After the eradication of Helicobacter pylori infection, relapse is a serious problem in Turkey.

Eradication of Helicobacter pylori (Hp) infection is strongly recommended in duodenal and gastric ulcer. In developed countries the recurrence rate is low; however, in Turkey, the Hp recurrence rate is suspected to be high as the prevalence of Hp infection is--as high as 70-80% in the asymptomatic population. We planned this study to determine the relapse rate of Hp infection after successful eradication therapy in Turkey. Fifty-two cases including 24 patients with duodenal ulcer and 28 patients with nonulcer dyspepsia were examined in this study. The eradication regimen was omeprazole 20 mg twice daily, clarithromycin 500 mg twice daily, and metronidazole 500 mg three times a day for 1 week. All patients underwent upper gastrointestinal tract endoscopy. At least four samples from antrum and corpus were taken to enable histologic diagnosis of Hp infection. After the eradication therapy, endoscopy was repeated at 1, 3, 6, and 12 months, and Hp-positive patients were dropped from study. With the use of this regimen, the Hp eradication rate was 92.3% (48/52). After the eradication of Hp infection, relapse rates were 6.97%, 27.5%, and 11.11% at 3, 6, and 12 months, respectively. The cumulative relapse rate for 1 year was 41.46%. The results of this study revealed that after the eradication of Hp infection, recurrence is encountered very often as a problem in Turkey. We concluded that hygienic and environmental factors can affect these high relapse rates.

Effects of a novel bombesin antagonist analogue on bombesin-stimulated gastric acid secretion and growth hormone release in the pentobarbital-anesthetized rat.

A new and specific bombesin receptor antagonist analogue, Leu13 psi [CH2NH]Leu14-bombesin, was studied for inhibition of bombesin-stimulated gastric acid secretion in pentobarbital-anesthetized rats. The analogue potently inhibited bombesin-stimulated gastric acid secretion in a dose-dependent fashion, exhibiting an ID50 of 0.66 mumol/250 g, which corresponds to a molar ratio of bombesin to antagonist of approximately 1:12. This agrees well with antagonist to agonist potency ratios previously reported for inhibition of bombesin-stimulated amylase release from guinea pig pancreatic acinar cells and the growth of murine Swiss 3T3 cells, suggesting functional similarities between the receptor sites involved. Conversely, the analogue failed to inhibit bombesin inhibition of growth hormone release in the sodium pentobarbital-anesthetized rat model and was, in fact, a weak agonist at higher dose levels. This indicates either that this system is not particularly bombesin-specific or that bombesin receptor recognition and signaling requirements are substantially different in the gut and hypothalamus.

Gastric, duodenal, and pancreatic somatostatin-like immunoreactivity during hypovolemic shock.

Because hypovolemic shock is known to cause gastric ulcers in animals and human beings, we investigated the tissue levels of somatostatin-like immunoreactivity (SLI) in the gastric corpus and antrum, duodenum, and pancreas during hypovolemic shock in rats. We studied male Wistar rats (N = 10 each) 15 min, 2 hr, and 12 hr after hypovolemic shock and compared results to a control group (N = 15). Two rats in both 2-hr and 12-hr groups showed gastric ulcers: three corporal and one antral. One animal developed multiple ulcers. In the gastric corpus and antrum and in the duodenum, tissue SLI showed significant decrease 15 min and 2 hr after shock. Gastric SLI remained low, whereas duodenal SLI recovered and rose above control level at 12 hr. Pancreatic SLI showed no significant changes during hypovolemic shock. Gastric tissue SLI levels that were significantly lower after shock than those of normal controls may have contributed to the peptic ulcer disease induced by hypovolemic shock in this experimental model.