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)

A patient with recurrent peptic ulceration and presumed Zollinger-Ellison syndrome whose serum gastrin concentration varied widely is reported. Two antisera, one directed predominantly against nonsulfated gastrin and the other measuring both sulfated and nonsulfated gastrin, showed that in addition to wide variation in gastrin levels, this patient secreted his gastrin predominantly in the sulfated G34 form. The possibility of variable serum gastrin levels, which may reflect either spontaneous vaiation in gastrin output from Z-E tumors or differing specificity of the antiserum utilized in the immunoassay, may be of importance in the diagnosis and management of patients with the Zollinger-Ellison syndrome. Because of gastrin heterogeneity in the Z-E syndrome, this study reinforces the concept that a broad spectrum antibody, detecting all gastrin components should be routinely used in detection of patients suspected of having the Z-E syndrome.
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PMID:Variability of serum gastrin levels in Zollinger-Ellison syndrome. Studies with two antisera to gastrin. 113 Mar 77

Our experience with a commercially available kit for the measurement of serum gastrin has been reported. Significant non-specific interference was noted by the addition of serum contents in the assay which lead to erroneous results. Use of gastrin free serum as a diluent in the standard curve was found to improve the mean recovery of added gastrin. With this modification the procedure was evaluated for its clinical application. In 30 normal subjects, the fasting mean gastrin level was 78.7 plus or minus 31.9 (S.D.) pg/ml; in 18 of these individuals the postprandial mean level was 118.3 plus or minus 26.7 (S.D.) pg/ml. In 15 patients with pernicious anemia the mean level was 912 plus or minus 779 pg/ml; and in 4 patients with Zollinger-Ellison (ZE) syndrome the mean gastrin level was 1950 plus or minus 379 (S.D.) pg/ml. A significant rise in gastrin level was noted in patients with kidney failure during and after dialysis (p smaller than 0.05).
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PMID:An improved radioimmunoassay of serum gastrin using commercial kit. 113 50

The relative concentrations of big gastrin (G-34) and little gastrin (G-17) were compared in the sera and tumours (gastrinomas) of Zollinger-Ellison syndrome patients. Big and little gastrins were identified in all 10 serum samples and in all 10 tumour biopsies examined. In serum, G-34 (range of concentrations 58-220 000 fmol/ml) was the major form of gastrin and G-17 (22-78 000 fmol/ml) was a minor component; the mean relative abundance of G-17/[G17 + G34]) in serum was 0-18 and the mean relative abundance of G-34 was 0-82. In tumour, however, the opposite was true: G-17 (49-869 000 pmol/g) was the major component and G-34 (45-464 pmol/g) a minor component, and the relative proportions of G-17 and G-34 were 0-73 and 0-27 respectively. Following an intravenous injection of porcine secretin (2-0 U/kg) there was a rapid increase in concentration of all forms of gastrin in the blood, but the increase in G-17 was proportionately greater than that of G-34 (relative abundance of G-17 in basal serum was 0-21 compared with 0-37, five minutes after secretin). Differences in the half lives of G-17 and G-34 may partly explain their relative abundancies in serum and tumour tissue.
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PMID:Relative abundance of big and little gastrins in the tumours and blood of patients with the Zollinger Ellison syndrome. 114 Jun 33

With better methods of diagnosis, patients will be identified earlier in the course of their disease and will often have atypical and borderline manifestations of the syndrome. Serum gastrin measurements with calcium and especially with secretin challenge will be the most important method of diagnosis. Any patient with acid hypersecretion who has a high serum gastrin level that does higher on secretin infusion should be considered to have the Zollinger-Ellison syndrome. A firm diagnosis of the Zollinger-Ellison syndrome should be made, if at all possible, prior to operation. At operation, a thorough search of the pancreas, duodenum, stomach, greater and lesser omentum and liver should be made for primary and secondary gastrinomas. If the preoperative data firmly establish the diagnosis of the Zollinger-Ellison syndrome, a total gastrectomy should be carried out even if no primary tumor is found. Similarly, a total gastrectomy should be done even if there are massive hepatic metastases. If total gastrectomy is not performed, the patient is apt to die of complications of acid hypersecretion. The only possible exceptions to the rule of always performing a total gastrectomy are in asymptomatic patients with easily excisable tumors or patients with tumors of the duodenum that are easily excisable, providing that in both instances after the excision of the tumor the output of gastric acid as measured at operation is immediately halted. All possible metastatic tumor tissue should be removed. The more tumor tissue removed, the longer the patient will survive. Metastases should be treated aggressively. They do not disappear after total gastrectomy in our experience, and they may kill patients. Patients should be followed after operation with serial measurements of serum gastrin concentrations and by hepatic scintillation scans and hepatic angiography. If hepatic metastases develop, intrahepatic artery infusions of 5-fluorouracil may slow tumor growth.
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PMID:Natural history and experience with diagnosis and treatment of the Zollinger-Ellison syndrome. 114 7

A collaborative study was conducted to determine interlaboratory variations in the measurement of gastrin by radioimmunoassay (RIA). A kit containing reagents for a communal RIA method, as well as test samples containing different amounts of human synthetic gastrin (SHG I) and test samples of serum from a fasting normal patient admixed with varying volumes of serum from a patient with the Zollinger-Ellison syndrome, was sent to each collaborating investigator. Each investigator was requested to measure the gastrin concentrations in test samples by means of the communal RIA method, as well as the RIA method utilized in his or her laboratory. Use of the communal RIA method resulted in no significant interlaboratory variation in the determination of gastrin concentration in SHG I test samples and a maximum two- to threefold variation in determination of gastrin serum test samples. In contrast, when individual RIA methods were used to measure gastrin concentrations, the amount of SHG I in test samples reported by one laboratory was significantly different than that reported by the other three. In addition, use of different RIA methods resulted in a 2- to 19-fold interlaboratory variation in serum gastrin measurements and the maximum variation was found when the gastrin in normal fasting serum was measured. Increased variations in results, when different RIA methods were used, may be due to differences in preparation and purification of labeled antigen, to differences in separation of bound from free hormone, and to differences in the antibodies themselves.
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PMID:Interlaboratory reproducibility of gastrin measurements by radioimmunoassay. 115 Nov 67

Plasma gastrin response to the intravenously administered secretin was investigated in various clinical entities. The marked increase of plasma gastrin was found in response to secretin in a case of suspected Zollinger-Ellison syndrome in contrast to various degrees of plasma gastrin decrease seen in patients with ordinary or postoperative recurrent peptic ulcer. The diagnostic value of secretin provocation test was stressed especially in relation to differentiation between Zollinger-Ellison syndrome and recurrent ulcer due to retained pyloric antrum kept away from the food-passing route, both of which are characterized by hypergastrinemia and acid hypersecretion.
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PMID:Diagnostic value of secretin provocation test. 115 84

The effect of exogenous glucagon and secretin on resting lower esophageal sphincter (LES) tone during endogenous hypergastrinemia was studied in 2 patients with proven Zollinger-Ellison Syndrome (ZES). Intravenous glucagon and in one patient secretin, in dosages which decrease LES pressure in normals during LES stimulation by exogenous gastrin, caused a decrease in resting LES pressure in the ZES patients. This drop in LES tone occurred both during concomitant serum gastrin rise caused by secretin and serum gastrin decline caused by glucagon. This finding suggests that the action of secretin on LES pressure may be independent on endogenous gastrin, while the glucagon effect on LES tone may be mediated through gastrin.
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PMID:Lower esophageal sphincter responses to enteric hormones in two patients with Zollinger-Ellison syndrome. 115 11

Whereas 67 patients with duodenal ulcer had fasting and 30-minute postprandial mean serum gastrin levels not substantially different from 32 normal subjects, they had substantially higher fasting and histamine-stimulated gastric acid secretion. The increased acid secretion found in patients with duodenal ulcer is not caused by increased serum gastrin levels. Ten patients with recurrent ulcer, after incomplete vagotomy and gastric resection, had high gastric acid secretion and normal serum gastrin levels. Three patients with recurrent ulcer following complete vagotomy and gastric resection, but with retained antrum, had both high gastric acid secretion and high fasting and postprandial secrum gastrin levels. Three patients with Zollinger-Ellison tumors had even higher basal acid outputs and serum gastrin levels. The combination of basic gastric acid secretory studies and serum gastrin determinations may identify three causes of recurrent ulcer: incomplete vagotomy, retained antrum, and Zollinger-Ellison tumor.
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PMID:Gastrin determinations in symptomatic patients before and after standard ulcer operations. 115 53

We have successfully grown six Zollinger-Ellison tumors in vitro with use of a monlayer tissue culture technique. The initial gastrin concentration in the medium varied between 0 and 100 ng per ml. Many cytoplasmic secretory granules were seen in the cells of one culture population. Gastrin secretion was stimulated by the addition of fresh medium to the culture flasks. Both the culture cells and the medium were found to contain primarily big gastrin (G-34) but smaller amounts of little gastrin (G-17) were also present. Gastrin concentration in the medium decreased with time in culture until no hormone was detected between 2 and 6 weeks, possibly because of endocrine cell dedifferentiation and an increased proportion of fibroblasts in the population.
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PMID:Culture of Zollinger-Ellison tumor cells. 116 4

Changes of the stomach, duodenum and small bowel due to gastrin-producing tumors are important signs for the diagnosis of Zollinger-Ellison syndrome. Peptic esophagitis and calcification of a gastrin producing tumor of the pancreas are typical changes in the Zollinger-Ellison syndrome.
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PMID:[Peptic esophagitis and tumor-calcification in the Zollinger-Ellison Syndrome (author's transl)]. 117 44


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