From basic science to future medical options for treatment of ulcerative colitis.
Both ulcerative colitis (UC) and Crohn's disease are considered the result of an unrestrained inflammatory reaction, but an explanation for the aetiopathogenesis has still not emerged. Until the predisposing and trigger factors have been clearly defined, therapeutic and preventive strategies for these disorders must, therefore, rely on interrupting or inhibiting the immunopathogenic mechanisms involved. Current therapies, such as glucocorticoids and 5-aminosalicylic acid, inhibit raised concentrations of interdependent, soluble mediators of inflammation, which may amplify one another or have parallel effects. Future medical options for treatment of UC aim at removing perpetuating antigens, blocking entry of inflammatory cells by manipulating adhesion molecules, targeting soluble mediators of inflammation by blocking proinflammatory molecules or by preserving endogenous suppressive molecules, or correcting genetic defects. It remains, however, to be determined whether targeting multi-inflammatory actions or a single key pivotal process is the better therapeutic strategy and whether subgroups of UC with different clinical courses will require different treatment approaches.
Rask-Madsen
J
J
Department of Medical Gastroenterology, Hvidovre Hospital, University of Copenhagen, Denmark.
D000917:Antibody Formation / Q000502:physiology*; D015551:Autoimmunity; D015815:Cell Adhesion Molecules / Q000502:physiology; D003093:Colitis, Ulcerative / Q000209:etiology* / Q000628:therapy*; D004195:Disease Models, Animal; D006801:Humans; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors*
D015815:Cell Adhesion Molecules; D018836:Inflammation Mediators