Biological therapy for inflammatory bowel disease information
Biological therapy, the use of medications called biopharmaceuticals or biologics that are tailored to specifically target an immune or genetic mediator of disease, plays a major role in the treatment of inflammatory bowel disease.[1] Even for diseases of unknown cause, molecules that are involved in the disease process have been identified, and can be targeted for biological therapy. Many of these molecules, which are mainly cytokines, are directly involved in the immune system. Biological therapy has found a niche in the management of cancer,[2][3] autoimmune diseases,[4] and diseases of unknown cause that result in symptoms due to immune related mechanisms.[5][6]
Inflammatory bowel disease (IBD), a collection of systemic diseases involving inflammation of the gastrointestinal tract,[7] includes two (or three) diseases of unknown causation: ulcerative colitis, which affects only the large bowel; Crohn's disease, which can affect the entire gastrointestinal tract; and indeterminate colitis, which consists of large bowel inflammation that shows elements of both Crohn's disease and ulcerative colitis.[8]
Although the causes of these diseases are unknown, genetic, environmental, immune, and other mechanisms have been proposed. Of these, the immune system plays a large role in the development of symptoms.[8] Given this, a variety of biological therapies (such as TNF inhibitors and interleukin antagonists) have been developed for the treatment of these diseases. Although the use of antibodies to treat diseases can be dated back to the 1800s, biologic therapy as we know it today is a relatively new concept for the treatment of inflammatory bowel disease.[9] The previous treatment options had many shortcomings, and the introduction of biological therapy changed the way physicians treat Crohn's disease and ulcerative colitis.[5][6] Even so, biologic therapy still has its faults such as high cost and risk of side effects. A lot of research is being done in fields like biosimilars and oral delivery to address these concerns.[10][11]
^Talpaz M, Kantarjian H, McCredie K, Trujillo J, Keating M, Gutterman JU (February 1987). "Therapy of chronic myelogenous leukemia". Cancer. 59 (3 Suppl): 664–7. doi:10.1002/1097-0142(19870201)59:3+<664::AID-CNCR2820591316>3.0.CO;2-Y. PMID 10822467. S2CID 29012197.
^Kalinski P, Mapara MY (June 2006). "9th Annual Meeting of the Regional Cancer Consortium for the Biological Therapy of Cancer. 16-18 February 2006, UPMC Herberman Conference Center, Pittsburgh, PA, USA". Expert Opinion on Biological Therapy. 6 (6): 631–3. doi:10.1517/14712598.6.6.631. PMID 16706609. S2CID 33990836.
^Weinblatt ME, Kremer JM, Bankhurst AD, Bulpitt KJ, Fleischmann RM, Fox RI, Jackson CG, Lange M, Burge DJ (January 1999). "A trial of etanercept, a recombinant tumor necrosis factor receptor:Fc fusion protein, in patients with rheumatoid arthritis receiving methotrexate". The New England Journal of Medicine. 340 (4): 253–9. doi:10.1056/NEJM199901283400401. PMID 9920948.
^ abHanauer SB, Feagan BG, Lichtenstein GR, Mayer LF, Schreiber S, Colombel JF, Rachmilewitz D, Wolf DC, Olson A, Bao W, Rutgeerts P (May 2002). "Maintenance infliximab for Crohn's disease: the ACCENT I randomised trial". Lancet. 359 (9317): 1541–9. doi:10.1016/S0140-6736(02)08512-4. PMID 12047962. S2CID 1905194.
^ abRutgeerts P, Sandborn WJ, Feagan BG, Reinisch W, Olson A, Johanns J, Travers S, Rachmilewitz D, Hanauer SB, Lichtenstein GR, de Villiers WJ, Present D, Sands BE, Colombel JF (December 2005). "Infliximab for induction and maintenance therapy for ulcerative colitis". The New England Journal of Medicine. 353 (23): 2462–76. doi:10.1056/NEJMoa050516. PMID 16339095.
^Hanauer SB (March 1996). "Inflammatory bowel disease". The New England Journal of Medicine. 334 (13): 841–8. doi:10.1056/NEJM199603283341307. PMID 8596552.
^ abPodolsky DK (August 2002). "Inflammatory bowel disease". The New England Journal of Medicine. 347 (6): 417–29. doi:10.1056/NEJMra020831. PMID 12167685.
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