gastrins and pepsinogen-(1-12)

Cancer of stomach is currently regarded as the final result of a staged multifactor process during which the microenvironment affects cells and causes their changes. One of the main triggering factors is Hp infection. Adenocarcinoma of stomach develops via stages of gastritis, precancerous changes, and cancer. The possibility to prevent cancer ensues from the potential irreversibility of premalignant processes in gastric mucosa, in the first place its atrophy; hence, the importance of its early diagnosis. The state of the endoscopic service in this country is inadequate for mass screening of patients with symptoms of dyspepsia. "GastroPanel", a new serological test for the diagnosis of gastric pathology provides information about histological and functional characteristics of gastric mucosa in the antral and fundal regions of the stomach. The method determines serum gastrin-17, pepsinogen-1, and IgG expressed in response to Hp infection. Our results demonstrate high diagnostic efficiency of "GastroPanel" as a screening technique for atrophic gastritis and assessment of stomach cancer risk.

Topics: Adolescent; Adult; Aged; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Mass Screening; Middle Aged; Neoplasm Staging; Pepsinogen A; Peptide Fragments; Stomach Neoplasms; Young Adult

The rise in serum gastrin and pepsinogen I after 5 days' treatment with the proton pump inhibitor pantoprazole (40 mg/day) was examined in eight duodenal ulcer patients with Helicobacter pylori infection and compared with eight in whom it had been eradicated. Before treatment, the post-prandial serum gastrin concentrations were higher in the H. pylori-positive than -eradicated patients (p less than 0.05). The median rise in pre-prandial serum gastrin concentrations on treatment was similar in the H. pylori-positive (41%) and -eradicated patients (45%). The rise in post-prandial serum gastrin was also similar in the H. pylori-positive (81%) and -eradicated patients (69%), resulting in significantly higher gastrin concentrations during treatment in the former. The median rise in serum pepsinogen I on treatment was greater in the H. pylori-positive (114%) than in the -eradicated patients (8%), resulting in significantly higher concentrations during treatment in the former. These observations indicate that eradication of H. pylori may be a means of moderating the hypergastrinaemia caused by acid-inhibitory therapy. They also indicate that H. pylori-related hypergastrinaemia is not due to an increase of the antral surface pH by the bacterium's urease activity.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adenosine Triphosphatases; Benzimidazoles; Duodenal Ulcer; Gastric Acidity Determination; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Omeprazole; Pantoprazole; Pepsinogen A; Pepsinogens; Peptide Fragments; Sulfoxides