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Ellison Syndrome (ellison + syndrome)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Occurrence and relapse of bleeding from duodenal ulcer: respective roles of acid secretion and Helicobacter pylori infection

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 6 2001
G. Capurso
Background: Helicobacter pylori infection, gastric acid hypersecretion and NSAID consumption may cause peptic ulcer. Aim: To investigate the respective roles of H. pylori and acid secretion in bleeding duodenal ulcer. Patients and methods: A total of 99 duodenal ulcer patients were referred for evaluation of acid secretion: seven with Zollinger,Ellison Syndrome; 14 with hypersecretory duodenal ulcer, defined by the coexistence of elevated basal acid output and pentagastrin acid output; and 78 duodenal ulcer patients with normal acid output. All non-Zollinger,Ellison Syndrome patients were H. pylori -positive and cured of infection. All patients were followed-up for a 36-month period, to assess the occurrence of bleeding episodes. Results: Twenty-nine patients had at least one bleeding episode in the 4 years before the study. Bleeding was more frequent in males and in patients on NSAIDs. The mean basal acid output was not higher among bleeders. In the 21 patients (14 hypersecretory duodenal ulcer, seven Zollinger,Ellison Syndrome) with basal acid output > 10 meg/h and pentagastrin acid output > 44.5 meg/h, the risk of bleeding was higher (OR 6.5; 95% CI: 2,21). In the follow-up period, three out of 83 (3.3%) non-Zollinger,Ellison Syndrome patients had a H. pylori -negative duodenal ulcer with bleeding. The risk of bleeding after H. pylori cure was not higher in hypersecretory duodenal ulcer patients (P > 0.3), nor among patients with previous bleeding episodes (P > 0.2). Conclusions: In H. pylori -positive duodenal ulcer patients, the coexistence of elevated basal acid output and pentagastrin acid output leads to a sixfold increase in the risk of bleeding. After H. pylori cure, gastric acid hypersecretion is not a risk factor for bleeding. However, duodenal ulcer recurrence with bleeding may occasionally occur in patients cured of H. pylori, even if acid output is normal. [source]

Review article: strategies to determine whether hypergastrinaemia is due to Zollinger,Ellison syndrome rather than a more common benign cause

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 10 2009
S. V. M. MURUGESAN
Summary Background, As there is considerable overlap between the fasting serum gastrin concentrations found in Zollinger,Ellison syndrome and various common conditions such as Helicobacter pylori infection and acid suppressing medication use, establishing the cause of hypergastrinaemia in individual cases can sometimes be difficult. Aim, To review the causes of hypergastrinaemia and the role of additional non-invasive investigations in hypergastrinaemic patients. Methods, Review of articles following a Pubmed search. Results, As gastrinomas may cause serious complications and be potentially life threatening, investigation of hypergastrinaemic patients should particularly focus on confirming or refuting the diagnosis of Zollinger,Ellison syndrome. Establishing the cause of hypergastrinaemia may be difficult when there is only a mild-to-moderate elevation of fasting serum gastrin concentration and concurrent treatment with proton pump inhibitor drugs and the presence of H. pylori infection can both confuse the clinical picture. A variety of provocative tests are therefore useful for establishing whether a hypergastrinaemic patient has a gastrinoma and current evidence suggests that the secretin test should be used first line. Conclusions, We suggest an algorithm for the investigation of patients found to have an elevated fasting serum gastrin concentration and address the roles of gastrin stimulation tests in current clinical practice. [source]

Review article: potential gastrointestinal effects of long-term acid suppression with proton pump inhibitors

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 6 2000
Laine
This review examines the evidence for the development of adverse effects due to prolonged gastric acid suppression with proton pump inhibitors. Potential areas of concern regarding long-term proton pump inhibitor use have included: carcinoid formation; development of gastric adenocarcinoma (especially in patients with Helicobacter pylori infection); bacterial overgrowth; enteric infections; and malabsorption of fat, minerals, and vitamins. Prolonged proton pump inhibitor use may lead to enterochromaffin-like cell hyperplasia, but has not been demonstrated to increase the risk of carcinoid formation. Long-term proton pump inhibitor treatment has not been documented to hasten the development or the progression of atrophic gastritis to intestinal metaplasia and gastric cancer, although long-term studies are required to allow definitive conclusions. At present, we do not recommend that patients be tested routinely for H. pylori infection when using proton pump inhibitors for prolonged periods. Gastric bacterial overgrowth does increase with acid suppression, but important clinical sequelae, such a higher rate of gastric adenocarcinoma, have not been seen. The risk of enteric infection may increase with acid suppression, although this does not seem to be a common clinical problem with prolonged proton pump inhibitor use. The absorption of fats and minerals does not appear to be significantly impaired with chronic acid suppression. However, vitamin B12 concentration may be decreased when gastric acid is markedly suppressed for prolonged periods (e.g. Zolllinger,Ellison syndrome), and vitamin B12 levels should probably be assessed in patients taking high-dose proton pump inhibitors for many years. Thus, current evidence suggests that prolonged gastric acid suppression with proton pump inhibitors rarely, if ever, produces adverse events. Nevertheless, continued follow-up of patients taking proton pump inhibitors for extended periods will provide greater experience regarding the potential gastrointestinal adverse effects of long-term acid suppression. [source]

The analysis of immunophenotype of gastrin-producing tumors of the pancreas and gastrointestinal tract

CANCER, Issue 9 2003
Larissa Gurevich M.D., Ph.D.
Abstract BACKGROUND Gastrinomas are located more frequently in the pancreas, which normally has no cells that can produce gastrin. They have a more aggressive course than other pancreatic endocrine tumors and extrapancreatic gastrinomas associated with multiple endocrine neoplasia Type 1 syndrome. The current study analyzed immunophenotypes of gastrinomas and compared them with other pancreatic endocrine tumors. METHODS Twenty-one formalin-fixed, paraffin-embedded specimens (15-tumors in the pancreas, 1 in the duodenum, 1 in the stomach, 1 in the liver, and 3 of unknown primary location) accompanied by Zollinger,Ellison syndrome and 17 other pancreatic endocrine tumor specimens were investigated. They were stained immunohistochemically for gastrin, chromogranin A, synaptophysin, insulin, glucagon, somatostatin, pancreatic polypeptide, calcitonin, serotonin, chorionic gonadotropin, adrenocorticotropic hormone, carcinoembryonic antigen, epithelial membrane antigen, and cytokeratin 19. RESULTS Gastrinomas coexpressed neuroendocrine and exocrine markers, including chromogranin A, synaptophysin, carcinoembryonic antigen, cytokeratin 19, and epithelial membrane antigen. Carcinoembryonic antigen was found in all 17 gastrinomas (100%), cytokeratin 19 was found in 15 of 17 (88.2%) gastrinomas, and epithelial membrane antigen was found in 16 of 18 (88.9 %) gastrinomas. Cytokeratin 19, epithelial membrane antigen, and carcinoembryonic antigen were not found to be present in the pancreatic endocrine tumors, but chromogranin A and synaptophysin were. Chorionic gonadotropin was found in 16 gastrinomas (100%), but only in 2 of 17 other pancreatic endocrine tumors (11.8 %). CONCLUSIONS Pancreatic gastrinomas were characterized by the coexpression of neuroendocrine markers, exocrine markers, and chorionic gonadotropin. Therefore, pancreatic gastrinomas made a special intermediate group of tumors, which phenotypically combined features of neuroendocrine and exocrine neoplasms. These findings suggested that sporadic pancreatic gastrinomas and other pancreatic endocrine tumors are different phenotypically and are possibly of different origin. Cancer 2003. © 2003 American Cancer Society. [source]