Detection of Helicobacter pylori cagA gene by polymerase chain reaction infaecal samples

Objective The polymerase chain reaction (PCR) has been extensively and succ essfully used to detect Helicobacter pylori in gastric juice and gastric bi opsies. In contrast, the results obtained using faeces as biological sample s for PCR are rather conflicting. This may be due to the presence of faecal inhibitory compounds (polysaccharides) which can inhibit the amplification reaction. The aim of this study was to characterize the H. pylori genotype in faecal samples by using specific primers for the cagA gene. To overcome the problem of contamination by polysaccharides, we used a filter-based ex traction technique already applied in a previous study, Methods Antral and body biopsies were obtained from 30 symptomatic patients undergoing upper endoscopy, PCR was used to detect the presence of H. pylo ri organisms in faecal samples by using primers selected for the urease gen e A. In addition, H. pylori organisms were characterized both in faecal sam ples and paraffin-embedded biopsies by PCR with specific primers for the ca gA gene. Results All patients showed a positive CLO test (rapid urease test) and evi dence of H. pylori by Warthin-Starry stain, PCR detected the urease A gene in the faecal samples of all patients, The cagA gene was detected in the fa ecal and biopsy samples of 18 subjects (60%). Duodenal ulcer and/or antral erosions were observed in 15 of the 18 cagA-positive patients (83.3%) and i n five of the 12 cagA-negative patients (41.7%). Endoscopic features of nor mal mucosa or gastritis were observed in three cagA-positive patients (16.7 %) and in seven cagA-negative patients (56.3%). cagA-positive status was fo und to be significantly related to the endoscopic features of duodenal ulce ration and/or antral erosions. Conclusions Our findings prove that faeces are suitable samples for the det ection of cagA status. Moreover, they confirm the existence of a significan t relationship between cagA-positive status and duodenal ulcer and/or antra l erosions. Eur J Gastroenterol Hepatol 11:251-256 (C) 1999 Lippincott Will iams & Wilkins.