Summary:We describe the development of radioimmunoassays to measure both human pepsinogen A and pepsinogen C concentrations in serum. The antibodies were raised in goats by immunization with purified pepsinogen A or C. The affinity constants of the respective antibodies were 20 · l O 10 1/mol and 7 · l O 10 1/mol.Pepsinogens A and C were labeled with Na 125I by the chloramine T method. The binding between labels and antibodies was inhibited by 0.50 at 0.82 ng pepsinogen A per tube and 2.1 ng pepsinogen C per tube. The detection limits of the assay of pepsinogen A and C were 0.12 μg/l and 1.8 μg/l, respectively.Pepsinogen A and C were purified and added to a patient serum, showing a good recovery in the radioimmunoassays. Serial dilution of another patient serum, which contained a high concentration of both antigens, showed curves parallel to the Standard curves. The intra-and interassay variations of these radioimmunoassays were evaluated. The intra-assay coefficients of Variation for pepsinogen A were found to vary from 0.03 to 0.102 at concentrations in serum in the normal r nge, while the inter-assay coefficient of Variation ranged from 0.118 to 0.194 at the same concentrations in serum. For the pepsinogen C radioimmunoassay we found intra-assay coefficients of Variation between 0.126 and 0.147 at concentrations in serum in the normal r nge, while the inter-assay coefficient of Variation ranged from 0.174 to 0.325 for the same sera.In 201 blood donors we found a me n serum concentration of pepsinogen A of 59 μg/l and a mean serum concentration of pepsinogen C of 15 μg/l. There was a significant relationship between these values (r = 0.779, p < 0.001).The concentrations of both pepsinogens were increased in 10 patients with duodenal ulcer (132 and 67 μg/l, respectively). Serum pepsinogen A was decreased in 14 patient« with partial gastrectomy (34 μg/l) and in 6 with achlorhydria (9 μg/l), accompanied by raised (34 μg/l) and!inormal (20 μg/l) mean pepsinogen C concentrations in the respective groups. In 4 patients with a total gastrectomy the mean serum concentration of both pepsinogen A and C reached the zero level (5 and 4 μg/l, respectively). These results not only underline the accuracy of the measurements but also point to their clinical relevance. ntro uction. § secrete^ by f un( jj c , pyloric and proximal duodenal Pepsinogen A and C are the proenzymes of pepsin A mucosa (1). Exocrine-secreted pepsinogens function and pepsin C, respectively, which belong to the group s zymogens for the main proteolytic activity of gasof gastric acid aspartic endoproteiiiases. Pepsinogen tric juice. There is also a small endocrine excretion of A is secreted by fundic mucosa, while pepsinogen C pepsinogens without a known function, but by exploiting this phenomenon, we can gain Informatioñ on the condition of the gastric mucosa by measurePepsin* *Α; EC 3 4.23.1 ment of the serum concentration of pepsinogen A and Pepsin C; gastricsin; EC 3.4.23.3 pepsinogen C (2, 3).

The yield of colonoscopic surveillance in familial CRC is substantially higher than the yield of screening reported for the general population.

Aim:To compare the efficacy of ranitidine bismuth citrate plus clarithromycin (RBC–C) vs. omeprazole plus amoxycillin (OME–AMO) in the cure of Helicobacter pylori infection.Methods:In this double‐blind, multicentre, parallel‐group study 122 H. pylori‐positive patients with active duodenal ulcer or gastritis, with confirmed history of duodenal ulcer, were randomized to treatment with ranitidine bismuth citrate 400 mg b.d. plus clarithromycin 500 mg b.d. or omeprazole 20 mg b.d. plus amoxycillin 1000 mg b.d. for 14 days, followed by 14 days of ranitidine bismuth citrate 400 mg b.d. or omeprazole 20 mg once daily, respectively, to facilitate ulcer healing. Endoscopy was carried out at the start of the study and 28 days after the end of treatment. At each endoscopy four biopsies were obtained from the antrum and four biopsies from the corpus, for rapid urease test, histology and culture. H. pylori infection was defined as a positive urease test, confirmed by histology or culture. Cure of H. pylori infection was defined as negative urease test, histology or culture from both sites.Results:Per‐protocol, all‐patients‐treated and intention‐to‐treat cure rates (95% confidence interval) were, respectively, 90% (81–89%), 90% (82–89%) and 84% (74–93%) for ranitidine bismuth citrate plus clarithromycin, and 39% (27–54%), 44% (31–57%) and 41% (29–53%) for omeprazole plus amoxycillin, P < 0.00001. Both regimens were well tolerated. Eight patients were lost to follow‐up, for lack of efficacy (one patient), adverse events (three patients) or refusal of second endoscopy (four patients).Conclusion:Ranitidine bismuth citrate 400 mg b.d. with clarithromycin 500 mg b.d. is superior to omeprazole 20 mg b.d. with amoxycillin 1000 mg b.d. Ranitidine bismuth citrate with clarithromycin is the first dual therapy with high cure rates and good tolerance, and is easy to take. It may therefore prove a suitable first‐line treatment in H. pylori infection.

A study has been done in 10 male healthy volunteers of the effect of oral omeprazole 20 mg daily for 3 days on the serum concentrations of Pepsinogens A and C in relation to changes in fasting serum gastrin and basal and pentagastrin stimulated gastric acid output. The concentrations of Pepsinogens A and C showed concomitant and variable but significant increases, and the Pepsinogen A, C ratio did not change during the 3-day course of omeprazole. The increments were also significantly correlated with the increase in fasting serum gastrin and with the reduction in pentagastrin stimulated acid output. The correlations were mainly due to the marked inhibition of gastric acid secretion and the corresponding increases in serum gastrin and Pepsinogens A and C in two subjects, as in the other 8 subjects the changes were only modest. There appears to be a relationship, therefore, between the degree of inhibition of acid by omeprazole and the parallel increases in both serum pepsinogens and fasting gastrin.

We have studied the effect on serum gastrin concentrations of weekly 3-day courses of 20 mg/day omeprazole followed by a 4-day period without medication (weekend therapy) for 4 weeks in 10 patients with duodenal ulcer. Basal and postprandial serum gastrin concentrations were measured in week 1, before (day 1) and immediately after the 3-day omeprazole course (day 4), and further on day 6 and day 8, immediately before the next course, and at similar intervals in week 4 (days 22, 25, 27, and 29). Basal serum gastrin concentrations were not significantly different from day 1, but postprandial peak gastrin concentrations on days 6, 8, 22, 25, 27, and 29 and integrated postprandial gastrin secretion on days 25 and 27 were significantly increased (p less than 0.01 to p less than 0.05). However, the increases in serum gastrin concentration were modest and clinically irrelevant. It is concluded that this intermittent weekend schedule of omeprazole therapy does not induce marked hypergastrinemia and may therefore be suitable for long-term therapy with this drug.