Helicobacter pylori and cagA gene detected by polymerase chain reaction in gastric biopsies: correlation with histological findings, proliferation and apoptosis
Abstract
CONTEXT AND OBJECTIVE: The virulence of Helicobacter pylori (HP) in gastroduodenal disease is related to pathogenicity islands (cagPAI) present in some strains. Infection with cagPAI induces IL-8 secretion, increases epithelial cell proliferation and may be important in carcinogenesis. Our objective was to detect HP and the cagA gene (cagPAI marker) by polymerase chain reaction (PCR) and to correlate these results to histological findings, epithelial cell proliferation and apoptosis. DESIGN AND SETTING: Retrospective, at the Surgical and Molecular Pathology Laboratory, Hospital Sírio-Libanês. METHODS: DNA samples isolated from 164 gastric biopsies were used for HP detection by PCR. cagPAI+ was identified in HP+ cases by cagA gene amplification. All cases were submitted to immunohistochemistry to evaluate cell proliferation, and TUNEL to detect apoptosis. Statistical analysis was performed to compare results. RESULTS: HP was detected in 67.7% of the patients, with good correlation between HP infection and moderate to severe gastritis, gastric ulcer and MALT lymphoma. There was a correlation between cagPAI+ strains and severe gastric diseases including cancer. The risk of gastric ulcer, adenocarcinoma and MALT lymphoma was 8.8 times higher for cagPAI+ patients. cagPAI+ infection was related to higher proliferation rates. The proliferation/apoptosis index was significantly higher for cagPAI+ patients. CONCLUSION: Cell growth deregulation in cagPAI+ patients could be demonstrated by the difference in the proliferation index. We believe that this explains the carcinogenic role of Helicobacter pylori.
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