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 function and histology were investigated in 24 patients with untreated chronic renal failure. At endoscopy nine patients had oesophagitis, 12 patients were considered to have gastritis, and the duodenum appeared inflamed in 20 patients. Endoscopic biopsies were taken at standard sites in the stomach and duodenum; gastritis was found in all patients, and 17 patients had duodenitis. Stimulated acid secretion was impaired in seven out of 20 patients and acid hypersecretion was found in a further two patients. Pepsin output correlated well with acid output in these patients. Fasting serum gastrin levels were elevated in 12 of the 19 patients tested. Patients with atrophic gastritis had low acid outputs and hypergastrinaemia, and when extensive gastritis was present, the patients tended to have more severe renal failure and hyposecretion of acid. Three patients were studied again after regular haemodialysis or renal transplantation and were found to show marked endoscopic and histological improvement.
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PMID:Gastric function and histology in chronic renal failure. 37 52

Recent experience with 40 patients with the Zollinger-Ellison syndrome at all Mayo Clinic suggests that traditional clinical criteria for diagnosis are often absent or invalid. Patients are younger have a shorter duration of symptoms, and often present without prior gastric surgery. Clinical, roentgenographic, and endoscopic findings indistinguishable from those of idiopathic duodenal ulcer or erosive duodenitis were the only presenting features in half of the patients in this series. Therefore, increased diagnostic use of serum levels of gastrin and gastric analysis appears desirable, particularly in patients selected for elective surgical treatment of duodenal ulcer disease, because specific therapeutic approaches may be required.
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PMID:A reappraisal of clinical, roentgenographic, and endoscopic features of the Zollinger-Ellison syndrome. 62 40

Biopsy specimens have been taken from five standard sites in the stomach and from the duodenal bulb in order to investigate the association of gastritis and duodenitis with duodenal ulcer. Twenty patients with chronic duodenal ulcer were investigated in this manner and in addition had gastric secretion tests and a radio-immune assay of serum gastrin under differing conditions. The patients were then treated either by a truncal vagotomy and pyloroplasty (TVP) or by a highly selective vagotomy without a drainage procedure (HSV). All the investigations were repeated three months postoperatively. Duodenal ulcer was usually associated with gastriitis, although this varied in extent and severity from patient to patient. In nearly all the patients, gastritis was present at the pyloric end of the stomach and along the lesser curve. In more than half of the patients, gastritis was also present in the body of the stomach but the fundus was usually spared. Chronic duodenitis was found in the duodenal bulb in all these patients. After vagotomy there was a marked increase in both the extent and severity of the proximal gastritis in both treatment groups but the distal gastritis remain almost unchanged. There was little change in the incidence of duodenitis after vagotomy but its severity was lessened. No correlation was found between the peak acid output (PAO) in response to Histalog and the severity of the gastritis or the duodenitis either before or after operation, with one exception. The postoperative PAO was significantly less in those patients who developed a severe proximal gastritis after vagotomy. No relationship was found between the severity of the distal gastritis and the levels of serum gastrin. No correlation was found between either the basal or peak acid output and the corresponding serum gastrin levels before or after vagotomy.
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PMID:Gastritis duodenitis, and circulating levels of gastrin in duodenal ulcer before and after vagotomy. 97 13

Although Helicobacter pylori is now accepted as the major aetiological factor in chronic gastritis in man, many of the factors which determine its pathogenicity are unknown. The organism has adapted to survive in the low-pH environment of the stomach, partly through its ability to buffer hydrogen ion by the hydrolysis of urea and by the presence of lectins on its surface, which bind to gastric mucosa and epithelial cells. After attachment, harmful toxins and enzymes have access to the gastric cells and cellular damage and an immune response ensues. In patients with duodenal ulceration, Helicobacter pylori-related gastritis predominantly affects the gastric antrum and has a high prevalence. Excessive gastrin production has been suggested as a potential aetiological factor linking infection with duodenal ulcer development. Perhaps more important is the association between gastric metaplasia of the duodenal epithelium, which is correlated with acid load and is more extreme in H. pylori positive patients with duodenitis. Organisms may subsequently spread from the gastric antrum into areas of gastric metaplasia in the duodenal bulb, leading to areas of chronic duodenitis and ultimately frank ulceration. It should not be overlooked, however, that other factors such as genetic predisposition, blood group, stress, drugs and smoking all have a role to play in the outcome, given the comparatively small number of patients in the general population infected with H. pylori who develop ulcer disease.
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PMID:Role of Helicobacter pylori in gastritis and duodenitis in man. 144 34

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

In 16 consecutive patients with systemic mastocytosis, we prospectively evaluated a variety of gastrointestinal functions and examined how they relate to the occurrence of gastrointestinal symptoms. Nine patients had either a duodenal ulcer or duodenitis. Hypersecretion of gastric acid was present in 6 patients, and in these patients the mean basal acid output was 20.7 +/- 4.1 mEq/h (range 14-39 mEq/h). Impaired small intestinal absorption occurred in 5 patients, although this was usually mild. The mean fractional emptying rate of liquids for all patients (14.7% +/- 2.3% per minute) did not differ from that for controls (10.7% +/- 0.6% per minute). Mean mouth-to-cecum transit time measured by breath hydrogen testing was the same among patients (87.7 +/- 6.7 min) and controls (86.7 +/- 8.0 min). Plasma histamine concentrations were increased in all patients (mean 1886 pg/ml, range 480-7450) and correlated with the basal acid output (r = 0.64, p less than 0.02) but not maximal acid output or the presence or absence of pain or diarrhea. Mean fasting plasma concentrations of motilin, substance P, and neurotensin from 6 patients did not differ significantly from controls, whereas gastrin and vasoactive intestinal peptide were significantly less than in controls (p less than 0.01). Gastrointestinal symptoms, consisting of abdominal pain or diarrhea, occurred in 80% of patients. Abdominal pain classified as dyspeptic was usually associated with acid-peptic disease of the duodenum and hypersecretion of gastric acid, whereas abdominal pain of a nondyspeptic character was not. Only in those cases of diarrhea consisting of greater than 200 g stool/day was gastric acid hypersecretion frequently found. Neither fecal urgency nor nondyspeptic pain could be accounted for by alterations of gastrointestinal transit. These results demonstrate that gastrointestinal symptoms, peptic disease, and mild malabsorption are much more common than described previously in patients with systemic mastocytosis. Furthermore, the results provide no evidence for the contention that altered gastrointestinal transit is involved in the pathogenesis of these symptoms.
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PMID:Gastrointestinal dysfunction in systemic mastocytosis. A prospective study. 339 14

Acid secretory behavior as well as gastrin levels were evaluated in 38 cases of chronic duodenitis. Basal HCl secretion was normal in 39% of cases, hypochlorhydria was observed in 29%, and hyperchlorhydria in 32%. Maximal acid output was normal in 71% of patients with duodenitis, decreased in 19%, and increased in 10%. Fasting serum gastrin was always within normal limits. The secretory behavior correlated with age but not with the histological pattern of duodenal mucosa. In chronic duodenitis, normal secretion or hypochlorhydria is the prevailing finding. This does not exclude the possibility of a peptic pathogenetic mechanism which could be involved in the rare cases of chronic duodenitis with hyperchlorhydria. Acid-peptic disease is not etiopathogenetic in the causation of most cases of chronic duodenitis.
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PMID:Is duodenitis always a peptic disease? 400 72

Seventy-five dialysis patients awaiting renal transplantation were studied. Investigations included single contrast barium meal, serum gastrin assay, gastric acid studies, and fiberoptic gastroduodenoscopy with multiple biopsies. Radiological studies revealed five duodenal ulcers and one gastric ulcer. Endoscopy showed gastroduodenal lesions in 57 patients (49%). Superficial gastritis was present in 50 patients (66.7%), atrophic gastritis in 11 (14.6%), and duodenitis in 30 (40%). Hypergastrinemia was observed in 48 patients (64%). Maximum acid output was markedly elevated in 33 patients. Acid hypersecretion was found to be correlated with the presence of endoscopic lesions and histological evidence of gastritis. Nine of the 11 patients with atrophic gastritis were acid hyposecretors and had low gastrin levels. Pretransplant gastric assessment identified a relevant number of gastroduodenal lesions in these patients. The increased risk of severe posttransplant ulceration justifies thorough gastric assessment and prophylactic antiulcer therapy in all renal transplant candidates.
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PMID:Assessment of the upper gastrointestinal tract in hemodialysis patients awaiting renal transplantation. 634 17

We studied the gastric response to severe head injury and multiple trauma in 53 patients admitted to the surgical intensive care unit at the University of Louisville. Twenty-two of the 32 patients with severe head injury could have endoscopy. Each patient had gastritis or duodenitis. Patients with severe head injury had a slightly higher rate of gastric acid secretion than did the other trauma patients without severe head injury, but the difference was not significant. Serum gastrin levels were normal in both groups and did not correlate with intracranial pressure. Pancreatic polypeptide levels were significantly higher in patients with severe head injury compared with the control trauma patients without head injury. Elevations in pancreatic polypeptide may be linked to increases in intracranial pressure. We conclude that erosive gastritis occurs commonly in patients with severe head injury and that severe head injury is associated with a marked increase in pancreatic polypeptide levels in the fasted, nongut-stimulated state. Gastrin levels are within normal limits. Head injury appears to specifically increase pancreatic polypeptide release, probably by influencing autonomic centers in the mid brain. Because the cephalic phase of pancreatic polypeptide release is vagalcholinergic, the data are consistent with the hypothesis that severe head injury increases vagal activity. Participation of vagal adrenergic fibers in this process cannot be excluded.
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PMID:Gastric response to severe head injury. 669 57

Controversial data have been reported on gastric acid secretion in patients with chronic pancreatitis. Moreover, studies on gastroduodenal morphological changes in patients with this disease and with other alcohol-related conditions have given different results. Basal and penta-gastrin-stimulated gastric secretion, histological changes of gastric and duodenal mucosa, and basal and meal-stimulated gastrin were measured in 21 patients with chronic alcoholic pancreatitis and in the following pair-matched groups: 21 chronic alcoholics and 21 control subjects (nonulcer dyspepsia), and in 19 patients with proven liver cirrhosis of alcoholic origin. No patient suffered from peptic ulcers. Moreover, gastric secretion was also measured in 51 patients with proven duodenal ulcers and in 34 healthy subjects. Basal acid output in patients with chronic pancreatitis was significantly higher (p less than 0.05) than in the other groups, except for the patients with duodenal ulcers. Peak acid output values in patient with chronic pancreatitis were similar to those measured in patients with duodenal ulcer, and they were higher than in the healthy subject group and in patients with liver cirrhosis, but statistical significance was not attained for patients with nonulcer dyspepsia. An increased frequency of duodenitis was found in patients with chronic pancreatitis, whereas an increased frequency of gastric metaplasia in the duodenal bulb was observed in all the patients with alcohol-related conditions considered. No relevant differences among the considered groups were found relating to gastric histological changes. Basal and meal-stimulated gastrin were similar in all the studied groups. This study suggests that in patients with chronic pancreatitis there is increased gastric secretion and probably an increased capacity for secretion of acid. Moreover, in patients with chronic pancreatitis, duodenitis seems to be frequent, but it probably is not directly related to chronic alcohol consumption.
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PMID:Gastric secretion, gastroduodenal histological changes, and serum gastrin in chronic alcoholic pancreatitis. 707 77


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