Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00790 (PGA)
 2,475 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pepsin 1, the ulcer-associated pepsin, occurred significantly more frequently in the gastric juice of those patients with duodenal ulcer who did not secrete A, B, or H antigens into gastric juice than in those secreting these antigens. This observation may explain the increased proportion of such non-secretors among patients with duodenal ulceration. In patients with gastric ulcer and non-ulcer dyspepsia, and in a miscellaneous group of patients, there was no association of pepsin 1 secretion with secretor status, suggesting that the association noted in duodenal ulceration is an indirect rather than a direct one. No increase of pepsin 1 occurred in group O patients with peptic ulcer, so that the increased proportion of such patients in peptic ulcer does not arise from differences in pepsin 1 secretion.
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PMID:Hereditary aspects of duodenal ulceration: pepsin 1 secretion in relation to ABO blood groups and ABH secretor status. 11 57

Intraduodenal instillation of hypertonic glucose significantly inhibited tetragastrin-induced gastric acid and pepsin outputs in man. The secretory volume of gastric juice was markedly decreased, whereas, acid concentration remained unchanged. Pepsin concentration, on the contrary, was reduced significantly. The degree of inhibition of pepsin output, therefore, was greater than that of acid output. No significant difference in the extent of inhibition of acid or pepsin output was observed between control subjects and patients with duodenal ulcer.
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PMID:Inhibition of gastric secretion by intraduodenal hypertonic glucose in patients with duodenal ulcer. 34 51

1. Electrophoretic separation of proteases from human gastric mucosal extracts of five patients with gastric ulcer, one with duodenal ulcer and three with gastric cancer were investigated by agar-gel electrophoresis at pH 8.3 and pH 5.0. 2. In the fundic mucosal study, there were seven faster moving proteases in all nine cases, but the slowest moving protease showed a slightly different picture in each case. In the antral mucosal study, two of eight cases showed mainly group II pepsinogens, seven of nine cases, however, showed the same results as in the fundic mucosal study. 3. In the cases of the nine mucosal extracts activated at pH 1.5 or pH 4.0, they all showed the same electrophoretic separation at each pH level. At these two pH levels, however, quite different electrophoretic patterns were observed. The presence of pepsin 3 appeared to diminish at the higher levels of pH, although that of pepsin 5 and pepsin 7 appeared to increase at pH 4.0 and above. Pepsin 6 appeared for the first time at pH 4.0 and existed at higher pH levels. 4. We thus conclude that electrophoretic patterns of pepsins in the gastric mucosal extracts are changeable depending on the pH level of the incubating medium, and further that diversity of pepsins in gastric juices may also depend on the pH level of gastric juices.
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PMID:Studies on the pepsinogens of human gastric mucosal extracts. 74 87

Metiamide was given orally in one dose of 200 mg in 23 sutdies in patients with duodenal ulcer, 4 in the basal state, 11 during histamine infusion, and 8 before insulin hypoglycemia stimulation. In the latter 8 patients insulin was given at another time without metiamide. In 17 studies acid secretion was suppressed by metiamide--up to 75% in the basal state, 53% after histamine, and 80% after insulin. Pepsin secretion was reduced to the same extent as H+ in the histamine studies but not in the basal (57%) or insulin (44%) studies, so that in the latter pepsin/acid ratios were 3-fold greater than in controls. Blood levels of metiamide were measured in 17 studies. In 10 out of 11 who showed inhibition of 40% or more, peak blood levels of metiamide were 0.45 mug/ml to 1.25 mug/ml. In 5 of 6 who did not show inhibition, blood levels were 0.05-0.4 mug/ml; in the sixth it was 0.8 mug/ml. Therefore a critical blood level for suppression of basal or stimulated secretion appears to be approximately 0.45 mug/ml.
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PMID:Inhibition of basal and stimulated gastric H+ and pepsin secretion in duodenal ulcer patients by metiamide, an H-2 histamine antagonist. 78 30

Gastric secretion was stimulated by intravenous infusion of 15 mug/kg/hr of pentagastrin before and 10 and 90 days after proximal gastric vagotomy in 16 duodenal ulcer patients. Postoperatively 15 ug/kg/hr of pentagastrin was also given in combination with 2 mug/kg/hr of carbacholine. Mean acid output in response to pentagastrin alone was reduced by 48 and 64 per cent at 10 and 90 days after the vagotomy, respectively. Mean pentagastrin-stimulated acid output and volume of gastric juice was significantly higher at 10 days than at 90 days after the operation. Mean pepsin output decreased also, but the decrease was not statistically significant. There was no significant effect of carbacholine on pentagastrin-stimulated acid output either at 10 or 90 days. Carbacholine increased pentagastrin-stimulated volume of gastric juice significantly at 10 but not 90 days postoperatively. The effect of carbacholine on pentagastrin-stimulated pepsin output was significant both 10 and 90 days after the vagotomy. Pepsin output in response to pentagastrin plus carbacholine 10 days after the operation was not significantly different from preoperative values. At 10 days postoperatively the increase in pentagastrin-stimulated volume of gastric juice by carbacholine was significantly greater than at 90 days. The corresponding differences of acid and pepsin outputs were not significant.
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PMID:Decrease in gastric secretion during the first three months after proximal gastric vagotomy in duodenal ulcer patients. 109 30

The gastric antisecretory effects of two dose levels of pirenzepine given at night were investigated in a group of healthy male volunteers. Compared with placebo, three days of treatment with pirenzepine 100 mg nocte or 150 mg nocte inhibited mean nocturnal intragastric acidity by 54% and 53%, respectively (p less than 0.01). The volume of gastric juice secreted was reduced by 47% and 52% (p less than 0.005), by 100 mg and 150 mg nocte, respectively. Each dose suppressed mean gastric acid output by 67% (p less than 0.001). Pepsin output was not significantly altered. There were no differences in effect between the two dose levels studied, but side-effects such as dry mouth were only seen with the higher dose. Pirenzepine 100 mg is the optimum dose which can conveniently be given at night. This will limit side-effects, and may be a useful treatment for patients with duodenal ulcer.
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PMID:Single nocturnal doses of pirenzepine effectively inhibit overnight gastric secretion. 286 23

One hundred and seven patients with active juxtapyloric ulcers and a history of chronic ulcer disease were treated with cimetidine. After ulcer healing 67 patients were selected for medical management, testing the value of cimetidine maintenance treatment. Time to healing was shorter for patients with duodenal ulcers when compared with those with active prepyloric ulcers. Recurrences were fewer for patients with pure duodenal ulcer disease (DUD) when compared with those with active or previous prepyloric ulcer disease (PUD). Patients whose ulcers were slow to heal and those with active or previous prepyloric ulcers (PUD) required a higher dose of cimetidine for effective control of their disease. All patients with slowly healing ulcers (more than 6 weeks) relapsed with 400 mg cimetidine at night. Among patients with relapse 46% with DUD and 31% with PUD were controlled by increasing cimetidine to 400 mg twice daily. Tests of acid secretion were of no value in predicting the rate of ulcer healing or relapse rate. Pepsin secretion studies, however, were of predictive value for patients with DUD but of indeterminate value for patients with PUD. Long-term cimetidine produced a significant decrease in pentagastrin-stimulated pepsin secretion (without treatment) in both patients with and without relapse. No significant changes in acid secretion were observed. As a result of these studies we recommend a cimetidine maintenance dosage of 400 mg twice a day for all patients whose ulcers are slow to heal on 1 g cimetidine a day and in patients with prepyloric ulcer disease regardless of rate of healing.
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PMID:Results of short- and long-term cimetidine treatment in patients with juxtapyloric ulcers, with special reference to gastric acid and pepsin secretion. 309 44

Duodenal ulcer therapy with H2 antagonists initially aimed to control acid secretion throughout the 24-h period, but recently nighttime suppression has been advocated. The effect of single nighttime regimens of cimetidine 400 mg BID, cimetidine 800 mg HS, ranitidine 150 mg HS, and placebo on 24-h intragastric acidity, nocturnal acid output, and pepsin secretion were studied in four healthy volunteers and four patients with healed duodenal ulcer. A nonrandomized dose of cimetidine 1200 mg HS was also studied. For all four treatments, daytime (0730-2230 h) intragastric acidity was reduced by 4-30% in the normals and by 10-44% in the duodenal ulcer patients (NS), while 24-h intragastric acidity was reduced by 44-46% and 40-64%, respectively (p less than 0.05). Reduction in nocturnal acid output was 82-96% in normals and 91-99% in duodenal ulcer, respectively. Pepsin concentration was unaffected by treatment but pepsin concentration was significantly (p less than 0.05) lower in patients than in normals. Mean 24-h gastric acid secretion was reduced by a single nighttime treatment with an H2-receptor antagonist, while nocturnal acid secretion was virtually abolished. H2 antagonists given only at night deserve further clinical evaluation to determine the minimal effective dose and optimal duration of suppression to achieve ulcer healing.
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PMID:A double-blind randomized study comparing different dose regimens of H2-receptor antagonists on 24-hour gastric secretion in normal subjects and duodenal ulcer patients. 309 64

The determination of serum pepsinogen A (= pepsinogen I) levels is of clinical importance in the study of duodenal ulcer, atrophic gastritis and gastric cancer. In the present study two different quantitative immunological techniques for serum pepsinogen A were compared: a radioimmunoassay (RIA) (Helsinki) and an enzyme-linked immunosorbent assay (ELISA) (Amsterdam). Serum samples of 177 subjects with various gastric diseases were tested in a double blind study. The correlation was excellent (r = 0.954 in the range 0-760 micrograms/l and r = 0.971 in the range 0-100 micrograms/l). The functional relationship between ELISA (x) and RIA (y), determined by weighted model II regression, was y = 1.12x-0.54. Initially the use of goat anti-PGA in the ELISA resulted in falsely high values in about 10% of the individuals. This was caused by circulating antibodies cross-reacting with goat IgG. This artefact was eliminated by pre-incubation of all samples with non-immune goat serum.
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PMID:Enzyme-linked immunosorbent assay and radioimmunoassay of serum pepsinogen A. 355 88

Gastric secretion was measured in nine patients with duodenal ulcer before, and after treatment for four weeks with omeprazole 20 mg or 40 mg daily. Basal acidity and acid output were affected variably by 20 mg, but inhibited totally by 40 mg daily. Sham feed stimulated acid output was reduced by 20 mg daily and completely inhibited by 40 mg daily. Maximal pentagastrin stimulated acid output was halved by 20 mg omeprazole daily and 84% inhibited by 40 mg daily. The reduction in acidity was always greater than the reduction of volume. Pepsin output after pentagastrin was little altered but with the reduced secretory volume pepsin concentrations were increased by both doses. The major cause of reduced aspirate acid output after omeprazole is decreased secretion of the primary acid component of the parietal cell by the proton pump H+K+ ATPase. Duodenogastric alkaline reflux is, however, markedly increased after omeprazole and is an additional factor in the resultant hypoacidity or even anacidity after this drug.
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PMID:Basal, sham feed and pentagastrin stimulated gastric acid, pepsin and electrolytes after omeprazole 20 mg and 40 mg daily. 393 37


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