To study prospectively the clinical evolution of different forms of spondyloarthropathy (SpA) in relation to the type of gut histology in ileocolonoscopic biopsy specimens.
Ileocolonoscopy was performed in 217 patients with SpA (149 men, 68 women). Three types of gut histology (normal gut histology and acute and chronic inflammatory gut lesions) were found. Clinical, laboratory, and radiological examinations were performed at start and 2 to 9 years later in 123 patients who were regularly monitored. For the remaining 94 patients clinical data were obtained by telephone.
Of the 123 patients monitored regularly, 40 (32%) had normal gut histology, and 28 (23%) had acute and 55 (45%) chronic inflammatory gut lesions. Acute lesions were preferentially found in patients with non-ankylosing spondylitis SpA (non-AS-SpA). In the groups with normal gut histology and with chronic gut inflammation, patients with ankylosing spondylitis (AS) and non-AS-SpA were present in equal numbers. At review, clinical evolution was identical in the 3 histological subgroups. Eight patients developed idiopathic inflammatory bowel disease (IBD), one with initially acute gut inflammation, 7 with initially chronic gut inflammation. All had active AS at review. Fourteen patients with non-AS-SpA developed AS; 13 of them had initially presented inflammatory gut lesions. Three patients in the telephone group also developed IBD; all had active AS at review and initially presented chronic inflammatory gut lesions. Persistently high inflammatory serum variables, HLA-B27 negativity in the presence of sacroiliitis or AS, and inflammatory gut lesions at the first ileocolonoscopy indicate patients with SpA are at risk for developing IBD.
Gut inflammation, mainly subclinical, could be demonstrated in 68% of patients with SpA. Acute gut inflammation was predominant in patients with reactive arthritis (ReA). The evolution to clinical remission was not influenced by the presence or the type of gut inflammation at start. Patients with non-AS-SpA with inflammatory gut lesions have greater risk of developing AS. One patient with Yersinia induced ReA developed AS and IBD. In total, 11 patients (66%) developed IBD, all initially presenting inflammatory gut lesions. Ten had chronic gut lesions, suggesting this type of gut inflammation is related to the inflammation of Crohn's disease. This type of gut inflammation, the persistence of high inflammatory serum variables, and the absence of HLA-B27 in patients with AS are risk factors for developing IBD.