Inflammatory Bowel Disease
even a highly specific screening test will have a high false-positive rate, thereby leading to unnecessary worry and work-up, or potentially even surgery. Third, we do not understand the mechanism by which SBA arises, both in CD and in general. It has been suggested that SBA may develop as a consequence of dysplasia. However, small bowel surveillance for dysplasia is no small undertaking, especially in patients with fibrostenotic disease. Finally, the diagnosis of SBA in CD is rarely made pre-operatively, as symptoms are relatively non-specific and an alarming proportion of patients present with SBA within one year of CD diagnosis (some of whom did not even have prior symptoms of CD). For all these reasons, it would be very difficult and cost-ineffective to screen for SBA in patients with CD. What is most sorely needed is a way to detect these cancers earlier. n
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Mark T Osterman, MD, is Assistant Professor of Medicine at the University of Pennsylvania School of Medicine. A former Rickover Science Institute attendee and United States Presidential Scholar, he attended Harvard University and graduated magna cum laude with a degree in chemistry. After graduating from Harvard Medical School, he was a medical intern and resident at Brigham and Women’s Hospital in Boston, Massachusetts. He subsequently completed his gastroenterology fellowship at
the University of Pennsylvania and simultaneously completed master of science coursework at the Center for Clinical Epidemiology and Biostatistics. He then joined the faculty at the University of Pennsylvania, where he has focused his clinical practice and research on the study of inflammatory bowel disease. He has authored a number of publications and has given multiple talks in this field.
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