משכחי כאבים פוגעים במערכת החיסון

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13/12/2006 | 12:05 | מאת: א

Some nonsteroidal anti-inflammatory drug (NSAID) painkillers may react with the immune system in a way that reduces the effectiveness of flu shots AND other types of vaccines, a University of Rochester study finds. The researchers said this is an important finding because an estimated 50 percent to 70 percent of Americans use NSAIDs for relief from pain AND inflammation. "For years, we have known that elderly people are poor responders to the influenza vaccine AND vaccines in general," principal investigator Richard P. Phipps, a professor of environmental medicine AND of microbiology AND immunology, said in a prepared statement. "And we also know that elderly people tend to be heavy users of inhibitors of cyclooxygenase such as Advil, aspirin, OR Celebrex. This study could help explain the immune system response problem," Phipps said. He AND his colleagues conducted studies on mice AND analyzed samples of blood from people who took part in early clinical trials of a new vaccine against human papillomavirus (HPV), which can cause cervical cancer. They found that some NSAIDs hinder a vaccine's ability to prompt the immune system to produce antibodies against a specific illness/infection. The researchers said their findings suggest that it may be wise for people to avoid taking any NSAIDs when they receive any vaccine. The study was published in the Dec. 1 online issue of the Journal of Immunology.

לקריאה נוספת והעמקה

מחקרים רפואיים מראים שמעכבי קוקס-2 הם בעלי פעילות אנטיאנגיוגנטית ופרו אפופטוטית ופועלים בצורה זו לעכב התפתחות גידולים ממאירים. מחקרים אחרים מראים שתרופות אלה מונעות התפתחות תהליכים סרטניים בגוף ומשפרים את הטיפול בתרופות כימותרפיות. ד"ר יוסף ברנר

13/12/2006 | 12:52 | מאת: א

אין ארוחות חינם. תרופות שמועילות ל א' פוגעות ב ב', ולהיפך. J Cardiovasc Pharmacol. 2006;47 Suppl 1:S76-81. Coxibs AND cancer prevention. • Yona D, • Arber N. Integrated Cancer Prevention Center, Tel Aviv Medical Center AND Sackler School of Medicine, Tel Aviv University, Israel. Preventive medicine is becoming a cornerstone in our concept of health. This is especially significant in regard to cancer, as cancer is predicted to become the leading cause of death, surpassing heart disease, by the end of this decade. The prevention of colorectal cancer (CRC) has become an important public health goal because of the high incidence of CRC, with more than 945,000 new cases expected worldwide in 2006, AND the considerable mortality AND morbidity associated, with more than 492,000 deaths expected worldwide in the same year. The past 2 decades have seen the emergence of chemopreventive agents that have 1 of 3 effects: inhibiting, delaying, OR reversing carcinogenesis. Notwithstanding a substantial body of evidence suggesting an inverse relationship between aspirin OR nonsteroidal anti-inflammatory drug use AND CRC incidence AND mortality, the use of traditional nonsteroidal anti-inflammatory drugs in the chemoprevention of CRC is limited by their gastrointestinal toxicity. The favorable gastrointestinal safety profile of selective cyclooxygenase-2 inhibitors has therefore made them particularly attractive for this purpose. There has been concern, however, that selective cyclooxygenase-2 inhibitors may increase the risk of cardiovascular events, possibly by reducing endothelial prostacyclin production while leaving platelet thromboxane A2 generation unopposed. In the intriguing jigsaw puzzle of cancer prevention, we now have a definite positive answer for the basic question "if," but several other parts of the equation (proper patient selection, ultimate drug, optimal dosage, AND duration) are missing. The most challenging task is to find the proper place for these interventions in the entire effort of cancer prevention, in subjects at risk for colorectal neoplasia, AND in those at risk for other tumors. The achievement of this important goal may contribute to the conversion of CRC into a truly preventable disease ---------------------------------------- 1: Annu Rev Med. 2006 Nov 13; [Epub ahead of print] NSAIDs AND Cancer Prevention: Targets Downstream of COX-2. • Cha YI, • Dubois RN. Department of Medicine, Cell AND Developmental Biology AND Cancer Biology, Vanderbilt University Medical Center AND Vanderbilt Ingram-Cancer Center, Nashville, Tennessee 37232-2279. Preclinical AND clinical studies have clearly shown a benefit of nonsteroidal anti-inflammatory drug (NSAID) use in reducing cancer risk. However, the adverse gastrointestinal AND cardiovascular side effects associated with NSAIDs AND COX-2 selective inhibitors (coxibs) have provoked more scrutiny of the precise role of specific downstream mediators in the prostaglandin (PG) signaling cascade. NSAIDs AND coxibs inhibit PG biosynthesis. One of the PGs produced at high levels in the tumor microenvironment is PGE2, which is thought to play a major role in cancer progression. Thus, a better understanding of PGE2 signaling could enable identification of novel AND safer therapeutic targets downstream of the cyclooxygenase enzymes. We review the emerging molecular mechanisms by which COX-2-derived PGE2 is involved in cancer progression AND delineate potential opportunities for development of novel pharmacologic approaches utilizing this pathway. Expected online publication date for the Annual Review of Medicine Volume 58 is January 7, 2007. Please see http://www.annualreviews.org/catalog/pub_dates.asp for revised estimates.

13/12/2006 | 13:16 | מאת: סקרנית

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