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Helicobacter pylori infection and peptic disease in coeliac disease

2000; Lippincott Williams & Wilkins; Volume: 12; Issue: 12 Linguagem: Inglês

10.1097/00042737-200012120-00004

1473-5687

Carolina Ciacci, Aniello Squillante, Domenico Rendina, Stefania Limauro, Carmela Bencivenga, Flora Labanca, Rita Romano, G. Mazzacca,

Microscopic Colitis

Objective To evaluateHelicobacter pylori(HP) and peptic disease prevalence in coeliac disease patients and in a control group. Design In the retrospective study, data collected on 690 upper endoscopies in coeliac patients, carried out between 1990 and 1997, were analysed. In the prospective study 263 consecutive adult patients were studied for follow-up of coeliac disease or suspected malabsorption/coeliac disease. Tests included routine blood tests; serum dosage of EMA; IgG anti-HP and, in a subgroup of participants, anti-CagA antibodies; upper endoscopy with multiple gastric and duodenal biopsies; histological examination of gastric and duodenal specimens with staining providing evidence for the presence of HP. Setting A centre for the treatment of malabsorptive diseases, University Federico II of Naples, Italy. Participants Adults with coeliac disease at the time of diagnosis and follow-up. Results In the retrospective study, peptic disease had a prevalence of 0.72% in the endoscopy series of coeliac patients examined. In the prospective study, the prevalence of HP infection was significantly lower in untreated coeliac patients when compared with treated patients and controls (20.7%, 32.4% and 55.3%, respectively;p= 0.001, X2). The prevalence of HP was related to both gender and age. It was found more frequently in men and the frequency increased with age in all groups. The study confirmed the low prevalence of peptic disease in coeliac patients compared with controls (0.9% vs 3.8%,p= 0.001). Conclusion Patients with coeliac disease show a significantly lower prevalence of HP infection and peptic disease when compared to controls. Gluten free diet-induced changes in the intestinal environment and/or the host immuno-response may explain the increased HP prevalence in treated coeliac patients.