OBJECTIVES: Although the host factors governing clinical outcomes subsequent to Helicobacter pylori infection have not yet been defined, it has been generally perceived that the development of the atrophic gastritis is determined more by host-related factors than by bacterial factors. It is very important to define the host factors controlling the pathway to atrophic gastritis, which is the precursor of gastric cancer. H. pylori infection is characterized by extensive infiltration of neutrophils. Myeloperoxidase in neutrophils amplifies the oxidative potential of hydrogen peroxides that induce gastric mucosal damage, and thus myeloperoxidase is suspected to play a role in H. pylori-induced gastric injury. The aim of this study was to elucidate the association of host myeloperoxidase genetic polymorphism with atrophic gastritis upon H. pylori infection. METHODS: Biopsy specimens taken from the gastric mucosa were examined histologically using the updated Sydney System in 127 Korean patients. The polymerase chain reaction-restriction fragment length polymorphism assay was used to characterize myeloperoxidase genotypes. RESULTS: The distributions of myeloperoxidase genotypes in Korea were 81.9% for myeloperoxidase (G/G) and 18.1% for myeloperoxidase (G/A). No myeloperoxidase (A/A) genotype was observed in 127 patients studied. The degree of active inflammation increased with the increase in H. pylori colonization. A strong positive correlation between the levels of neutrophil infiltration and gastric atrophy was found in the myeloperoxidase (G/G) genotype but not in myeloperoxidase (G/A). CONCLUSIONS: These results suggest that myeloperoxidase genotype is a critical determinant in the pathogenesis of atrophic gastritis subsequent to H. pylori infection. More work is needed to clarify the functional relevance of myeloperoxidase genetic polymorphisms to gastric cell injury.
OBJECTIVES: Although the host factors governing clinical outcomes subsequent to Helicobacter pylori infection have not yet been defined, it has been generally perceived that the development of the atrophic gastritis is determined more by host-related factors than by bacterial factors. It is very important to define the host factors controlling the pathway to atrophic gastritis, which is the precursor of gastric cancer. H. pylori infection is characterized by extensive infiltration of neutrophils. Myeloperoxidase in neutrophils amplifies the oxidative potential of hydrogen peroxides that induce gastric mucosal damage, and thus myeloperoxidase is suspected to play a role in H. pylori-induced gastric injury. The aim of this study was to elucidate the association of host myeloperoxidase genetic polymorphism with atrophic gastritis upon H. pylori infection. METHODS: Biopsy specimens taken from the gastric mucosa were examined histologically using the updated Sydney System in 127 Korean patients. The polymerase chain reaction-restriction fragment length polymorphism assay was used to characterize myeloperoxidase genotypes. RESULTS: The distributions of myeloperoxidase genotypes in Korea were 81.9% for myeloperoxidase (G/G) and 18.1% for myeloperoxidase (G/A). No myeloperoxidase (A/A) genotype was observed in 127 patients studied. The degree of active inflammation increased with the increase in H. pylori colonization. A strong positive correlation between the levels of neutrophil infiltration and gastric atrophy was found in the myeloperoxidase (G/G) genotype but not in myeloperoxidase (G/A). CONCLUSIONS: These results suggest that myeloperoxidase genotype is a critical determinant in the pathogenesis of atrophic gastritis subsequent to H. pylori infection. More work is needed to clarify the functional relevance of myeloperoxidase genetic polymorphisms to gastric cell injury.