Comparison of different permeability probes in patients with spondylarthropathy and noninflammatory rheumatic disease: What is the effect of NSAIDs?

Abstract

relates to the presence of CagA. The evolution of 1-1. pylori related gastritis was studied in relation to cagA and to duration of follow-up, in patients with either persistent or cured H. pylori infection. Dyspeptic patients entered the study starting in 1984. H. pylori infection was assessed by culture and histopathology of antral biopsies. The grading of activity of gastritis, superficial epithelial damag e (SED), atrophy and intestinal metaplasia (IM) was based on the updated Sydney classification. CagA status was determined by specific serum IgG antibodies. H. pylori eradication was attempted with bismuth-, or ppi-antibiotic combination therapies. Results of 265 patients were available for analysis. The median follow up was 5.3 years (range 1.1-12.5). Group I consisted of 124 patients with persisting H. pylori infection. Group II consisted of 141 patients in whom H. pylori eradication was achieved. CagA results were available in 185/265 patients (94 of group I; 91 of group II) of whom 140 (76%) were infected with a CagA ÷ strain. Pretreatment degrees of activity, SED, atrophy and IM were similar (ns) in group I and II. Higher degree of activity and SED was found in CagA+ infected patients (p < 0.0001). The degree of activity, SED, atrophy and IM remained unchanged over the years in group I. After successful H. pylori eradication, the degree of activity and SED improved significantly (p < 0.001), irrespective of the CagA status. The degree of atrophy improved from 2.2 to 1.2 (p < 0.001) in CagA+infected patients, however, the degree of atrophy remained unaffected in CagA-neg infected patients (from 1.8-1.6; ns). The degree of IM remained unchanged after successful H. pylori eradication, irrespective of the CagA status. Mean degrees of gastritis in group I and II, after a follow-up period less than 4 years or more than 4 years, were similar (ns). In conclusion, atrophy is partially reversible in CagA+infected patients, but IM remains unchanged. In CagA-neg H. pylori infection, atrophy and IM appeared irreversible. The length of follow-up in this cohort did not influence the observed degrees of activity, SED, atrophy and IM. Whether partial reversibility of atrophy will lead to reduction in cancer risk requires further prolonged observation.