[Cellular renewal of the gastric mucosa in patients with chronic gastritis and portal hypertension].

UNLABELLED: Portal gastropathy is common finding in patients with portal hypertension (PH) caused by liver cirrhosis, but influence of H. pylori on pathogenesis and natural history of this lesion is still not completely cleared up. The goal of the study was to evaluate histological changes in gastric mucosa at the patients with liver cirrhosis and portal hypertension and to establish role of H. pylori in development of portal gastropathy and related atrophy of gastric mucosa. The gastric biopsy was obtained from 54 patients (36 men and 18 women) in the age from 22 till 73 years. The diagnosis of liver cirrhosis was confirmed at 39, and chronic hepatitis at 15 patients. H. pylori was revealed in 37 patients. Four groups of the patients were discharged: I - 11 patients without attributes PH; II - 12 patients with PH, but without esophageal varicose phlebectasia; III - 17 patients with a varicose phlebectasia of esophagus - grade I, and IV - 14 patients with a varicose phlebectasia of esophagus - grade II. Proliferative activity in gastric mucosa was evaluated by immunostain for Ki-67. Patients from group III had more prominent inflammation, but only 35% of them were H. pylori (+). Gastric mucosa atrophy was frequently observed in this group. Severe atrophy of gastric mucosa was detected in patients in group IV but they had less activity of gastritis and only 29% of them were H. pylori (+). Nonmetaplastic type of atrophy was dominated in patients with portal hypertension. Proliferative activity in antral portion of gastric mucosa was decreased from 55% in group II to 23% in group-IV (P <0,01), but proliferation remained on the same level in corpus mucosa. Cellular proliferation had positive correlation with inflammation grade in groups II and III (P <0,05). The negative correlation of cellular proliferation with glandular atrophy was detected in patients with severe PH. Local discirculation, which depends on infringement of vascular permeability in gastric mucosa at patients with PH, may abolish trophic effect of gastrin and decrease cell proliferation activity.

CONCLUSION: The downstroke of cellular proliferation in gastric mucosa at patients with severe PH cause nonmetaplastic type of atrophy. H. pylori promotes faster development of glandular atrophy in gastric mucosa at early stages of PH via exacerbation of inflammatory mechanisms.