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Objectives. Study the articular involvement present in inflammatory bowel disease, mainly in Crohn disease (CD) and ulcerohaemorrhagic rectocolitis (UHRC), the genetic and immune mechanism underlying the occurrence of these disorders and their complications, response to therapy, as well as the value of the immunoserology tests. Material and methods. The group of 204 patients that were monitored, consisted of two subgroups: 50 patients with CD, and 154 patients with UHRC and have been enrolled in a prospective longitudinal study. The patients were included in the study group according to strictly established criteria, taking into account the underlying inflammatory bowel disease that triggered the respective articular disorders, have been assessed according to a protocol including both individual parameters (clinical, biological), endoscopic, histopathologic, radiographs, RMN, CT evaluation. Results. 93 patients had joint manifestations. 65 of them had developed due articular lesions in ulcerative colitis and 28 Crohn's disease. In ulcerative colitis Joint damage occurred as follows: 58.5% sacroiliitis (38 cases), ankylosing spondylitis 7.7% (5) 10.7% acute arthritis (7). In Crohn's disease were detected: sacroiliac 35.8% (10 patients), 42.9% peripheral arthritis (12), acute arthritis 7.1% (2 cases), reactive arthritis 14.2% (4) with germs Salmonella (3) and Shigella (1). In 71 patients from those with articular manifestations of detecting the presence of HLAB27. Conclusions. Joint damage was correlated with the severity, type of inflammatory bowel disease (IBD) reflecting the state of activity. Joint manifestations were detected mainly in ulcerative colitis increased, unlike the literature. [ABSTRACT FROM AUTHOR]

Bolile inflamatorii intestinale (boala Crohn şi rectocolita ulcero-hemoragică) rămân un capitol deschis cercetării din cauza frecvenţei (în creştere în ultimele decade), particularităţilor clinico-evolutive a suferinţei digestive şi extradigestive, a enigmelor patogenetice, sursă a dificultăţilor terapeutice. Tipare genetice specifice, mutaţii genice favorizează răspuns imun aberant la antigeni din mediu sau la autoantigeni provocând o inflamaţie intestinală cu potenţial înalt de cronicizare; citokinele eliberate şi alte mecanisme încă necunoscute pot firesponsabile de manifestările extradigestive. Autorii sistematizează date recente privind patogeneza formelor clinico-evolutive, posibilităţi moderne de diagnostic, posibilităţile şi limitele măsurilor terapeutice moderne în artropatiile care însoţesc boala inflamatorie intestinală. [ABSTRACT FROM AUTHOR]