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 metaplasia of the duodenal mucosa in biopsy specimens of healed duodenal ulcer and in surgical specimens of perforated duodenal ulcer was investigated using mucin histochemistry and the indirect immunoperoxidase method. Endoscopic methylene blue test was performed prior to biopsy. All specimens from areas showing no dye absorption revealed varying degrees of gastric metaplasia characterized by heterotopic occurrence of gastric-type foveolar cells mainly at the tips of stunted intestinal villi. On average, 31.8% of the total surface length of duodenal mucosa taken from areas showing no dye absorption was occupied by the metaplastic cells. They showed strong reactivities for periodic acid-Schiff (PAS) and galactose oxidase-Schiff sequences, while alcian blue and paradoxical concanavalin A staining, class III, were negative. Immunoperoxidase-PAS double staining revealed a few gastrin and somatostatin cells in foci of gastric metaplasia, but almost no cells containing motilin, secretin, cholecystokinin and gastric inhibitory peptide. Such endocrine cells were scattered in nonmetaplastic mucosa. While such metaplastic change has been regarded as a self-defence mechanism or adaptation of the duodenal mucosa against acid, a local decrease of normal endocrine cells, which allegedly function as acid receptors, may lead to alterations of gastroduodenal interaction. It is suggested that gastric metaplasia is important as one of the pathophysiological mechanisms involved in the recurrence of duodenal ulcer.
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PMID:Gastric metaplasia in duodenal ulcer. Histochemical considerations of its pathophysiological significance. 318 9

The patient described here, with malignant non-beta islet cell tumor of the head of the pancreas, was treated by resection of the tumor and metastases. Additional pathology of perforated duodenal ulcer and pyloric stenosis required vagotomy and pyloroplasty. The maintenance of normal gastrin levels after the operation indicates a good prognosis. We believe that the low-risk Zollinger-Ellison patient should be treated surgically and the tumor removed. When no tumor can be detected, parietal cell vagotomy should be performed to assist the pharmacological control of the gastric acid hypersecretion. Extensive surgery, such as total gastrectomy, is no longer the treatment of choice and is reserved for the so-called "cimetidine failure."
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PMID:Conservative surgery in Zollinger-Ellison syndrome: report of a case with an eight-year follow-up. 359 93

A patient with a multiple-hormone-producing islet cell carcinoma, who had previously been successfully treated with streptozotocin, was given three further infusions of this drug because of the redevelopment of gastric hypersecretion. Although some evidence of damage to the gastrinsecreting cells was obtained, the fasting plasma gastrin was not significantly altered and the patient died from a perforated duodenal ulcer. Serum insulin levels were considerably reduced and the patient became mildly diabetic but the main complication of treatment was a severe though reversible renal tubular defect. At necropsy considerable quantities of gastrin, but low levels of insulin and glucagon were extracted from a tumour metastasis.
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PMID:Further studies on streptozotocin therapy for a multiple-hormone-producing islet cell carcinoma. 432 97

In a prospective randomized clinical trial, gastric acid secretion was compared in patients after simple closure, proximal gastric vagotomy with closure, or truncal vagotomy with pyloroplasty performed for perforated duodenal ulcer. The basal and pentagastrin- and insulin-stimulated acid outputs were similar after either proximal gastric or truncal vagotomy; they were also comparable with the postoperative acid values after corresponding procedures performed electively for chronic duodenal ulcer. Conversely, the basal and maximum acid outputs after simple closure of perforation were no different from the preoperative acid outputs of a group of duodenal ulcer patients matched for age and sex. The efficacy of acid reduction by emergency proximal gastric and truncal vagotomy was shown by the respective ulcer recurrence rate of 3% (1/34) and 6% (2/32) compared with 43% (15/35) after simple closure (p less than 0.01). Acid secretory data and serum gastrin levels did not predict ulcer relapse in patients after simple closure of perforation.
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PMID:Gastric acid secretion and its predictive value after vagotomy for perforated duodenal ulcer. 637 69

Cushing's ulcers of the duodenum are well known complications of neurosurgery, head trauma, and other causes of increased intracranial pressure. Perforation of Cushing's ulcer of the duodenum is infrequently described. That the use of high-dose corticosteroids for cerebrovascular infarct in an aphasic patient may obscure the symptomatology and physical findings of a perforated Cushing's ulcer has not been described to our knowledge. We report a patient with a large left hemispherical infarct and resultant aphasia who developed a perforated duodenal ulcer and extensive chemical peritonitis while receiving high dose corticosteroids for increased intracranial pressure. She was unable to register any complaints and the typical physical findings of perforated duodenal ulcer with chemical peritonitis were virtually absent. A high index of suspicion must be maintained for a perforated Cushing's duodenal ulcer in the patient receiving high dose dexamethasone despite the presence of nonspecific symptomatology and abdominal findings. Elevated serum gastrin levels, as in this patient, may also indicate the patients with increased intracranial pressure who are at greater risk for developing Cushing's ulcer.
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PMID:Occult duodenal perforation complicating cerebral infarction: new problems in diagnosis of Cushing's ulcer. 711 24

A psammomatous endocrine tumor of the duodenum associated with a perforated duodenal ulcer, acute diffuse peritonitis and multiple organ failure is described. Histologic evaluation of the tumor shows a mixed pattern, with solid and glandular structures. Immunohistochemical stains further show cytoplasmic storage of gastrin and somatostatin. Apical CEA staining is also demonstrated in glandular areas of the tumor.
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PMID:[Duodenal endocrine tumor associated with ulcerous perforation]. 818 13

The authors describe the case of a 51-year-old male with Zollinger-Ellison syndrome manifested by epigastralgia, nausea, vomiting, hypergastrinemia and multiple endocrine neoplasia type 1. History included a Billroth II procedure for a perforated duodenal ulcer. Multiple metastatic liver lesions were found that were gastrin-negative and chromogranin-positive. Endoscopy revealed a large ulcerated gastro-jejuno-colonic fistula which was surgically repaired. Pre- and postoperative imaging studies, including the highly sensitive somatostatin-receptor scintigraphic scan using In-pentetreotide, have consistently failed to disclose other tumors. Recent reports indicate that most Zollinger-Ellison syndrome-associated gastrinomas are small, easily overlooked lesions located in the proximal duodenum rather than in the pancreas as formerly believed. In the present patient therapy with omeprazole and alpha-interferon has produced complete remission of the Zollinger-Ellison syndrome and a stabilization of tumor growth has occurred during the last 7 years, allowing the patient to live a normal life. This peculiar response to therapy is discussed.
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PMID:Liver metastases of endocrine tumour associated with multiple endocrine neoplasia type 1: a sustained response to interferon therapy or a peculiar benign course? 1110 Mar 30

We report a patient with insulinoma associated with Zollinger-Ellison syndrome. A 67-year-old woman was first admitted to our hospital for an abdominal mass. Abdominal computed tomography (CT) revealed a large pancreatic tumor, which was then diagnosed as an unresectable pancreatic adenocarcinoma. At the age of 71, she presented symptoms of hypoglycemia. Fasting blood glucose was 21 mg/dl and plasma immunoreactive insulin level was 846 microU/ ml. Plasma gastrin, glucagon, vasoactive intestinal polypeptide and somatostatin levels were all normal. At the age of 73, hypoglycemic attacks occurred more frequently and she was admitted to our hospital. Abdominal CT scan showed multiple liver metastases. Chemotherapy with 5-fluorouracil and doxorubicin was performed. Three months later, she had an emergency laparotomy because of a perforated duodenal ulcer. Plasma gastrin level was 1,960 pg/ml at that time. Gastric hypersecretion was well controlled with a proton pump inhibitor (lansoprazole) but she died of widespread cancer dissemination 8 years after her first admission. On autopsy, histologic examination revealed a mixed acinar-endocrine carcinoma of the pancreas. Immunohistochemical stains were positive for insulin, gastrin, and alpha1-antitrypsin.
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PMID:Insulinoma with subsequent association of Zollinger-Ellison syndrome. 1139 7

A patient admitted for acute abdomen was incidentally found with elevated serum calcium level. In surgery, under conservative treatment of the hypercalcemia, a perforated duodenal ulcer was found and simple closure was performed. Postoperatively, calcium level continued to rise, parathyroid hormone was elevated and ultrasonographic examination showed a lesion in the right anterior neck, while serum gastrin level was normal, thus documenting the diagnosis of primary hyperparathyroidism. Conservative treatment had no effect on calcium level and the patient was subjected to emergency neck exploration, where a large parathyroid adenoma was removed. After surgery, calcium and PTH levels were normalized and the patient was discharged on the 5th postoperative day. Peptic ulcer and its complications are usual manifestations of primary hyperparathyroidism, with or without increased gastrin level. On the other hand, cases of a perforation of peptic ulcer as the first clinical manifestation of primary hyperparathyroidism are extremely rare.
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PMID:Peptic ulcer perforation as the first manifestation of previously unknown primary hyperparathyroidism. 2148 67