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 realisation that circulating gastrin is heterogeneous necessitates a reappraisal of gastrin's role in the increased incidence of duodenal ulcer disease that occurs in chronic renal failure. Radioimmunoassays employing region-specific antisera have been used to examine renal and extrarenal factors controlling serum gastrin concentration in patients with chronic renal failure. The present study has shown that basal serum gastrin concentrations measured with a carboxyl-terminal specific antibody were significantly higher in eight patients with chronic renal failure treated by dietary restriction (388+/-196 pM) than in 14 patients with chronic renal failure treated by haemodialysis (28.7+/-4.6 pM). However, basal gastrin concentrations in both groups of patients were significantly higher than in 25 normal subjects (12.3+/-1.8 pM) and showed significant negative correlations with maximal gastric acid secretion (p < 0.01). Markedly raised basal gastrin concentrations were observed only in chronic renal failure patients who were also achlorhydric. Although the peak postprandial increment in big gastrin concentration in 11 chronic renal failure patients (34.0+/-7.5 pM) was significantly greater (p < 0.05) than in 25 normal subjects (19.5+/-4.6 pM), the little gastrin responses were not significantly different. In addition, clearance of exogenous little gastrin was similar in four chronic failure patients (clearance half time: 8.1+/-0.7 min) and four normal subjects (clearance half time: 6.5+/-1.2 min). These studies suggest that the human kidney is unimportant in the metabolism of little gastrin. As circulating little gastrin is six times more potent than big gastrin in stimulating acid secretion, these studies suggest that the raised gastrin concentrations observed in patients with chronic renal failure have little significance in terms of their increased incidence of duodenal ulcer disease.
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PMID:Serum gastrin in patients with chronic renal failure. 746 64

It is known that Helicobacter pylori (H. pylori) plays an important role in gastritis and peptic ulcer disease in the general population. Although upper gastrointestinal mucosal lesions have been one of the most common complications in patients with chronic renal failure, quite few reports are available regarding the prevalence of H. pylori and its influence on the upper gastro-intestinal tract. The present study was conducted to examine whether H. pylori is involved in the pathogenesis of upper gastrointestinal mucosal lesions in dialysis patients. The subjects consisted of 43 dialysis patients with upper gastro-intestinal tract symptoms. Thirty-four patients without any known kidney disease were used as controls. Gastric mucosa and gastric juice were obtained endoscopically. For the determination of H. pylori, culture of biopsy specimens from the gastric mucosa and histopathological examination with hematoxylin-eosin stain were used. Concentrations of serum gastrin and gastric juice ammonia were also measured. H. pylori was observed in 53.5% of the dialysis group and 64.0% of the controls. Gastro-duodenal lesions in H. pylori-positive dialysis patients included atrophic gastritis, superficial gastritis, erosive gastritis, and gastric ulcer. In the dialysis group, ammonia concentrations in the gastric juice were higher in patients with H. pylori than in those without H. pylori (489.1 +/- 35.8 mu g/ml vs 67.0 +/- 19.2 mu g/ml, p < 0.001). The former value was also higher than that seen in the H. pylori-positive controls (152.4 +/- 18.7 mu g/ml, p < 0.01). Serum levels of gastrin were significantly higher in patients with H. pylori than in patients without H. pylori (ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Role of Helicobacter pylori in gastro-duodenal mucosal lesions in patients with end-stage renal disease under dialysis treatment]. 747 17

Endocrine abnormalities in patients with chronic renal failure are well documented. The present study aimed to assess the influence of long-term erythropoietin (EPO) therapy on endocrine abnormalities in hemodialyzed patients. Two groups of hemodialyzed patients, each of which comprised 17 subjects, were examined. The first group was treated by EPO (EPO group) while the second one did not receive this hormone (No-EPO group). A complete biochemical and hormonal check-up was performed before and at the 3, 6, 9, and 12 month points of the study period. Normal values for the estimated parameters were obtained in appropriately selected sex- and age-matched healthy subjects. After EPO therapy, an increase of the hematocrit value from 21.8 +/- 0.9 to 32.6 +/- 0.9% was observed, which was accompanied by a significant decline of plasma ferritin and saturation of transferrin. In patients of the No-EPO group, a significant although less marked rise of the hematocrit value (21.4 +/- 0.4 to 24.2 +/- 0.6%) was also noticed. EPO therapy did not change plasma levels of electrolytes (Na, K, Ca, inorganic phosphate), osteocalcin, creatinine, glucose, and alkaline phosphatase as well as plasma concentrations of calcium-related hormones (PTH, calcitonin, 1,25[OH]2D3), vasopressin, and triiodothyronine. EPO treatment induced a significant decrease in somatotropin, prolactin, follitropin, lutropin, ACTH, cortisol, plasma renin activity, aldosterone, noradrenaline, adrenaline, dopamine, glucagon, pancreatic polypeptide, and gastrin plasma levels and an increase in plasma insulin, estradiol, testosterone, atrial natriuretic peptide, thyrotropin, and thyroxine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Function of endocrine organs in hemodialyzed patients of long-term erythropoietin therapy. 762 22

In a rat model of chronic renal failure, we recently reported that hypergastrinemia was associated with increased stomach weight and parietal cell and enterochromaffin-like (ECL) cell density. In this study, the role of gastrin in mediating trophic effects of uremia on the gastric mucosa was examined by chronic immunoneutralization of endogenous gastrin in the sub-total nephrectomy uremic rat model. Three weeks after surgery, the rats were uremic (azotemic and hypertensive). Uremic rats had a significant increase in corpus mucosal height (17%), parietal cell density (14%), ECL cell density (27%), and basal gastric mucosal blood flow (63%). These effects were specifically inhibited by chronic administration of gastrin-specific monoclonal antibody (5 mg ip every other day) in the 3-wk postoperative period. Uremic rats also had an increase in stomach weight (23%), corpus mucosal area (8%), arterial blood pressure, and serum creatinine and a decrease in body weight. Gastrin immunoneutralization did not alter these effects. The findings suggest that elevated levels of endogenous circulating gastrin in uremic rats mediate, in part, the trophic response observed in the gastric mucosa.
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PMID:Gastrin mediates the increase in gastric cell growth in uremic rats. 773 85

Hypopepsinogenaemia A is often found in patients with gastric atrophy and gastric surgery. In these conditions serum pepsinogen C provides additional diagnostic information, especially when expressed as pepsinogen A:C ratio. Hyperpepsinogenaemia A has been shown in patients with duodenal ulcer disease, Zollinger-Ellison syndrome, hypertrophic gastropathy, chronic renal failure, and during omeprazole treatment. As patients with hyperpepsinogenaemia A often overlap in symptoms, endoscopical findings, and serum gastrin values, this study has evaluated whether measurement of serum pepsinogen C in subjects with hyperpepsinogenaemia A can help in differentiating clinical conditions. Serum concentrations of pepsinogen A and C were measured in serologically Helicobacter pylori negative blood transfusion donors (127) as reference population, and in patients with Zollinger-Ellison syndrome (24), duodenal ulcer (50), hypertrophic gastropathy (5), and chronic renal failure (50), and also in reflux oesophagitis patients on longterm omeprazole treatment (28). A low pepsinogen A:C ratio was found in all patients with hypertrophic gastropathy. A pepsinogen A:C ratio above the critical value of 4.7 was found in 14 (70.0%) of the Zollinger-Ellison patients, two (9.5%) of the duodenal ulcer patients, 11 (25.6%) of the patients with chronic renal failure, and in one (7.1%) of the patients receiving longterm omeprazole treatment. In fact, all but three hyperpepsinogenaemia A patients with a pepsinogen A:C ratio greater than 4.7 and normal renal function had the Zollinger-Ellison syndrome. In patients with hyperpepsinogenaemia A, a low pepsinogen A:C ratio may point to hypertrophic gastropathy, while a pepsinogen A:C ratio greater than 4.7 is suggestive for the Zollinger-Ellison syndrome.
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PMID:Diagnostic value of serum pepsinogen C in patients with raised serum concentrations of pepsinogen A. 824 94

The prevalence of Helicobacter pylori (H. pylori) was investigated in 164 consecutive patients with different degrees of renal function; group I (normal renal function) n = 84, group II (chronic renal failure, CLCR > or = 5 < 90 ml/min) n = 45, group III (haemodialysis therapy) n = 35, to test the hypothesis that the resulting different concentrations of urea in the gastric juice would have an influence on the colonization of the gastric mucosa by these urea-splitting bacteria. As every individual method for the detection of H. pylori shows disadvantages, the results of the detection methods used (urease test, Warthin-Starry stain, bacterial cultivation, direct examination of the processed sample by phase-contrast microscopy) were combined in a cumulative evaluation. These calculated cumulative indices for the antrum and corpus showed no statistically significant differences between the studied groups. The prevalence of H. pylori ranged from 34 to 54%. The histopathological findings were similar in all groups. In spite of the fact that patients with renal dysfunction had significantly higher levels of serum gastrin (P < 0.05), there was no influence on the gastric juice pH value. The relationship between the cumulative index and ammonia concentration in gastric juice was found to be linear (P < 0.05). The higher urea levels in the blood and gastric juice of patients with renal failure do not seem to be a risk factor for infection with H. pylori.
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PMID:Prevalence of Helicobacter pylori in patients with chronic renal failure. 839 2

Thirty patients with chronic renal failure (CRF) and 30 age- and sex-matched controls were assessed for gastrointestinal diseases by gastroscopy, serum gastrin determination, and routine clinical and laboratory evaluation. Biopsy specimens from their gastric oxyntic mucosa were immunohistochemically stained with monoclonal antibodies against serotonin (5-hydroxytryptamine) and chromogranin A, the latter staining all gastric endocrine cells, the former disclosing serotonin-containing enterochromaffin (EC) cells only. The average EC cell density (cells/mm2) in the CRF patients was significantly lower than in the controls: 2.6 vs 12.9 (p = 0.0005). The EC cell counts also correlated negatively with serum gastrin values (p = 0.0031). The densities of the chromogranin-positive cells did not differ between CRF patients (74 cells/mm2) and controls (76 cells/mm2) (p = 0.7559). We conclude that, in addition to the previously known findings of hypoacidity, persistent hypergastrinaemia, and G and parietal cell hyperplasia, CRF also reduces the number of oxyntic EC cells. The negative correlation between EC cell density and serum gastrin levels reflects the complex interplay between different endocrinological activities in the gastrointestinal tract.
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PMID:Enterochromaffin cell density in the gastric mucosa of patients with chronic renal failure. 870 42

Feeding problems, anorexia and vomiting are common in infants and children with chronic renal failure (CRF), and play a major role in the growth failure often found in this condition. However, the gastroenterological and nutritional aspects of CRF in children have received little attention, hence therapeutic interventions are usually empirical and often ineffective. Gastritis, duodenitis and peptic ulcer are often found in adults with CRF on regular haemodialysis and following renal transplantation. Despite persistent hypergastrinaemia, gastric acid secretion is decreased rather than increased in most of these patients, and active peptic disease appears to be promoted by the removal of the acid output inhibition (neutralisation of gastric acid by ammonia) that follows active treatment. Helicobacter pylori, on the other hand, does not seem to play a significant role in the pathogenesis of peptic disease in CRF. Gastro-oesophageal reflux has been found in about 70% of infants and children with CRF suffering from vomiting and feeding problems, and thus appears to be a major problem in these patients. In a number of symptomatic patients with CRF, gastric dysrhythmias and delayed gastric emptying have also been found; hence there appears to be a complex disorder of gastrointestinal motility in CRF. Serum levels of several polypeptide hormones involved in the modulation of gastrointestinal motility [e.g. gastrin, cholecystokinin (CCK), neurotensin] and the regulation of hunger and satiety (e.g. glucagon, CCK) are significantly raised as a consequence of renal insufficiency, and can be reverted to normal by renal transplantation. Furthermore, several other humoral abnormalities (e.g. hypercalcaemia, hypokalaemia, acidosis, etc.) are not uncommon in CRF. By directly affecting the smooth muscle of the gut or stimulating particular areas within the central nervous system, all these humoral alterations may well play a major role in the gastrointestinal dysmotility, anorexia, nausea and vomiting in patients with CRF. Specific pharmacological and nutritional interventions should thus be considered for the treatment of vomiting and feeding problems in CRF.
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PMID:Gastrointestinal function in chronic renal failure. 874 22

Several factors are involved in the persistence of endocrine alterations after renal transplantation, among which the following are to be mentioned: 1) duration of chronic uraemia before renal transplantation; 2) residual function of the patients' native kidneys; 3) quality of function of the renal graft; 4) modulation of secretion, transport, and degradation of hormones, and/or 5) altered target organ responsiveness to hormones induced by immunosuppressive drugs (glucocorticoids, azathioprine, cyclosporin A) or altered internal environment. In kidney transplant patients the following endocrine abnormalities are to be mentioned: dissociation of the physiological relationship between aldosterone synthesis and function of the renin-angiotensin system, abnormal volumetric regulation of arginine vasopressin secretion, suppressed responsiveness of cortisol secretion to stimulatory manoeuvres, persistent secondary hyperparathyroidism, relative deficiency of insulin (induced by glucocorticoid therapy), with consequent carbohydrate intolerance or even diabetes mellitus, suppressed response of gastrin and pancreatic hormone secretion to a test meal, and reduced responsiveness of atrial natriuretic peptide secretion to central hypervolaemia. Episodes of acute graft rejection are characterized by endocrine alterations similar to those seen in patients with acute or chronic renal failure.
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PMID:Function of endocrine organs in kidney transplant patients. 986 33

This study deals with the setting up of human serum calcitonin radioimmunoassay (hCT-RIA) using the high titer and specific antibody which was prepared by our own laboratory. The final dilution of the antibody titer was 1:1,200,000 when the binding rate of Bo/T was 30%. The antibody's affinity constant (Kd) was 2.25 x 10(11) L/M. No cross reaction was found between the antibody and the following eight different peptide hormones and proteins, viz.: TSH, T3, T4, ACTH, PTH, BGP, Insulin and Gastrin. The coefficients variation of intra and inter assay were 3.2% and 9.0%, respectively. The mean recovery rate of CT was 99.8%. The sensitivity of this assay was 9.4 pg/ml. The examination of this methodology showed that all its indices met the demands of RIA. There was no difference in the mean value of serum CT between the two sexes in 232 normal subjects, but the serum CT concentration in those aged of sixty and over of men and women, were much lower than those aged of fourty group. Mean CT concentration was low in the patients with primary osteoporosis, but were significantly higher in those suffering from medullary thyroid carcinoma, primary hyperparathyroidism crisis and chronic renal failure.
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PMID:[The setting up of human serum calcitonin radioimmunoassay and its clinical application]. 1045 98


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