Loss of FHIT expression in gastric mucosa of patients with family histories of gastric cancer and Helicobacter pylori infection

AIM: To answer the question whether FHIT gene expression is affected by the family history of gastric carcinoma and the presence of Helicobacter pylori (Hpylori) in the gastric mucosa of patients with dyspepsia.METHODS: FHIT gene expression in two different topographic sites of the gastric mucosa of twenty-one patients with dyspepsia and with or without familial gastric carcinoma, infected or not infected with H pylori, was evaluated by reverse transcription-PCR (RT-PCR) and IMAGE QUANT methods. A rapid urease test and histopathological examination were used to determine H pylori colonization.RESULTS: In the gastric mucosa of patients with family histories of gastric carcinoma, the amount of FHIT protein mRNA was reduced down to 32%, and for patients with H pylori colonization, to 24% in comparison to controls with dyspepsia and without cancer in the family. FHIT expression was independent of the topography of specimens (corpus vsantrum), and for the control patients it was less sensitive to infection with H pylori. A considerable statistical difference in FHIT levels was observed in the gastric mucosa from the corpus of patients with family histories of gastric carcinoma in respect to H pylori colonization (P = 0.06). Macroscopic evaluation of the gastric mucosa demonstrated that pathologic changes classified according to the Sydney system had no significant influence on FHIT expression within each tested group of patients.CONCLUSION: Loss of FHIT expression was observed in patients with dyspepsia and family histories of gastric carcinoma, especially those infected with H pylori. Such results may constitute an early indication of the development of gastric carcinoma, which is associated with family factors including heredity and H pylori infection. The loss of the FHIT gene may serve as a marker for early diagnosis and prevention of gastric carcinoma, especially in context of early monitoring of H pylori infection in individuals with a record of familial stomach cancer.

Gastric ghrelin in relation to gender,stomach topography and Helicobacter pylori in dyspeptic patients

AIM： To investigate the level of gastric ghrelin in stomach mucosa of dyspeptic patients in relation to Helicobacter pylor/（H pylori） infection, bacterial cytotoxicity, topography and gender.METHODS： The study comprised 40 premenopausal women （19 H pylori positive） and 48 men （17 H pylori positive） with functional dyspepsia. All gastric biopsy specimens revealed normal mucosa or non-atrophic gastritis. Gastric ghrelin concentration was determined by Enzyme linked immunosorbent assay. The cagA and vacA strains of bacterial DNA were identified by multiplex polymerase chain reaction.RESULTS： In general, infection with H pylori caused an increase in gastric ghrelin level regardless of gender and stomach topography. Significantly more hormone was present in both, non-infected and H pylori positive female samples, as compared to males. The distribution of bacterial strains showed cagA（＋） vacA slml and cagA（-） vacA s2m2 genotypes as the most common infections in the studied population. A tendency to higher ghrelin levels was observed in less cytotoxic （cagA negative） strain-containing specimens from the antrum and corpus of both gender groups （without statistical significance）. CONCLUSION： An increase in gastric ghrelin levels at the stage of non-atrophic gastritis in H pylori positive patients, especially in those infected with cagA（-） strains, can exert a gastroprotective effect.