Pyrin Gene Polymorphisms and H. pylori-associated Dyspepsia: A Sri Lankan Study

Abstract

Background/Aim: A considerable high number of dyspeptic patients were reported even with the decreasing prevalence of H. pylori in Sri Lanka. Several microbial, host, and environmental factors may associate with the disease outcome. Pyrin secreted by the white blood cells may modulate the inflammatory process by assembling inflammasome complexes in response to pathogen infection. This study focused on the role of pyrin gene polymorphism in gastric mucosal severity and H. pylori infection. Materials and Methods: Among the ninety dyspeptic patients three gastric biopsies were taken and the presence of H. pylori, yeast species and the gastric mucosal severity was determined. EDTA blood was used for DNA extraction and identification of pyrin gene polymorphism. 12 MEFV gene mutations were tested. Results: Most of the patients (61%) had mild chronic gastritis. Among them 11.1% specimens gave positive bands for NL1/LS2 PCR of yeast DNA. H. pylori was positive in 17 patients. No homozygous mutations were found in the MEFV gene. The most common three heterozygous mutations were E148Q (45%), P369S (5%), M680I (11.6%). No significant difference was observed between the presence of the gene polymorphism, gastric mucosal severity or the presence of H. pylori and yeast species in the study group. Conclusion: The absence of homozygous mutations in the MEFV gene suggests that it is not a main factor contributing to gastric mucosal severity. The presence of H. pylori and yeasts reinforce the concept that stomach is a non-sterile environment.