title: Course of gut inflammation in spondylarthropathies and therapeutic consequences.
abstract: Gut inflammation plays a crucial role in the pathogenesis of spondylarthropathies (SpA) since ileocolonoscopic studies have demonstrated the presence of gut inflammation in different forms of this concept: in ankylosing spondylitis (AS) (60%), in enterogenic (90%) and urogenital reactive arthritis (20%), in undifferentiated SpA (65%), in the pauciarticular and axial forms of psoriatic arthritis (16%), in late onset pauciarticular juvenile chronic arthritis (80%) and in acute anterior uveitis (66%). The strong relationship between gut and joint inflammation was demonstrated by performing a second ileocolonoscopy: remission of the joint inflammation was always connected with a disappearance of gut inflammation, whereas persistence of locomotor inflammation was mostly associated with the persistence of gut inflammation. During further evolution 20% of the non-ankylosing spondylitis SpA patients can develop AS. About 6% of the total group SpA patients, in whom inflammatory bowel disease (IBD) was excluded, developed Crohn's disease 5 to 9 years later. All these patients initially presented with gut inflammation, which indicates that this finding has prognostic value. The high prevalence of evolution to IBD in SpA patients confirms the thesis that both disease entities bear common pathogenic mechanisms, and confirms the place of IBD in the concept of SPA. Sulphasalazine (SASP), a successful drug in the treatment of IBD, has demonstrated its effectiveness in the treatment of SpA. The beneficial effect of the drug in this disease entity could be due to its anti-inflammatory effect on the gut wall, by normalizing its permeability and by preventing the entrance of antigens through the defective gut wall. However, SASP could not prevent the evolution to IBD.
authors.affiliation: Department of Rheumatology, University Hospital, Ghent, Belgium.
authors.forename: H
authors.initials: H
authors.lastname: Mielants
authors.forename: E M
authors.initials: EM
authors.lastname: Veys
authors.forename: C
authors.initials: C
authors.lastname: Cuvelier
authors.forename: M
authors.initials: M
authors.lastname: De Vos
mesh_terms: D001172:Arthritis, Rheumatoid / Q000473:pathology* / Q000628:therapy*; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000473:pathology* / Q000628:therapy*; D013167:Spondylitis, Ankylosing / Q000473:pathology / Q000628:therapy; D014605:Uveitis / Q000473:pathology / Q000628:therapy