Histopathological and Endoscopic Correlation of Gastric Lesions in Endoscopic Gastric Biopsies

AbstractBackground and Aims. Gastric cancer, because of its aggressive evolution and the high mortality associated with it, remains one of the most debated subjects in medical literature with Helicobacter pylori (HP) as a major risk factor. Chronic inflammation caused by HP infection represents the initial site of the predisposing and afterwards premalignant lesions for gastric carcinoma. The purpose of this study was to evaluate the prevalence of HP infection, of predisposing and premalignant lesions on gastric biopsies, as well as to identify the correlations between them.Material and method. A retrospective cross-sectional study was performed on gastric biopsies collected endoscopically from a single region, antrum or corpus, and from different regions, between January 2012 and July 2014. Incidence of HP infection, of predisposing and premalignant gastric lesions, the correlation of HP infection and these lesions, were evaluated.Results. HP infection was diagnosed in 32.81%. Predisposing and premalignant lesions were present in 53.64% of biopsies with most of them in the antrum. HP infection stands out for the under 50 yo group (p=0.001). No correlation between frequency of HP infection and predisposing and premalignant lesions was observed.Conclusions. Prevalence of HP infection in our study suggests that besides HP infection, other factors are also involved in gastric cancer development. Biopsies from different regions of the gastric mucosa do not offer extra information regarding HP infection prevalence but may be helpful in evaluating incidence and extension of predisposing and premalignant lesions.

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The Interaction between GSTT1, GSTM1, and GSTP1 Ile105Val Gene Polymorphisms and Environmental Risk Factors in Premalignant Gastric Lesions Risk

BioMed Research International ◽

10.1155/2017/7365080 ◽

2017 ◽

Vol 2017 ◽

pp. 1-9 ◽

Cited By ~ 8

Author(s):

Anca Negovan ◽

Mihaela Iancu ◽

Valeriu Moldovan ◽

Simona Mocan ◽

Claudia Banescu

Keyword(s):

Alcohol Consumption ◽

Gene Polymorphisms ◽

Premalignant Lesions ◽

Gastric Lesions ◽

Gstm1 Gene ◽

Increased Risk ◽

Gstp1 Ile105val ◽

Gastric Biopsies ◽

H Pylori ◽

Genotype Versus

The study investigated the possible influence of GSTM1, GSTT1, and GSTP1 gene polymorphisms as predisposing factors for premalignant gastric lesions as well as their interaction with H. pylori infection, gastrotoxic drugs, smoking, and alcohol consumption. In this study, 270 patients with a complet set of gastric biopsies and successfully genotyped were finally included. The GSTM1 gene polymorphism had significant contribution in mild/severe endoscopic lesions (p=0.01) as well as in premalignant lesions (p=0.01). The GSTM1 null genotype increased the risk for mucosal defects in H. pylori-negative patients (OR = 2.27, 95% CI: 1.20–4.37) and the risk for premalignant lesions in patients with no alcohol consumption (OR = 2.13, 95% CI: 1.19–3.83). The GSTT1 deleted polymorphism did not significantly increase the risk for premalignant lesions in the absence of gastrotoxic drugs (OR = 1.82, 95% CI: 0.72–4.74). The combined GSTT1T1 and GSTM1 null polymorphisms were borderline correlated with an increased risk for premalignant lesions (OR = 1.72, 95% CI: 1.00–2.97). The wild-type GSTP1 Ile/Ile genotype versus the variant genotypes Ile/Val + Val/Val was significantly associated with a decreased risk of gastric atrophy/intestinal metaplasia (OR = 0.60, 95% CI: 0.37–0.98). In conclusion, the GSTM1 and GSTT1 null genotypes increased the risk for premalignant and endoscopic gastric lesions, modulated by H. pylori, alcohol, or gastrotoxic drug consumption, while the presence of the GSTP1Val allele seemed to reduce the risk for premalignant lesions.

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The angiotensinogen gene polymorphism, lifestyle factors, associated diseases and gastric areas of inflammatory and preneoplastic lesions in a Romanian sample of patients

Revista Romana de Medicina de Laborator ◽

10.2478/rrlm-2019-0032 ◽

2019 ◽

Vol 27 (4) ◽

pp. 401-411

Author(s):

Mădălina Anciuc ◽

Florin Tripon ◽

George-Andrei Crauciuc ◽

Simona Mocan ◽

Anca Negovan

Keyword(s):

Lifestyle Factors ◽

The Body ◽

Gastric Body ◽

Gastric Lesions ◽

Preneoplastic Lesions ◽

Variant Genotype ◽

Gastric Biopsies ◽

Complete Set ◽

Inflammatory Drugs ◽

Nicotine Consumption

Abstract 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.

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