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)

Gastric secretory and excretory parameters and serum gastrin levels were assessed in 66 patients with chronic glomerulonephritis (CGN) with intact renal activity and those with chronic renal failure (CRF) of varying severity. Gastrin has been shown to participate in acidogenesis control, while proteolytic activity of the gastric content was not dependent on the blood level of this digestive hormone. The administration of pentagastrin stimulated active gastric juice excretion of nitrite residue that can be used for curative purposes.
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PMID:[Current clinical evaluation of indicators of the secretory and excretory function of the stomach in patients with chronic glomerulonephritis]. 272 41

Elevated serum gastrin (SG) has been reported in chronic renal failure (CRF). We studied SG levels in relation to various humoral and gastroduodenal histopathologic findings in 20 controls, 12 uremics under conservative therapy (CT), 27 patients on regular dialysis (RDT) and 8 transplanted patients (Tx). SG and parathyroid hormone (PTH) levels were estimated by radioimmunoassay (RIA), in addition serum BUN, creatinine, Ca++PO4---and alkaline phosphatase (predialysis in RDT) were determined. 20 patients (12 on CT and 8 on RDT) underwent pentagastrin (PG) stimulation test and upper gastrointestinal endoscopy with biopsy of gastric and duodenal mucosa. The mucosal samples were stained for mucopolysaccharides (MPS), nucleic acid (NA) and alkaline phosphatase (AP), and divided into intense, normal or faint staining. Mean SG was 688.71 pg/ml (CT cases), 636.2 pg/ml (RDT cases) and 280.6 pg/ml (Tx cases), all values being significantly higher than controls (118.46 pg/ml). SG level had a linear correlation with serum creatinine in CT patients and predialysis creatinine in RDT patients, but not with other parameters studied (BUN, Ca++,PTH,PO4---AP). The incidence of gastroduodenal erosions (40%) had a significant negative correlation with SG. They were more frequent with normal MPS stain (p = 0.01) and NA staining (p less than 0.001) than faint staining of gastric mucosa biopsy. The acid response to PG stimulation was inversely correlated with SG. We believe that elevated SG is compensatory to a decreased response of the gastroduodenal mucosa to PG. Mere retention of SG does not explain its elevation as its correlation with serum creatinine existed not only in patients on CT, but also in RDT patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum gastrin in chronic renal failure: morphological and physiological correlations. 315 79

In 40 young patients with chronic renal failure (CRF) on maintenance hemodialysis and 22 control subjects, (1) basal and test meal-stimulated gastrin concentrations, (2) basal and pentagastrin-stimulated gastric acid outputs, and (3) endoscopic examinations were studied. Age-matched CRF patients with control subjects had higher circulating gastrin levels both in the fasting and the test meal-stimulated state and they also had hypochlorhydria. After a test meal, the peak increment of serum gastrin in the CRF patients was more prolonged and greater than in controls. Endoscopic findings showed that the most predominant lesion in the CRF patients was hemorrhagic gastritis. Nine (64.2%) out of 14 patients were hyposecretors and none were hypersecretors. Patients with hyposecretion had higher gastrin levels as well as the same incidence of abnormal endoscopic findings as patients with normosecretion. It is concluded that hypergastrinemia in young CRF patients might be due to a combined effect of impaired renal clearance capacity and overproduction of gastrin associated with hypochlorhydria and also that the cause of gastritis in the young CRF patients might partly be due to a relative impairment of the mucosal defensive mechanism to acid. Our data suggest that the parietal cell response to gastrin in CRF patient may be impaired.
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PMID:Hypochlorhydria and hypergastrinemia and their association with gastrointestinal bleeding in young patients with chronic renal failure. 317 1

Twenty-nine patients with chronic renal failure were examined both during the predialytic stage and after active treatment (dialysis, transplantation) for upper GI diseases. They underwent a gastric dose-response secretion test, gastroduodenoscopy, radiologic upper GI series, and fasting serum gastrin determination. Upper GI diseases increased in the active treatment stage. At the time of examination, patients with these diseases had a positive ulcer history, duodenitis, duodenogastric reflux, and blood group O more often in the predialytic stage. Their stimulation sensitivity to pentagastrin and their acid secretion capacity were greater, and they were less achlorhydric. Their fasting serum gastrin level was also lower. They had less endoscopically discovered gastritis, but microscopically, with regard to gastritis, they did not differ from those who did not develop upper GI complications. In conclusion, in chronic renal failure upper GI findings increase after the active treatment. Secretion tests and endoscopy performed before active treatment give an indication of those who will develop upper GI complications during active treatment.
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PMID:Upper gastrointestinal findings in chronic renal failure. 329 37

Our previous secretin provocation studies in normal volunteers and unoperated duodenal ulcer patients suggested that the gastrin rise in gastrinoma may be an exaggeration of the normal response rather than paradoxical. We report further studies in various clinical settings having normogastrinemia (normal, n = 17; unoperated duodenal ulcer, n = 13; primary hyperparathyroidism, n = 7) and hypergastrinemia (postvagotomy, n = 5; hypochlorhydria, n = 7; achlorhydria, n = 10; chronic renal failure, n = 10; gastrinoma, n = 5). Under all nongastrinoma conditions, there were similar gastrin rises of 9-19% between 2 and 5 min after bolus intravenous GIH secretin (2 CU/kg), which fell to baseline by 8 min, except for chronic renal failure. In chronic renal failure, gastrin remained elevated from 7 to 30 min and was significantly different (p less than 0.05) at 10-30 min compared to all other nongastrinoma conditions except hyperparathyroidism. Peak rises occurred within 5 min in all entities, but only three gastrinoma patients had positive secretin provocation tests by the predefined criterion of a gastrin rise greater than 200 pg/ml. The results of secretin provocation in various clinical entities with and without hypergastrinemia further support the hypothesis that the gastrin rise in gastrinoma is an exaggeration of the normal response. The prolonged gastrin rise seen in chronic renal failure may be due to altered renal clearance, inasmuch as other hypergastrinemic states had responses similar to normal and duodenal ulcer.
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PMID:Secretin provocation: gastrin results in various clinical situations. 334 35

Gastrin releasing peptide(GRP)-like immunoreactivity in human plasma was measured using radioimmunoassay of neuromedin C (NMC) in 83 healthy and 58 diseased subjects. In the healthy group, the mean value of fasting GRP-like immunoreactivity was 2.1 +/- 1.4 (mean +/- SD) pmol/L. There was a slight positive correlation between the GRP-like immunoreactivity values and aging. Postprandial serial measurements demonstrated that GRP-like immunoreactivity showed no response to a significant elevation of serum gastrin concentration. The group with chronic renal failure on hemodialysis gave the highest value, 7.1 +/- 2.1 pmol/L (p less than 0.01). There were no statistical differences between the healthy controls and groups with peptic ulcer, liver cirrhosis, diabetes mellitus or carcinomas, although some cancer patients had a marked increase in GRP-like immunoreactivity value.
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PMID:Plasma GRP-like immunoreactivity in healthy and diseased subjects. 340 99

Conflicting results are reported in the literature on the structure and function of gastric mucosa in patients with chronic renal failure (CRF). In the present endoscopic study of 68 CRF patients on conservative treatment (regular dialyses or transplantations had not yet been undertaken), we sought to clarify whether CRF leads to hypertrophic or hypotrophic phenomena in gastric mucosa, as interpreted by the presence and grade of gastritis and by the thickness of the gastric mucosa. We found that the mean progression of gastritis in both antrum and body was significantly slower than expected in CFR patients, and that the thickness of both antral and body mucosa was significantly lower in CFR patients than in non-CRF controls. Furthermore, although the thickness of the oxyntic body mucosa in CRF showed a positive correlation to serum gastrin (SeGa) levels and even though 12 of the patients showed high SeGa levels corresponding to those seen in the Zollinger-Ellison synbdrome (300-1500 ng/l), the thickness of the oxyntic body mucosa in CRF patients did not exceed that seen in control subjects with normal SeGa. We conclude that CRF exerts inhibitory effects on the gastric mucosa resulting in retardation in the progression of chronic gastritis and hypotrophy of the gastric mucous membrane.
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PMID:Reduced thickness of gastric mucosa and retarded progression of chronic gastritis in patients with renal failure. 341 44

To gain further understanding of the peptic complications encountered in renal transplant surgery, 84 patients (19 with chronic renal failure on dietary treatment, 29 on regular dialysis treatment, 36 with a well-functioning renal transplant) were studied with regard to gastric acid secretion capacity and serum concentrations of gastrin and group I pepsinogens (PG I). The mean duration of preoperative dialysis treatment of the dialysed patients was 13.7 months. The mean length of postoperative follow-up of the transplant patients was 10.1 months. There was no significant difference between the mean gastric acid secretion of the three groups of patients. All the means were within the reported reference interval for healthy controls. However, 26% of the non-dialysed, 17% of the dialysed and 28% of the transplant patients had gastric hyposecretion. The mean serum concentration of gastrin was elevated in all patient groups and unaffected by normalization of renal function through transplantation, unlike PG I, which was normalized by the procedure. Thus, in the present era of treatment of chronic renal failure with a relatively short period of dialysis treatment, the frequent gastric hypoacidity, which is known to be peculiar to non-dialysed uraemic patients, seems also to characterize dialysis and transplant patients.
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PMID:The effect of renal transplantation on gastric acid secretion and on the serum levels of gastrin and group I pepsinogens. 390 74

In 68 patients with chronic renal failure (CRF), 15 patients with duodenal ulcer and 15 normal subjects, basal plasma gastrin levels and basal and stimulated gastric acid secretion were measured. Two antisera were used: antiserum R2702 with specificity for human G34 and its N-terminal fragments [G34] and antiserum 2604 with specificity for the four main components of gastrin (total gastrin). Basal gastrin concentrations of both total gastrin and G34-like immunoreactivity (G34LI) were significantly higher in the CRF patients than in the other two groups, irrespective of dialysis. Total gastrin levels were not correlated with serum creatinine levels. Total gastrin levels were significantly decreased during hemodialysis, but G34LI levels showed no significant change. A small amount of total gastrin was detected in the dialysate by antiserum 2604. As to the postprandial gastrin release, in the first 30 min, the pattern of response in the patients with CRF was similar to that of the normal subjects, but the peak value was attained later, and the response was more rather prolonged. Gastric analysis showed a low basal acid out put and impaired acid secretion in response to secretagogue. It is concluded that (1) one of the predominant circulating forms of gastrin in CRF is G34LI, and (2) the hypergastrinemia in the CRF patients is probably due to reduced removal of gastrin by kidneys, increased gastrin production by impairment of the negative acid feedback mechanism induced by parietal cell dysfunction or reduced parietal cell sensitivity to gastrin by atrophic gastritis.
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PMID:Hypergastrinemia and achlorhydria in chronic renal failure. 400 Mar 43

Fasting serum gastrin was measured by radioimmunoassay in 89 patients with chronic renal failure. When the serum creatinine level was used as an index of the degree of renal impairment serum gastrin rose proportionately with the degree of renal failure. Haemodialysis did not significantly alter serum gastrin levels but renal transplantation tended to return them towards normal. This study indicates that the kidney has a role in the degradation of gastrin.
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PMID:Hypergastrinaemia in chronic renal failure. 455 Aug 71


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