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)

If recurrent peptic ulceration follows partial gastrectomy with Billroth II reconstruction, retained antrum on the duodenal stump may be the culprit. Moderate hypergastrinemia and a high basal acid output (BAO) to maximal acid output (MAO) ratio on gastric analysis should alert the clinician. Careful filling of the afferent loop on barium meal or technetium 99m scanning may verify the diagnosis. The secretin provocative test may be helpful in distinguishing retained antrum from the Zollinger-Ellison syndrome by eliciting a decrease in serum gastrin levels in patients with retained antrum and an increase in serum gastrin levels in patients with Zollinger-Ellison syndrome.
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PMID:Serum gastrin levels in the differential diagnosis of recurrent peptic ulceration due to retained gastric antrum. 62 3

In ten Heidenhain pouch (HP) dogs who previously had undergone parietal cell vagotomy (PCV) with gastroduodenostomy, the antral nerves were cut, and the PCV thus converted to a selective gastric vagotomy (SGV). Mean gastric emptying rate was unaffected but antral motility changed considerably, the stomach became big and slack, and the emptying of a food-barium meal became purely passive. While the duodenal bulb was often filled with gastric content before antral denervation, this happened very seldom afterwards. Fasting, food-stimulated and 24-hour HP acid secretion increased significantly after denervation, but this was not accompanied by any significant changes in serum gastrin concentration. This indicates that other factors than gastrin must be responsible for the increased HP acid response to a meal after antral denervation.
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PMID:Antral denervation of parietal cell vagotomized dogs. Effect upon gastric emptying and motility, Heidenhain pouch acid secretion and serum gastrin concentration. 83 73

Heidenhain pouch (HP) dogs were studied. After gastroduodenostomy (GD) gastric emptying time was unaffected, but cineradiography showed that the strength of the antral contractions diminished considerably, while the number of peristaltic waves increased. "Circus movements" of the barium meal through the GD to the duodenum and back to the stomach through the pylorus occurred. No significant changes in food-stimulated HP acid secretion or serum gastrin response were observed. After parietal cell vagotomy (PCV) gastric emptying and motility was unaffected, but food-stimulated HP acid secretion and serum gastrin response increased significantly. After addition of a GD to PCV gastric emptying time decreased significantly but similar changes in antral motility occurred as after GD alone. The food-stimulated HP acid secretion and serum gastrin response became significantly reduced. Fasting HP acid secretion and serum gastrin concentration were not significantly altered by any of the surgical procedures.
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PMID:Gastroduodenostomy in dogs with and without parietal cell vagotomy. Effect upon gastric emptying and motility, Heidenhain pouch acid secretion and serum gastrin concentration. 83 81

From the experience of treating 91 patients with a proven recurrent ulcer we consider that if a proven ulcer is shown to be present and a gastrin-secreting tumour is excluded an appropriate reoperation will almost always produce a successful result (94 per cent). Before subjecting patients to reoperation all attempts must be made to secure a precise diagnosis. The following investigations should be performed: barium meal, panendoscopy of the upper gastrointestinal tract, determination of maximum acid output (with insulin test and gastrin analysis if appropriate), and cholecystography. Before accepting a diagnosis of recurrent ulcer at least 2 of the first 3 tests should be postive. If the primary operation was a resection we advocate vagotomy alone as the second operation, provided there are no local complications such as stenosis, bleeding, or fistula. If the primary operation was a vagotomy and the recurrence is associated with a positive response to the insulin test we advocate revagotomy and antrectomy. If the insulin test is negative we normally repeat the test; if it is still negative then we use antrectomy alone.
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PMID:Assessment and treatment of recurrent peptic ulceration. 111 90

No change was observed in fasting Heidenhain pouch (HP) acid secretion and fasting serum gastrin concentration following parietal cell vagotomy (PCV) in six dogs whereas significant increase in food-stimulated pouch secretion and serum gastrin concentration was observed. The increase in pouch secretion after PCV took place mainly in the first 2 h after meal. The maximum serum gastrin concentration was reached at 15 min after feeding before as well as after PCV. Maximum in HP secretion was reached later, at 120 min before and at 90 min after surgery. Gastric emptying studies, using a food-barium meal, showed a slight decrease in the emptying rate after PCV in two dogs, while it was unchanged in the others. Cineradiography showed an unaffected antral motility in all dogs after PCV.
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PMID:Parietal cell vagotomy in dogs. Influence on heidenhain pouch acid secretion, serum gastrin concentration, gastric emptying and motility. 118 54

Fourteen patients with clinically obvious gastro-oesophageal reflux were examined by conventional barium meal radiology. Neither exogenous penta-gastrin nor cholecystokinin appeared to influence the radiological competence of the gastro-oesophageal junction in ten of thos patients. The remaining four patients were used as controls and normal saline was injected instead of the active preparation. Radiological competence was unaffected. The significance of these findings is discussed.
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PMID:The effect of penta-gastrin and cholecystokinin on radiological gastro-oesophageal competence. 120 44

Today the upper gastrointestinal endoscopy is the diagnostic tool of choice to detect peptic gastroduodenal lesions. In case of substantial gastric outlet obstruction or strong suspicion of perforated ulcer, an upper gi-transit with barium or water soluble contrast medium in suspected perforated ulcers may be useful. Gastric ulcers are endoscopically controlled up to their complete healing and biopsies taken at each endoscopy in order to rule out gastric cancer. In contrast, duodenal ulcers are rarely malignant and uncomplicated duodenal ulcers, correctly treated with omeprazole over 8 weeks do not necessarily need a final endoscopic control. Since about 5% of duodenal ulcers treated with H2 blockers or mucosal protective agents do not heal within 8 weeks however, an endoscopic control of the healing is recommended. In peptic ulcer patients tests for detection of helicobacter pylori are only needed in presence of a hard indication for immediate eradication: Frequent ulcer recurrencies, complicated ulcer disease or very painful ulcer relapses, because the eradication therapy is often not well tolerated and the patient compliance therefore compromised. 30% of helicobacter infected patients have antibiotic resistant strains and there is no sufficient longterm experience with the eradication therapy available (4) to 8 weeks after treatment of the helicobacter pylori infection the effect on ulcer healing and infection should be verified. Determinations of plasma gastrin levels in peptic ulcer patients are mandatory in patients with suspected Zollinger-Ellison syndrome or patients with treatment resistant ulcers or recurrent ulcers after vagotomy or partial gastric resection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diagnosis of peptic ulcer disease]. 147 69

161 cases of chronic gastritis (including 59 superficial gastritis, 86 atrophic gastritis, 16 superficial gastritis combined with atrophic gastritis) typed in deficiency syndrome (including 64 Spleen-deficiency syndrome, 97 Spleen-Kidney-deficiency syndrome) were studied clinically with modern medicinal multiple-index. The gastroscope image, pathologic changes of gastric mucosa, stomach barium meal examination, gastric acid, serum gastrin, urine pepsinogen, urine 17-ketosteroid, vegetative nerve function, peripheral blood picture, etc. were selected as observation indices. The preliminary findings showed that in Spleen-deficiency patients, the superficial gastritis constituted the majority, the asthenic stomach constituted the minority, the gastric secretion and the serum gastrin were on the high side, the urine pepsinogen, the adrenocortical function and the hemoglobin were on the low side, but the white blood cell was rather normal; otherwise, in Spleen-Kidney deficiency patients, the atrophic gastritis and the asthenic stomach constituted the majority, the gastric secretion decreased, the serum gastrin level was higher, while the urine pepsinogen, the adrenocortical function, white blood cell and the hemoglobin were on the low side. It was also found that in certain same inflammation changes, the gastric secretion of the Spleen-Kidney-deficiency syndrome was markedly than that of Spleen-deficiency syndrome. With the treatment method of invigorating the Spleen and reinforcing the Spleen-Kidney, each index was relatively improved. The degree of seriousness to inflammation changes of gastric mucosa and the disturbance or imbalance of gastric secretion function were reflected from the Spleen-deficiency and the Spleen-Kidney-deficiency syndromes of chronic gastritis. It is suggested that hemopoiesis and hypothalamo-adenohypophysial-adrenal cortical axis be influenced.
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PMID:[Deficiency syndrome of chronic gastritis]. 220 29

The interrelations among fasting serum gastrin, serum creatinine, gastric acid secretion variables, and G-cell densities were analyzed in 47 patients with chronic renal failure (CRF). The patients also underwent gastroscopy and radiologic upper gastrointestinal barium examination. It is suggested that the hypergastrinemia seen in CRF is related to several factors: gastric acidity, grade of renal failure, G-cell density, and basal gastrin secretion rate. With regard to serum gastrin two different populations can be found, the cutting-off point being 300 ng/l. Although the group with high gastrin levels included significantly more patients with gastric body atrophy than the other group (4 of 11 versus of 1 of 36), most of them had no atrophy, which indicates that (an)other mechanism(s) is responsible for the hypergastrinemia. In the relation between serum gastrin and gastric acidity also, two differently behaving subgroups emerged. In the first, strong acidity change corresponded to minor gastrin change, whereas in the other, minor acidity change corresponded to marked gastrin change. The correlation coefficients between gastrin and acidity were high within both subgroups. During regular dialysis patients preserve the characteristics delineated from non-dialyzed values. Patients with signs of duodenal ulcer disease had high maximal acid output and low serum gastrin. Otherwise no associations were found between GI findings and the variables studied.
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PMID:Serum gastrin in chronic renal failure: its relation to acid secretion, G-cell density, and upper gastrointestinal findings. 259 56

A 14-year-old case was reported with a primary postbulbar duodenal ulcer, which was confirmed by barium meal study and duodenoscopy. In the preoperative study, the patient showed marked gastric hyperacidity: maximal and peak acid output were 0.980 and 1.434 mEq/kg/hr, respectively. As previously described, hyperacidity appears to be a main factor in the pathogenesis of postbulbar duodenal ulcer. Fasting and postprandial serum gastrin secretion was not thought to be responsible for gastric hyperacidity in the present case. Upon histological investigation, the operatively resected stomach did not suggest a possible relationship between hyperacidity and an enlarged parietal cell mass.
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PMID:Gastric acid secretion in a child with postbulbar duodenal ulcer. 260 5


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