Thomson... | |
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