Effect of Helicobacter pylori and eradication therapy on gastrointestinal permeability. Implications for patients with seronegative spondyloarthritis.

Abstract

OBJECTIVE: Disruption of intestinal barrier function, followed by increased antigen load, may possibly trigger joint inflammation. In seronegative spondyloarthritis (SpA) both gut inflammation and altered intestinal permeability have been reported. We evaluated the influence of Helicobacter pylori and nonsteroidal antiinflammatory drugs (NSAID) on gastrointestinal (GI) permeability in SpA. Twenty SpA patients (7 women, mean age 47 +/- 13 SD yrs), 30 patients with endoscopic gastritis (EndG; 17 women, mean age 48 +/- 14 yrs), and 35 healthy controls (16 women, mean age 40 +/- 15 yrs) were studied. No patient was undergoing antisecretory therapy. In the SpA group, 8 patients were chronically taking NSAID and 12 took NSAID occasionally, none during the month before the study. All subjects were assessed for gastroduodenal (sucrose) and intestinal (lactulose/mannitol) permeability test and H. pylori status (urea breath test). RESULTS: H. pylori affected GI permeability in both SpA and EndG patients. After eradication therapy, sucrose excretion remained increased in SpA and reverted to normal in EndG patients, whereas lactulose/mannitol test became comparable to controls in both groups. SpA patients taking chronic NSAID had increased gastroduodenal permeability only when H. pylori-positive. In SpA patients, GI permeability did not correlate with clinical activity or biochemical inflammation. CONCLUSION: In SpA, H. pylori and NSAID contribute to impaired GI permeability. Eradication therapy may help to maintain epithelial barrier function and possibly influence clinical improvement in patients with SpA.