The aim of our study was to evaluate the association between variant genotype of angiotensinogen (AGT) c.-58A>C, lifestyle factors and clinical factors and corporeal extension of gastric inflammatory and preneoplastic lesions.
Methods: Our study included 209 subjects who underwent a complete set of gastric biopsies, followed by genotyping. They were included to study inflammatory gastric changes and preneoplastic lesions and were grouped according to the localization of changes.
Results: No significant statistical associations were noticed between AGT c.-58A>C genotypes and the corporeal extension of the inflammation or preneoplastic injury groups. Extending preneoplastic lesions to the gastric body was associated with smoking habits (p=0.01) and additionally, there was a significant association between nicotine consumption and the body extension of preneoplastic lesions (p=0.01). The use of acenocoumarol was frequently associated with the progression of histological lesions to preneoplastic lesions (p=0.01). Compared with the wild-type AA genotype, the combined genotypes AA+CC of AGT c.-58A>C were significantly associated with the progression of inflammatory gastric lesions’ according to the regular ingested doses of nonsteroidal anti-inflammatory drugs (NSAIDs).
Conclusion: The AGT c.-58A>C polymorphism is not associated with extension of the gastric lesions. In accordance with nicotine and alcohol consumption, the acenocoumarol co-treatment and multiple cardiac pathologies are associated with the corporeal progression of these injuries. The age below 70 years and NSAIDs treatment for the patients with heterozygous AC genotype and variant homozygous CC genotype for the mentioned SNP have been associated with the corporeal extension of gastric inflammation.
