H. pylori Infection and Visceral Hypersensitivity in Patients with Irritable Bowel SyndromeGerards C.a · Leodolter A.a · Glasbrenner B.b · Malfertheiner P.a
aDepartment of Gastroenterology, Hepatology and Infectiology, Otto von Guericke University, Magdeburg, and bMedical Clinic II, St. Franziskus Hospital, Münster, Germany
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Background/Aim: Irritable bowel syndrome (IBS) is characterized by abdominal pain and changes in stool habits. Visceral hypersensitivity (VH) is a key factor in the pathophysiology of IBS. The role of Helicobacter pylori infection in the induction of VH in the upper gastrointestinal tract is controversially discussed. The aim of this study is to evaluate the value of rectal barostat in eliciting abdominal symptoms in patients with IBS in relation to H. pylori infection. Patients and Methods: 31 patients (19 female, 12 male, mean age 45.6 ± 10 years) with normal colonoscopy and clinical signs of IBS were examined by rectal barostat (pressure-controlled balloon distension in the rectum). Induction of typical abdominal discomfort (far from the balloon) defined the examination positive. Level of nonpainful perception (L1), feeling of defecation (L2), and pain or stool urgency (L3) were registered in comparison with a healthy control group (CG; n = 15, 9 female, 6 male). The H. pylori status was defined by 13C-urea breath test (n = 46). Results: Typical abdominal discomfort was induced in 9 patients (pain group, PG) by pressure-controlled rectal distension (H. pylori status: 8 positive, 1 negative). Patients not presenting with abdominal pain to rectal distension (nonpain group, NPG) were all H. pylori negative (p < 0.001). L3 as an indicator of VH was reached at a lower pressure threshold in PG than in NPG or CG (p < 0.05). The perception was not different between NPG and CG (p > 0.05). Conclusions: The induction of typical abdominal discomfort in patients with IBS by the use of rectal barostat occurred predominantly in H. pylori infected patients and suggests that H. pylori infection may be involved in triggering VH in patients with IBS. Further studies in larger patient groups and after H. pylori eradication therapy are needed to confirm and extend this observation.
© 2001 S. Karger AG, Basel
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