Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The serum concentrations of immunoreactive gastrin and immunoreactive calcitonin were measured in 13 fasting patients with achlorhydria and pernicious anaemia and in 10 age- and sex-matched fasting control subjects. All patients had highly elevated concentrations of gastrin in serum (1468 +/- 336 pg/ml, mean "/- SEM). The mean concentration in the controls was 35.2 +/- 6.4 pg/ml. No difference in the concentration of calcitonin was found between the pernicious anaemia patients and the controls, the levels being 0.93 +/- 0.08 and 0.89 +/- 0.03 ng/ml, respectively. Suppression of endogenous gastrin secretion in 5 of the patients by intragastric acid administration was not accompanined by any decrease in calcitonin concentration in serum. The findings suggest that chronically elevated endogenous gastrin is without influence on calcitonin secretion.
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PMID:Serum calcitonin in hypergastrinaemia due to achlorhydria. 57 6

Three urinary excretion tests of vitamin B12 absorption were done in 12 patients with classic pernicious anemia. The 24-hour urinary excretion of radioactivity was 2.1% +/- 0.7% (mean +/- SEM) of the ingested dose of cyanocobalamin-57 Co. When cyanocobalamin-57 Co was mixed with hog intrinsic factor in water, excretion increased to 15.6% +/- 1.6%. When cyanocobalamin-57 Co and intrinsic factor were given in two separate capsules, which is now a frequent practice, excretion was 9.5% +/- 2.2%. In 6 patients, use of the results obtained with capsules could have led to an incorrect diagnosis. When cyanocobalamin-57 Co and intrinsic factor are given in separate capsules, binding of radioactive vitamin to intrinsic factor may be incomplete due to inadequate mixing in the stomach or to binding of intrinsic factor to blocking antibody in the gastric juice. The classic technique in which intrinsic factor and cyanocobalamin-57 Co are mixed in water before administration should be used.
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PMID:Spurious Schilling test results obtained with intrinsic factor enclosed in capsules. 120 May 29

Patients with Addisonian pernicious anaemia are alleged to generate antibodies directed against the gastrin receptor. We purified IgG from 15 patients with pernicious anaemia and 15 healthy controls in an effort to show attenuation of gastrin specific binding in vitro and inhibition of gastrin stimulated acid secretion in vivo. Binding of the IgG fraction was determined in a radioreceptor assay utilising the rat pancreatic carcinoma cell line AR42J which expresses high affinity gastrin binding sites (Kd = 5 x 10(-10)). In comparison with control serum, there was no significant displacement (p = 0.10) of human gastrin-17 binding by pernicious anemia samples at either 0.3 mg protein/ml (control (mean (SEM)) 1489 (131) cpm; patients 1858 (174) cpm) or 3 mg protein/ml (control 1930 (110); patients 2195 (107) cpm). The effect of intravenous and intragastric IgG on acid secretion in the anaesthetised rat was determined over a 60 minute period after stimulation with 1 microgram/kg human gastrin-17. A bolus injection of IgG (60-200 mg/kg) had no significant effect (p = 0.50) on gastrin stimulated acid output (29.21 (1.28) mumol H+/h) compared with control (27.48 (4.70) mumol H+/h). Similarly, instillation of 800 mg/kg IgG directly into the stomach for 90 minutes also failed to influence gastrin stimulated acid output (29.69 (3.22) mumol H+/h). Thus, we have been unable to confirm previous reports of an IgG from patients with pernicious anaemia capable of blocking gastrin receptor binding or gastrin stimulated acid secretion.
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PMID:Absence of a gastrin inhibitory factor in the IgG fraction of serum from patients with pernicious anaemia. 238 8

Measurement of N-nitroso compounds in gastric juice by different methods has given conflicting results. In order to resolve this controversy, we have assessed endogenous nitrosation by the independent N-nitrosoproline excretion test in subjects who had previously undergone gastric juice analysis by one of these methods. Ten Polya gastrectomy, 10 pernicious anaemia and nine matched control subjects were fed 380 mg of nitrate in beetroot juice and 500 mg proline. N-nitrosoproline (N-Pro) synthesised intragastrically from these precursors, and quantitatively excreted by the kidneys, was measured in 24 hour urine samples (collection checked by creatinine clearance). N-Pro excretion (mean +/- SEM) was reduced (p less than 0.01) in pernicious anaemia (1.1 +/- 0.8 ng/day) compared with matched control (18.0 +/- 7.2 ng/day), and also tended to be lower (NS) in polya gastrectomy (3.2 +/- 2.3 ng/day). Twenty four hour intragastric pH was monitored on a separate occasion in 23 of the 29 subjects; 13 were hypoacidic (pH greater than 4 greater than 50% of 24 hours) and 10 were acidic. N-Pro yields were reduced (p less than 0.01) in the hypoacidic group (0.9 +/- 0.6 ng/day) compared with the acidic group (17.9 +/- 6.6 ng/day), and N-Pro was negatively associated with mean intragastric pH (tau = -0.53, p = 0.001). We conclude that endogenous synthesis of this specific N-nitroso compound is favoured by low rather than high pH. These results are concordant with those previously reported in gastric juice from the same subjects and suggest that nitrosation is chemically rather than bacterially mediated, contrary to the nitrosamine hypothesis of gastric carcinogenesis.
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PMID:Urinary N-nitrosoproline excretion: a further evaluation of the nitrosamine hypothesis of gastric carcinogenesis in precancerous conditions. 355 92

The sulfation of gastrin in serum, antrum and duodenum was studied in 22 normo- and 20 hypergastrinemic patients. The ratio between gastrin-17 and gastrin-34 was measured in antrum and duodenum. The degree of sulfation was reduced in the antrum of hypergastrinemic patients (35.3 +/- 1.3%, mean +/- SEM) compared with 48.0 +/- 2.1% in normo-gastrinemic patients (p less than 0.001). The degree of sulfation in serum and duodenum was similar to that of the antral gastrins in all patients. The percentage of gastrin-34 in antrum was increased (7.3 +/- 0.7%) in hypergastrinemic compared with 4.9 +/- 0.3% in normogastrinemic patients (p less than 0.01). In the duodenum the percentage of gastrin-34 was similar in normo- and hypergastrinemia. When classified according to clinical diagnosis, sulfation of antral gastrin was normal in duodenal ulcer (47.6 +/- 4.5%) but decreased in gastric ulcer (36.7 +/- 1.6%, p less than 0.01) and pernicious anemia (31.3 +/- 1.9%, p less than 0.001) compared with 48.2 +/- 2.2% in control patients. In pernicious anemia a larger proportion of antral gastrins occurred as gastrin-34 (8.2 +/- 0.9%) compared with 4.8 +/- 0.4% in control patients (p less than 0.01). Our study suggests that both sulfation and proteolytic processing of the gastrin precursor is diminished in hypergastrinemia of antral origin.
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PMID:Decreased sulfation of serum and tissue gastrin in hypergastrinemia of antral origin. 397 77

The concentrations of gastrins containing the active C-terminal tetrapeptide amide (mainly gastrin-34 and gastrin-17) and the N-terminal tridecapeptide fragment of gastrin-17 were measured in antral and duodenal biopsy specimens. The antral concentration of the N-terminal gastrin fragment was much higher in patients with active duodenal ulcer (33.4 +/- 6.8 nmol g-1, mean +/- SEM, n = 15) than in controls (5.6 +/- 2.9 nmol g-1, n = 10), patients with gastric ulcer (5.6 +/- 1.8 nmol g-1, n = 10) or patients with pernicious anaemia (7.7 +/- 2.5 nmol g-1, n = 6). No differences were found between the groups regarding gastrin-34 and gastrin-17 concentrations. In duodenal extracts, the N- and C-terminal gastrin concentrations were similar in all groups of patients. These data suggest that the posttranslational processing of antral gastrin is abnormal in patients with active duodenal ulcer disease.
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PMID:Abnormal processing of antral gastrin in active duodenal ulcer disease. 643 50

The basal concentrations of sulfated and non-sulfated gastrins in serum were measured radioimmunochemically in healthy subjects and in normo- and hyper-gastrinemic diseases. The degree of sulfation in patients with duodenal and gastric ulcer, chronic pancreatitis, gallstone disease, and chronic renal failure were similar to that of healthy controls, in whom 37.7 +/- 1.9% (mean +/- SEM) of serum gastrins were sulfated. In eight patients with the Zollinger-Ellison syndrome 57 +/- 5.4% of the gastrins were sulfated (p less than 0.005, compared with controls). In patients with pernicious anemia (no. = 20) only 24.4 +/- 2.0% of the gastrins were sulfated (p less than 0.005, compared with controls). An inverse correlation (r = -0.63, p less than 0.01) was found between the degree of sulfation and the total gastrin concentration in pernicious anemia but not in gastrinoma patients. The results indicate that diseases with increased synthesis of gastrin are accompanied by an abnormal degree of sulfation.
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PMID:Variations in the sulfation of circulating gastrins in gastrointestinal diseases. 666 33