Genotyping of Helicobacter pylori in paraffin-embedded gastric biopsy specimens: Relation to histological parameters and effects on therapy

OBJECTIVES: Colonization with Helicobacter pylori can lead to GI disease. Bacterial genotypes and host factors, such as acid production, can influence the progress of disease. We investigated H. pylori genotypes and histological parameters in the same paraffin-embedded gastric biopsy specimens. METHODS: Paraffin-embedded antrum and corpus biopsy samples from 75 gastroesophageal reflux disease patients were histologically examined and tested for H. pylori vacA (s and m regions), cagA, and iceA genotypes. Patients were investigated at baseline (58 H. pylori positive and 17 H. pylori negative) and after treatment with omeprazole with or without additional antibiotic therapy. RESULTS: Genotyping at baseline was complete in 52 (90%) of the 58 H. pylori positive patients. Multiple genotypes were detected in eight (14%) of these. Genotypes were highly consistent between antrum and corpus biopsy specimens at baseline and in follow-up samples. Genotypes from paraffin sections matched those from corresponding cultured strains in 10 selected cases. In the antrum, the degree of inflammation was associated with vacA s1 and cagA+ genotypes, and the degree of neutrophil activity was associated with the cagA+ genotype. In the corpus, the degree of inflammation was significantly associated with vacA s1, cagA+, and iceA1 genotypes and the degree of atrophy was associated with vacA s1, m1, and cagA+ genotypes, whereas the degree of neutrophil activity was associated with vacA s1 and cagA+ genotypes. vacA s2 and cagA strains appeared more resistant to antibiotic therapy, irrespective of resistance to clarithromycin. CONCLUSIONS: Our findings confirm the relevance of the H. pylori genotypes for the severity of gastric disease and the efficacy of antibiotic therapy

Quantitative assessment of gastric corpus atrophy in subjects using omeprazole: A randomized follow-up study

OBJECTIVES: Atrophy of the gastric mucosa most frequently results from chronic Helicobacter pylori infection and is a risk factor for the development of gastric cancer. Profound acid suppression has been suggested to accelerate the onset of gastric mucosal atrophy. The aim of the present study was to evaluate the effects of H. pylori eradication and acid inhibition by omeprazole on gastric atrophy by means of quantitative analysis of tissue morphology. METHODS: Corpus biopsy specimens were obtained during endoscopy in 71 gastroesophageal reflux disease (GERD) patients at baseline and after 3 and 12 months. A total of 48 subjects were H. pylori positive and 23 were H. pylori negative. All subjects received omeprazole 40 mg once daily after the first endoscopy for 12 months. After randomization, 27 of the 48 H. pylori-positive patients also received eradication therapy. In hematoxylin and eosin-stained slides the volume percentages of glands (VPGL), volume percentages of stroma (VPS), and volume percentages of infiltrate (VPI) were measured in the glandular zone of the mucosa. The results were evaluated by computerized morphometric analysis. RESULTS: In the eradication group, the mean VPGL increased from 63.0% to 67.7% and 71.5% after 3 and 12 months (p<0.001), respectively. The mean VPS and VPI decreased from 33.1% and 4.0% to 29.3% and 3.0% and to 26.4% and 2.1% (p<0.001 and p=0.04), respectively. Patients with the lowest VPGL at baseline showed the largest increases of VPGL after eradication treatment as compared to patients with high a VPGL at baseline. In the H. pylori-persistent group the VPI showed a significant increase (p=0.01), and in the H. pylori-negative group VPGL increased significantly from 71.9% to 75.2% (p=0.03) after 12 months. CONCLUSIONS: Eradication of H. pylori leads to restitution of the volume percentage of glandular epithelium to normal levels, even during treatment with proton pump inhibitors. Whether this effect can also be seen in patients with marked atrophy needs further investigation