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Rapid Responses to:
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Electronic letters published:
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Dr Shamsul A Bhuiyan, MBBS,MD. Mount Sinai School of Medicine(Cabrini), Dr Shah M. Mukhtadir, MD. Dr Shahabuddin Haq, MBBS
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drshamsulbd{at}gmail.com Dr Shamsul A Bhuiyan, et al.
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Colorectal cancer (CRC) is the third most common cancer in USA and 2nd leading cause of death overall with ninety percent occurring after the age of fifty. Twenty-five percent of patients have family history, and the question is, how effective would ASA be in this population as a preventive measure? Also people who have mutation in APC tumour suppressor gene, 100s to 1000s of polyps at young age, are 100% life time risk of developing colorectal cancer. Will this group of people get benefits if we use ASA as preventive measure? Same thing can be thought for HNPCC (hereditary non polyposis colorectal cancer—mutation in DNA mismatch repair genes). On the other hand, in the case of inflammatory bowel disease, ASA is shown to increase risk with increase extent and duration of disease. Since an ulcerative colitis patient has a chance to develop cancer, will this group benefit from ASA? No doubt that many peoples are on ASA because of their medical condition like CAD, S/P stent placements, TIA, atherosclerosis, headache, arthritis,and fever. These groups will get benefits as a protective measure for CRC somehow. The question is how beneficial would it would if ASA being used only as prophylaxis for CRC in general population considering all those disadvantages of ASA. Which would be better? Doing a colonoscopy in a patient that has risk factors or using ASA for long time only for preventive measure for CRC. In consideration of recurrence of adenoma, will it be really great to use rather than colonoscopy? Even if we use ASA for prevention and recurrence, ultimately we have to do sigmoidoscopy and colonoscopy that are diagnostic and therapeutic. There is no doubts that evidence pointing to an association between aspirin and reduced cancer risk is largely derived from epidemiologic studies, although laboratory experiments and a few clinical trials have provided support for this idea. Conflict of Interest:None declared |
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Mary B. Barton, M.D., M.P.P. Agency for Healthcare Research and Quality, Marion Torchia, Manuscript Coordinator
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mary.barton{at}ahrq.hhs.gov Mary B. Barton, et al.
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Editor Annals of Internal Medicine To the Editor: We want to respond to the complaint expressed by Dr. Til Sturmer and colleagues, regarding the posting on the AHRQ Web site of the report, “The Use of Aspirin to Prevent Colorectal Cancer: A Systematic Review.” The appendixes were inadvertently omitted from the Web posting. The mistake has been corrected, and the full systematic review is now available on the Web site at http://www.ahrq.gov/clinic/uspstf07/aspcolo/aspcoloes.pdf. We regret the frustration this error has caused. Sincerely, Mary B. Barton, M.D., M.P.P. Scientific Director U.S. Preventive Services Task Force Marion M. Torchia Manuscript Coordinator Agency for Healthcare Research and Quality Conflict of Interest:None declared |
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Til Sturmer, MD, MPH Brigham and Women's Hospital, Harvard Medical School, Til Sturmer, Julie E. Buring, and Robert J. Glynn
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til.sturmer{at}post.harvard.edu Til Sturmer, et al.
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The authors of the review papers on aspirin (1) and nonsteroidal anti -inflammatory drugs (NSAIDs) (2) for the primary prevention of colorectal cancer (CRC) ignore important limitations of observational studies, raise concerns unlikely to be valid (1), and fail to include the analysis on NSAIDs from the Physicians' Health Study (PHS) that was published in the time period covered (3). The authors correctly discuss shortcomings of randomized trials showing no protection in men and women, i.e. low dose and short duration (1). They fail, however, to address shortcomings of observational studies on regular long-term drug use, i.e. unmeasured confounding, as an alternative explanation for the reduced risk of CRC observed in most of these studies. Specifically, regular long-term drug use is associated with difficult to measure healthy characteristics. These healthy characteristics of long- term adherers may be associated with reduced risks independent of drug effects as evinced by reduced risks for many adverse outcomes in adherers to placebo. This can lead to paradoxical relations in observational studies (4). To reduce the magnitude of this problem, we excluded regular users of aspirin and NSAIDs from the PHS, thus studying only new regular users, and observed no reduction of CRC risk with aspirin (5) and NSAIDs (3). Unfortunately, the referenced detailed assessment of the quality of each of the studies (1,2) was not available from AHRQ or the authors. However, the authors mentioned concerns about our aspirin analysis in the PHS because of contamination by intervention and a reduced standardized mortality ratio for CRC compared with the U.S. population (1). Randomized aspirin treatment does not threaten the validity of our post-trial study of self-selected aspirin use. Any carry-over of putative aspirin effects would bias the results towards observing a reduced CRC risk in post-trial aspirin users. Reduced standardized morbidity ratios (5) are ubiquitous in volunteer studies and generally do not bias measures of relative risk. Finally, since only three cohort studies of NSAIDs and CRC are included in their analysis (2), the failure to include our observational study on NSAIDs and CRC in the PHS (3) largely reduces the value of the summary estimates. Taken together, we believe that the authors overstate the overall benefits from aspirin (1) and NSAIDs (2) on CRC. Putting greater weight on randomized evidence and observational studies with new- user designs would tip the harm to benefit balance even more towards harm for individuals at average risk for CRC. Conflict of Interest:None declared |
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