HELICOBACTER-PYLORI INFECTION AND GASTRIC-SECRETION IN DUODENAL AND GASTRIC-ULCER PATIENTS - THE EFFECT OF ERADICATION AFTER ONE-YEAR

The mechanism by which Helicobacter pylori (HP) predisposes to duodena l and gastric ulcers remains still unclear. It is possible that Hp inf ection impaires gastric secretion. Evaluation of gastric acid and mucu s secretion before and after Hp eradication would let to estimate the influence of Hp infection on gastric secretion. To evaluate the effect of Hp infection on gastric acid and gastric mucous secretion before a nd one year after Hp eradication. We examined 28 Hp positive peptic ul cer disease patients (10 - gastric ulcer GU, 18 - duodenal ulcer DU) b efore and one year after antibacterial treatment. Gastric acid output was examined basely (BAG) and in response to pentagastrin (6 mu g/kg) (MAO) using Kay's standard method. Some components of gastric mucus as fucose, galactose, hexosamines and sialic acid were measured using ca lorimetric methods basaly and after pentagastrin stimulation. :Plasma gastrin concentration was measured in 20 patients (6-GU, 14-DU) by rad ioimmunoassay before and one year after eradication. Hp status was det ermined by rapid urease test (CLO) and histology (Giemsa stain). One y ear after Hp successful eradication gastric acid secretion was signifi cantly reduced - BAO: 3,31 vs 1,474 mmo:/h; MAO: 19,63 vs 14,85 mmol/h , p<0,05. Plasma gastrin concentration decreased significantly from 9, 783 to 6,017 pmol/l, p<0.05, In patients with ineffective eradication we did not observe any significant changes in gastric acid secretion. An evident, but not statistically significant, decrease of sialic acid output in eradicated patients was noted. The study has shown the sign ificant influence of Hp infection on, gastric acid secretion. Those re sults support the hypothesis that increased gastric acid secretion may be one of the pathogenic mechanism of Hp infection inducing mucosal d amage.