Etiology and pathophysiology of inflammatory bowel disease - Environmentalfactors

Authors
Citation
T. Andus et V. Gross, Etiology and pathophysiology of inflammatory bowel disease - Environmentalfactors, HEP-GASTRO, 47(31), 2000, pp. 29-43
Citations number
256
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
HEPATO-GASTROENTEROLOGY
ISSN journal
01726390 → ACNP
Volume
47
Issue
31
Year of publication
2000
Pages
29 - 43
Database
ISI
SICI code
0172-6390(200001/02)47:31<29:EAPOIB>2.0.ZU;2-W
Abstract
Environmental factors play an important role in the pathophysiology of infl ammatory bowel disease. There is a strong and consistent association betwee n smoking and Crohn's disease, and between nonsmoking and ulcerative coliti s. Despite extensive research, the exact pathophysiological mechanisms for these associations remain unclear. In spite of this, some clinical trials w ith nicotine-patches showed beneficial effects for the treatment of ulcerat ive colitis. Associations of Crohn's disease and ulcerative colitis with ot her environmental factors are weaker like the association with use of oral contraceptives ol those less well investigated such as the association with childhood hygiene. Most studies suggesting a potential pathogenetic role o f Mycobacterium paratuberculosis or an effect of tuberculostatic therapy in Crohn's disease could not be reproduced by others. Perinatal or childhood infections by viruses like measles are heavily debated, but not proven to b e causal for inflammatory bowel disease. Coagulation disorders have been de scribed as protecting from inflammatory bowel disease, suggesting hypercoag ulability to be a pathogenetic factor. Some studies described that appendec tomy may prevent the onset of ulcerative colitis in man and mice. Other env ironmental factors such as hydrogen sulfide, tonsillectomy, diet, blood tra nsfusions, and Listeria also require confirmation. There are, however, conv incing data from genetic animal models and twin studies that environmental factors as the intestinal bacterial flora interact with susceptible hosts t o cause inflammatory bowel disease. Inflammatory bowel diseases have multif actorial etiologies, which require a differentiated approach for treatment and prevention.