Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of human urogastrone (0-25 mug. per kg. per hour intravenously) in four male patients with proven Zollinger-Ellison syndrome (z.e.s.) and in four healthy control subjects have been studied. After urogastrone in z.e.s. patients gastric acid volume and concentration decreased and basal acid output was reduced by 50-82%; the concentrations of intrinsic factor and pepsin in gastric juice increased by 60-300%; and peak plasma-gastrin concentration increased by 127-164% of basal concentration. A significant negative correlation between increase in plasma-gastrin concentration and decrease in acid output was observed (r=-0-72, P less than 0-01). Ulcer pain was relieved 30-60 minutes after the beginning of urogastrone infusion. These results suggest that urogastrone can inhibit the endogenously stimulated acid hypersecretion in z.e.s.
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PMID:Effect of urogastrone in the Zollinger-Ellison syndrome. 5 Dec 36

Three experiments were carried out in each of 6 healthy students on separate days, in a randomized order. Intravenous saline infusions were given for one hour basally in each experiment. During the second hour either pentagastrin, pentagastrin and somatostatin, or somatostatin alone were given. Gastric juice was collected continuously during all experiments. Somatostatin decreased the volume of gastric secretion and the concentrations of acid and pepsin, and output of acid, pepsin, and intrinsic factor (IF). The plasma gastrin concentration was not changed by somatostatin. A rebound effect was seen on pepsin and IF outputs after cessation of somatostatin, and on blood sugar concentration. The present study suggests that somatostatin acts on gastric secretion either directly or by mechanisms other than by inhibition of gastrin. The rebound of pepsin and IF indicates a release-inhibiting action on these substances similar to the effect of somatostatin on the release of some hormones.
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PMID:The effect of somatostatin on pentagastrin-stimulated gastric secretion and on plasma gastrin in man. 33 22

Gastric morphology, function, and immunology was studied in 68 patients with pernicious anemia (PA), 183 of their first-degree relatives, and 354 control subjects. The PA relatives and controls were comparable in age and sex distribution. In both groups, mean gastric acid output decreased and mean fasting serum gastrin levels and the prevalence of atrophic gastritis increased with age. The total prevalence of chronic gastritis was similar in the two groups, but severe atrophic gastritis of the body of the stomach (AGB), achlorhydria, parietal cell antibodies, and a raised fasting serum gastrin level were significantly more common in PA relatives than in controls. Of the PA relatives 23 had severe AGB which was indistinguishable from the gastric mucosal lesion found in PA probands and was, as a rule, accompanied by several other characteristics of type A gastritis. These included a normal antrum (78%), slight or absent inflammatory cell infiltration in the gastric mucosa (70%), achlorhydria (91%), high fasting serum gastrin level (83%), parietal cell antibodies (65%), and intrinsic factor antibodies (22%). The mean age and the proportion of subjects with slight and moderate AGB of all AGB subjects was significantly lower in PA relatives than in controls. This suggests an early onset and a rapid progression from mild to severe AGB in PA relatives. Thus, the PA relatives appear to consist of two populations, one with a high and one with little or no proneness to severe AGB. This bimodal distribution suggests the participation of a single major factor, probably genetic, in the pathogenesis of severe AGB in PA relatives.
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PMID:Gastric morphology, function, and immunology in first-degree relatives of probands with pernicious anemia and controls. 43 34

34 subjects including 5 probands with pernicious anemia, 3 probands with severe atriphic body gastritis and 26 of their first-degree relatives were studied gastroscopically, bioptically, functionally and immunologically. In general, members of the same family revealed a trend to behave similarly with respect to the parameters studied. Signs of A-gastritis (severe atrophy of gastric body glands with a normal or almost normal antrum, achlorhydria, hypergastrinemia and parietal cell antibodies), with intrinsic factor antibodies in the gastric juice and diminished intrinsic factor secretion without anemia were found both in families of probands with atrophic gastritis and pernicious anemia. This suggests a close etiopathogenetic relation of this type of mucosal lesion to overt pernicious anemia. Determination of HCl output and serum gastrin level enabled us to distinguish two differently behaving subgroups in the series, one of them with characteristics of overt adult pernicious anemia. Very low intrinsic factor secretion was found almost exclusively in connection with the presence of intrinsic factor antibodies in the gastric juice and always with severe atrophy of gastric body glands.
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PMID:Gastric lesion and pernicious anemia: a family study. 63 45

261 subjects with a normal body mucosa or with superficial gastritis used as controls for an atrophic gastritis series have been followed up for 23--27 years. Of them, 41 died during the earlier and 63 during the present follow-up period. In all, 141 subjects were reexamined in 1976--1977 and 16 answered a questionnaire. None of the subjects had gastric carcinoma or an adenomatous polyp. One patient diagnosed and reported earlier had died of gastric carcinoma during the present period of observation. Of the subjects with normal body mucosa 58% had developed superficial and 14% atrophic gastritis. Of those with superficial body gastritis 42% had developed atrophic gastritis and 18% showed an improvement of the gastritic changes. It should be noted, however, that earlier examinations were performed with blind biopsy and the present with direct vision gastroscopic biopsy. The state of the antral and body mucosa was similar in 53%, antral changes dominated in 33% and the changes in the body in 14%. Intestinal metaplasia was found in 36%, atypical epithelium in 6%, parietal cell antibodies in 0.5% and intrinsic factor antibodies in 0.5%. The fasting serum gastrin level was above 100 ng/ml in 10%. Only 2 cases fulfilled the morphological, functional and immunological criteria of type A gastritis. The present controls differed from the atrophic gastritis series in that the topography of gastritis was different and in that the incidence of metaplasia, atypia, gastric antibodies and high serum gastrin levels was markedly lower.
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PMID:Long-term observation of subjects with normal mucosa and with superficial gastritis: results of 23--27 years' follow-up examinations. 72 97

The mean concentration of gastrin in serum was determined in healthy fasting persons (n = 27), it amounted to 56.8 pg/ml (SD = 19.8 PG/ML). The values of gastrin in serum of patients, who were grouped by endoscopicbioptic criteria of antral mucosa and who exceptionally showed diffuse inflammation of gastric mucosa, amounted to 73.2 pg/ml in patients with mild superficial gastritis (n = 24), to 73.4 pg/ml in those with severe superficial gastritis (n = 55), to 82.3 pg/ml in patients with chronic atrophic gastritis (n = 11) and to 70.7 pg/ml in those with chronic atrophic gastritis and intestinal metaplasia (n = 17). The concentration of serum gastrin in patients with additional pathological processes of gastric or duodenal mucosa was also determined. Patients with gastric resection according to Billroth II (n = 15) revealed gastrin values of 47.8 pg/ml, those with duodenal ulcer (n = 5) of 58.5 pg/ml, with gastric ulcer (n = 50) of 61.3 pg/ml, with polyps in stomach (n = 10) of 109.6 pg/ml and with neoplasms of the stomach (n = 27) of 77.7 pg/ml. Gastrin values were not correlated to age or sex. The difference between the mean gastrin concentrations of the mentioned groups of patients however is not marked enough and the range of values is too wide to characterize those groups by specific gastrin levels. The determination of gastrin in serum of fasting patients is not helpful for diagnosis of gastritis without antibodies to intrinsic factor or for diagnosis of certain localized pathological conditions in stomach or duodenum obviously.
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PMID:[Serum gastrin levels in patients with changes of gastric or duodenal mucosa (author's transl)]. 93 97

Purified human urogastrone was given by intravenous infusion to 12 normal volunteer subjects and measurements made of gastric acid, pepsin and intrinsic factor secretion, and of plasma gastrin concentration. Clinical, haematological, and biochemical screening tests were made throughout the period of study. Urogastrone inhibited acid and intrinsic factor secretion whether stimulated by pentagastrin, histamine, or insulin, but had a much less marked effect on gastric pepsin output. Plasma gastrin levels did not alter significantly. Limited dose-response studies showed that 0-25 mug urogastrone kg--1 hr--1 resulted in inhibition of acid output of 80% and was not associated with clinical side-effects. No significant alteration in any of the haematological or biochemical measurements was observed in any of the subjects.
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PMID:Effect of urogastrone on gastric secretion and plasma gastrin levels in normal subjects. 110 12

Achlorhydria that is due to antrum sparing atrophic gastritis is a characteristic finding in pernicious anemia. As a consequence of this achlorhydria serum gastrin level rise. Usually several signs are required for assessing a pernicious anemia: megaloblastic anemia, low serum cobalamin level, positivity of a Schilling test, low level of intrinsic factor in the gastric juice, existence of anti-intrinsic factor antibodies in plasma and/or in gastric juice. In this study the usefulness of the serum gastrin level is assessed. We report here the results in investigating sixteen patients with a pernicious anemia. All had: megaloblastic changes on bone marrow examination, serum cobalamin level lower than 150 pg/ml. For 14 patients the performed Schilling test was positive. For 2, no Schilling test was done, but anti-intrinsic factor antibodies were elevated. Serum gastrin levels were higher than 250 pg/ml (254 to 1770 pg/ml). In our patients with pernicious anemia, as a result of hypo or achlorhydria, serum gastrin increase was higher than in any other cause of hypochlohydria: anti-acid treatment, vagotomy... Measurement of serum gastrin is easy. High levels are simple to explain if found together with a sparing antrum atrophic gastritis and/or a low level of serum cobalamin. Serum gastrin measurement may be a cornerstone to rapid and reliable diagnosis of pernicious anemia.
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PMID:[Importance of hypergastrinemia in diagnosis of Biermer's disease in adults]. 142 72

In many patients with low serum levels of vitamin B12, the absorption of the free vitamin has been normal. The present study, using a total body counter 57CoB12 absorption method that clearly separated those with intrinsic factor deficiency from controls, found that of 94 patients with low B12 levels and intact stomachs in whom the absorption of free and bound B12 was determined, 44 (47%) had normal absorption of both. However, 20 of the 94 (21%) with normal absorption of free B12 had low absorption of bound B12. The remainder (32%) had low absorption of both free and bound B12. All patients with high serum gastrin levels had low bound B12 absorption, but so did 21% of those patients with normal serum gastrin levels.
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PMID:Bound vitamin B12 absorption in patients with low serum B12 levels. 160 68

Anti-parietal cell antibody has been reported in nearly all patients with pernicious anaemia in past studies, in contrast with anti-intrinsic factor (IF) antibody which occurs in only 50-70% of such patients. However, observations in the more diverse patient population at our hospital suggest that these prevalences, originally described in predominantly elderly, white patients of European origin, no longer apply. Anti-IF antibody was found in 70% of the 324 patients, with blacks (84%) and Latin Americans (69%) having a significantly higher prevalence than whites (55%). In contrast, only 55% of the 266 patients tested had anti-parietal cell antibody. It was noteworthy that this low rate was similar in all racial groups. However, patients lacking anti-parietal cell antibody were significantly younger than those who had the antibody (54.8 +/- 17.8 vs 59.6 +/- 16.2 years, P = 0.022). Overall, a striking 30% of all patients had anti-IF antibody but not anti-parietal cell antibody, while only 13% had the latter antibody without having anti-IF antibody. This pattern was particularly striking among black patients. An interesting incidental observation was that gastrin levels were not associated with antibody status, but were significantly higher not only among women than among men but also among white and black patients than among Latin-American patients. The findings show that anti-parietal cell antibody is not found nearly as often in pernicious anaemia as has been reported in the past, and thus has no value as a diagnostic tool in pernicious anaemia. They also suggest clues to different expressions of pernicious anaemia or of its immunologic response, particularly among younger patients with the disease.
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PMID:Reassessment of the relative prevalences of antibodies to gastric parietal cell and to intrinsic factor in patients with pernicious anaemia: influence of patient age and race. 162 26


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