Nine patients with Helicobacter pylori-related antral gastritis and history of duodenal ulceration were studied before and at 1 and 7 months after eradication of the infection by a 4-week course of tripotassium dicitrato bismuthate, metronidazole, and amoxycillin. The median basal gastrin concentration before eradication was 30 ng/l (range, 20-60) and fell to 20 ng/l (5-20) at 1 month (p less than 0.02) and 15 ng/l (5-20) at 7 months (p less than 0.01) after eradication. The integrated gastrin response to a peptide meal was 3650 ng/l.min (range, 1875-6025) before treatment compared with 1800 ng/l.min (range, 1200-3075) at 1 month (p less than 0.01) and 1312 ng/l.min (875-2625) at 7 months (p less than 0.03). Daytime intragastric pH (0900-2100 h) was similar before treatment (median, 1.4; range, 1.1-2.1) and at 1 month (1.4; 1.1-2.3) and 7 months (1.4; 1-2.2) after eradication. In five of the patients nighttime acid output (2300-0900 h) was also studied and was similar before (median, 86 mmol/10 h; range, 52-114) and at 1 month (76 mmol/10 h; 50-143) and 7 months (94 mmol/10 h; 63-106) after eradication. In conclusion, eradication of H. pylori is accompanied by a sustained fall in serum gastrin concentrations but is not accompanied by an early or late reduction of daytime intragastric acidity or nighttime acid output.

The mechanism of the hypergastrinaemia associated with Helicobacterpylori infection is unknown. It may be an effect of the ammonia produced by the bacterium near the antral epithelial surface. We In an attempt to elucidate the mechanism of the hypergastrinaemia associated with H pylori infection, we have examined the effect of inhibiting the bacterium's urease activity and ammonia production on serum gastrin in duodenal ulcer patients. Patients and methods STUDIES IN PATIENTS WITH H PYLORI INFECTIONSix patients confirmed endoscopically to have duodenal ulceration within the previous year but currently in clinical remission were studied. Their median age was 39 years (range 26-52) and three were women. In each patient, an antral biopsy specimen obtained endoscopically within the preceding three months had shown gastritis associated with H pylori like organisms.The patients reported fasted and a venous blood sample was removed at 8 am for gastrin determination. Immediately after this they drank 50 ml water and further blood samples were taken at 30 minute intervals for two hours. At 10 am they took a standard meal consisting of two beef cubes (OXO Ltd, Croydon, England) dissolved in 200 ml water at 50°C. Further blood samples were taken at 10 minute intervals for 70 minutes and a final one at 90 minutes after the OXO drink. Immediately after this sample a "C urea breath test was performed to measure H pyloni urease activity. For this they drank 250 ml Ensure Plus (Abbott Laboratories, England) to delay gastric emptying, followed by 0 4 MBq 14C urea (Amersham International) in 25 ml water. Breath samples for 14C-Co2 analysis were obtained at 10 minute irtervals for 90 minutes.

Helicobacter pylori possesses unusually high urease activity that lowers the urea concentration and raises the ammonium concentration of the gastric juice in infected people. The value of measuring urea and ammonium concentrations in gastric juice obtained during upper gastrointestinal endoscopy as a means of diagnosing the presence and eradication of the infection was assessed. Twenty four subjects with the infection and 14 in whom it had been eradicated were examined. Their Hpylori status was confirmed by antral biopsy and 14C urea breath test. The median (range) gastric juice urea concentration in infected subjects was 0-8 mmol/I (0.5-2.9 mmol/l), which was lower than th9t in the uninfected subjects (2.1 mmolIl ,(1I0-3-7 mmol/l)) (p<0001). The median gastric juice ammonium concentration in infected subjects was 3.4 mmol/l (10-13-0 mmol/l), which was higher than that in the uninfected subjects (0.64 mmol/l (0.02-1.4 mmol/l)) (p<0001). Though the two groups overlapped in respect of their urea and ammonium concentrations, they were completely different when the urea: ammonium ratios were calculated -the ratios ranged from 0 04-0*7 (median 0.26) and from 1-1-113 (median 3.4) in infected and uninfected subjects respectively (p<0001

Aim-To assess the value of measuring the gastric juice urea: ammonium ratio in detecting Helicobacter pyloni infection in patients with chronic renal failure.

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.