Gastroduodenal Disease, Helicobacter pylori, and Genetic Polymorphisms

Over the past 20 years, there has been marked progress in our understanding of the role of genetic and environmental factors in the etiology of gastroduodenal disease. Helicobacter pylori infection now is recognized to be the most important environmental factor for both noncardia gastric cancer and peptic ulcer disease. The likelihood of the infection resulting in significant disease depends on genetic polymorphisms influencing the virulence of the organism. However, the specific pattern of disease induced by the infection is determined to a great extent by genetic polymorphisms in the host that govern the local gastric immune response elicited. Genetic factors also are important in the treatment of gastroduodenal diseases. Polymorphisms of host CYP2C19 influence the pharmacokinetics and clinical efficacy of proton pump inhibitor therapy.

Abbreviations used in this paper:  cagPAI, cag pathogenicity island , DU, duodenal ulcer , EM, extensive metabolizer , HLA, human leukocyte antigen , iceA, induced by contact with epithelium , IL, interleukin , MHC, major histocompatibility complex , PM, poor metabolizer , PPI, proton pump inhibitor