2011, nr. 3 - Academia de Ştiinţe a Moldovei

Ştiinţe MedicaleIndiferent de rezultatele studiilor, fumatul nu va fi recomandatbolnavilor cu CU, deoarece efectul asuprabolii se nivelează de acţiunea nefavorabilă asupra sistemelorcardiovascular şi respirator.Totalizând cele expuse, putem presupune că factoriide mediu, asociaţi cu BII, posibil, îşi exercită acţiuneaprin intermediul florei intestinale (spre exemplu,particularităţile alimentaţiei, factorii igienici etc.)şi al sistemului imun, iar dereglările florei intestinaleşi ale statutului imun la persoanele cu susceptibilitategenetică conduc spre apariţia inflamaţiei cronice înintestin.Concluzii. Interacţiunile dintre susceptibilitateagenetică, caracterul atacului antigenic al microfloreiintestinale şi caracterul răspunsului imun la aceastăagresiune antigenică sunt mecanisme complexeşi necesită studiere în continuare. În mod schematicaceste legături sunt reprezentate în figura 2. Caracterulşi particularităţile acestor interacţiuni, probabil,determină nu doar apariţia BII, dar şi fenotipul bolii,exprimat prin varianta clinico-evolutivă.Bibliografie selectivă1. Lakatos P. Environmental factors affecting infl ammatorybowel disease: have we made progress? In: Dig.Dis., 2009, 27(3), p. 215-225.2. Kaser A., Zeissig S., Blumberg R. Genes and environment:how will our concepts on the pathophysiologyof IBD develop in the future? In: Dig. Dis., 2010, 28(3), p.395-405.3. Fiocchi C. The multifactorial pathogenesis of IBD.Inflam. bowel disease – Diagnostic and therapeutic strategies.Falk Symposium 154. Moscow, 2006, p. 21-22.4. Kirsner J.B., Spencer J.A. Family occurrence ofulcerative colitis, regional enteritis, and ileocolitis. In:Ann. Intern. Med., 1963,; 59, p. 133-144.5. Jewell D.P. Genetic basis of infl ammatory boweldisease. Inflammation in the intestinal tract: pathogenesisand treatment. Falk symp. 169, 2009, Kiev, p. 17-19.6. 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