Please can you give a brief introduction to ulcerative colitis (UC) and Crohn’s disease (CD)?
Ulcerative colitis and Crohn’s disease are idiopathic (we don’t know the cause) inflammatory diseases (IBD) of the colon and/or small bowel. They are chronic in that we do not have a medical cure and are differentiated from IBS (irritable bowel syndrome) by inflammation that causes ulcerations of the GI tract.
The inflammation and ulceration lead to symptoms of bleeding, diarrhea, abdominal pain that may be associated with “systemic” symptoms of weight loss, fever, night sweats and/or “extraintestinal symptoms” such as joint pains and arthritis, skin nodules or ulcers, inflammation of the eye, or inflammation of the liver.
How many people are affected by inflammatory bowel disease (IBD) and what proportions are affected by UC and CD respectively?
It has been estimated that 1‐2 million Americans are affected with nearly the same numbers of patients with UC and CD.
How is IBD typically treated and do treatments usually differ for UC and CD?
The treatments for UC and CD overlap greatly and are determined by the location and severity of inflammation.
Patients with mild colitis (inflammation of the colon) are treated with 5‐ASA drugs such as sulfasalazine, mesalamine, olsalazine or balsalazide. In addition, budesonide, a locally active steroid can be targeted to the end of the small intestine or colon.
More moderate to severe disease is treated with prednisone, a systemic steroid and then once the disease is controlled, maintenance to prevent recurrent inflammation is treated long‐term with immunemodulating medications such as azathioprine, mercaptopurine or methotrexate.
Patients who don’t respond or cannot get off of steroids are treated with biologic agents that target a chemical of inflammation (TNF) or, most recently that target integrins on lymphocytes that prevent inflammatory cells from getting out of the blood stream and into tissues.
Please can you explain what a biologic therapy is?
In contrast to “conventional” therapies which are chemicals, biologic therapies are usually antibodies that have been created through cells or bacteria which can be designed to target protein structures.
How have biologics changed the treatment landscape for UC and CD?
Since the first introduction of infliximab (Remicade) in 1998 biologic therapy has significantly changed the prognosis for patients with moderate‐severe UC and CD by their ability to actually heal the intestinal ulcers and prevent subsequent ulcers from forming.
When we accomplish healing we prevent symptoms and subsequent complications and are able to reduce the need for surgery to remove affected segments of bowel.
Is there still a need for additional new treatment options for patients with moderately to severely active UC or CD?
While our current treatments are very effective and are able to improve and maintain the quality of life of the vast majority of our patients, there remain a sizeable proportion of patient who have an incomplete or inadequate response to even our most intensive therapies.
What do you think the future holds for UC and CD treatments?
We are getting smarter about how to “optimize” and “personalize” our current therapies for individual patients by measuring both blood levels and responses to treatment combinations and as we learn more about the immune and inflammatory processes we continue to develop more potent and, yet, safer treatments that can “target” (e.g. smart bombs) compounds and minimize the long‐term use of steroids that, while highly effective, are associated with the greatest number of side effects.
Where can readers find more information?
CCFA.org
About Stephen B. Hanauer, MD
Stephen B. Hanauer completed a medical degree, with honors, at the University of Illinois in Chicago. His postdoctoral training included an internship and residency in internal medicine, as well as a fellowship in gastroenterology, at the University of Chicago. He rose through academic ranks to become Professor of Medicine and subsequently was awarded the Joseph B. Kirsner Chair in Medicine and was designated Chief of the Section of Gastroenterology, Hepatology and Nutrition where he served from 2000-2014. He was recruited as the Medical Director of the Digestive Health Center at Northwestern Medicine and is Professor of Medicine in the Northwestern Feinberg School of Medicine as of January 1, 2014.
Dr. Hanauer is board certified in internal medicine and gastroenterology by the American Board of Internal Medicine and the American Board of Gastroenterology, respectively.
He holds membership in several professional societies and is a Fellow of American Gastroenterological Association, the American College of Gastroenterology and the American College of Physicians. In connection with the American Gastroenterological Association (AGA), Dr. Hanauer served as chair for the Inflammation, Immunology, and Inflammatory Bowel Disease Section, subsequently also serving as Councilor for Clinical Research on the governing board and as chair of the Clinical Practice Section. He is the current President-elect of the American College of Gastroenterology and a prior member of the Specialty Board of the American Board of Internal Medicine. Among his many honors, Dr. Hanauer received the AGA Fiterman Foundation Joseph B. Kirsner Award in Gastroenterology in 2001 and the Janssen Award for Clinical Excellence in 2004. He has served as a Member and Chair of the U.S. Food and Drug Administration Advisory Panel for Gastrointestinal Disorders and is a member and ex-Chairman of the International Organization for Inflammatory Bowel Disease.
Dr. Hanauer has authored hundreds of peer-reviewed journal articles, books and book chapters, abstracts, monographs, and editorials. Dr. Hanauer is ex-Editor-in-Chief of Nature Clinical Practice Gastroenterology & Hepatology and currently serves as Associate Editor (IBD) of Clinical Gastroenterology and Hepatology. He is also a member of the editorial boards of numerous journals, including the American Journal of Gastroenterology, and Inflammatory Bowel Diseases.
Genetic variant identified as potential predictor for severe ulcerative colitis