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Robert T Jensen - One of the best experts on this subject based on the ideXlab platform.
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Secretin and Calcium Provocative Tests in the Zollinger-Ellison Syndrome
Annals of Internal Medicine, 2020Co-Authors: Harold Frucht, Rakesh Vinayek, J M Howard, Jerry D. Gardner, Stephen A Wank, Paul N Maton, Denis M. Mccarthy, James I. Slaff, Robert T JensenAbstract:Abstract Study Objective:To evaluate criteria of positivity for and usefulness of both the secretin and calcium gastrin-provocative tests in patients with the Zollinger-Ellison Syndrome. Design:Pro...
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Zollinger-Ellison Syndrome: Recent advances and controversies
Current Opinion in Gastroenterology, 2013Co-Authors: Hisato Igarashi, Robert T JensenAbstract:Purpose of reviewTo review the recent advances and current controversies in patients with Zollinger–Ellison Syndrome (ZES).Recent findingsRecent advances in the management of ZES include: improved understanding of the pathogenesis of gastrinoma and pancreatic neuroendocrine tumors, new prognostic cl
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Management of the Zollinger-Ellison Syndrome in pregnancy.
American journal of obstetrics and gynecology, 1997Co-Authors: C. A. Stewart, B Termanini, F Gibril, Vito D. Corleto, Vince E. Sutliff, H C Weber, Robert T JensenAbstract:There is almost no information on the management of patients with functional pancreatic endocrine tumors such as Zollinger-Ellison Syndrome during pregnancy. The purpose of this study was to develop an approach for the management of such cases during pregnancy on the basis of experience with five recent cases. Five women with Zollinger-Ellison Syndrome who had seven pregnancies were the subject of this study. Each patient had an initial evaluation to confirm the diagnosis and to establish gastrinoma location and for the presence or absence of multiple endocrine neoplasia type I. In patients with Zollinger-Ellison Syndrome diagnosed before conception, various medical or surgical treatments were established before conception and were used to control acid secretion throughout the pregnancy. The presence of upper gastrointestinal symptoms during pregnancy, maternal and fetal complications, gender, and weight of the infant were determined in all cases. Acid control was determined in four of the five patients during six pregnancies. The interval between the onset of Zollinger-Ellison Syndrome and the subsequent pregnancy varied from 0.6 to 9.9 years (mean 6.9 +/- 1.7 years). Zollinger-Ellison Syndrome was unrecognized before pregnancy in two patients (40%); it was diagnosed between 0.2 and 2.4 years after the pregnancy. In three patients the time of diagnosis varied from 2.6 to 9 years before pregnancy. All patients had symptoms from gastric hypersecretion and elevated fasting serum gastrin levels that varied from 20% above normal to 37-fold above normal with mean of 2536 pg/ml (range 124 to 6970 pg/ml). Four of the five patients (80%) had positive secretin and calcium provocative tests. Two patients had multiple endocrine neoplasia type I. The five patients had seven pregnancies. Acid secretion was treated during pregnancy with antacids only (one patient), ranitidine alone (one patient), prior curative gastrinoma resection (one patient, two pregnancies), prior parietal cell vagotomy with incomplete tumor resection (one patient, two pregnancies), and prior parathyroidectomy and use of ranitidine in a patient with multiple endocrine neoplasia type I. In five pregnancies in three of the cases, no gastric antisecretory medications were needed during pregnancy. The mean acid secretion during pregnancy was 11.9 mEq/hr (range 0 to 42 mEq/hr). In the two cases with poor acid control and unrecognized Zollinger-Ellison Syndrome mild fetal complications occurred. It is possible for patients with Zollinger-Ellison Syndrome to have pregnancies that are not complicated by gastric acid hypersecretion. If the Zollinger-Ellison Syndrome is diagnosed before pregnancy, curative resection with parietal cell vagotomy may obviate the need for gastric antisecretory drugs. If metastases are present or the diagnosis of Zollinger-Ellison Syndrome is made after conception, ranitidine in the lowest possible dose should be used to control acid secretion. If acid secretion in uncontrolled, the dose may be increased or omeprazole may be used.
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Management of the Zollinger-Ellison Syndrome in pregnancy.
American Journal of Obstetrics and Gynecology, 1997Co-Authors: Stewart Ca, F Gibril, Termanini B, Vito D. Corleto, Vince E. Sutliff, H C Weber, Robert T JensenAbstract:Abstract OBJECTIVE: There is almost no information on the management of patients with functional pancreatic endocrine tumors such as Zollinger-Ellison Syndrome during pregnancy. The purpose of this study was to develop an approach for the management of such cases during pregnancy on the basis of experience with five recent cases. STUDY DESIGN: Five women with Zollinger-Ellison Syndrome who had seven pregnancies were the subject of this study. Each patient had an initial evaluation to confirm the diagnosis and to establish gastrinoma location and for the presence or absence of multiple endocrine neoplasia type I. In patients with Zollinger-Ellison Syndrome diagnosed before conception, various medical or surgical treatments were established before conception and were used to control acid secretion throughout the pregnancy. The presence of upper gastrointestinal symptoms during pregnancy, maternal and fetal complications, gender, and weight of the infant were determined in all cases. Acid control was determined in four of the five patients during six pregnancies. RESULTS: The interval between the onset of Zollinger-Ellison Syndrome and the subsequent pregnancy varied from 0.6 to 9.9 years (mean 6.9 ± 1.7 years). Zollinger-Ellison Syndrome was unrecognized before pregnancy in two patients (40%); it was diagnosed between 0.2 and 2.4 years after the pregnancy. In three patients the time of diagnosis varied from 2.6 to 9 years before pregnancy. All patients had symptoms from gastric hypersecretion and elevated fasting serum gastrin levels that varied from 20% above normal to 37-fold above normal with mean of 2536 pg/ml (range 124 to 6970 pg/ml). Four of the five patients (80%) had positive secretin and calcium provocative tests. Two patients had multiple endocrine neoplasia type I. The five patients had seven pregnancies. Acid secretion was treated during pregnancy with antacids only (one patient), ranitidine alone (one patient), prior curative gastrinoma resection (one patient, two pregnancies), prior parietal cell vagotomy with incomplete tumor resection (one patient, two pregnancies), and prior parathyroidectomy and use of ranitidine in a patient with multiple endocrine neoplasia type I. In five pregnancies in three of the cases, no gastric antisecretory medications were needed during pregnancy. The mean acid secretion during pregnancy was 11.9 mEq/hr (range 0 to 42 mEq/hr). In the two cases with poor acid control and unrecognized Zollinger-Ellison Syndrome mild fetal complications occurred. CONCLUSIONS: It is possible for patients with Zollinger-Ellison Syndrome to have pregnancies that are not complicated by gastric acid hypersecretion. If the Zollinger-Ellison Syndrome is diagnosed before pregnancy, curative resection or resection with parietal cell vagotomy may obviate the need for gastric antisecretory drugs. If metastases are present or the diagnosis of Zollinger-Ellison Syndrome is made after conception, ranitidine in the lowest possible dose should be used to control acid secretion. If acid secretion in uncontrolled, the dose may be increased or omeprazole may be used. (Am J Obstet Gynecol 1997;176:224-33.)
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Studies on the interrelation between Zollinger-Ellison Syndrome, Helicobacter pylori, and proton pump inhibitor therapy
Gastroenterology, 1997Co-Authors: H C Weber, David Venzon, Robert T Jensen, David C. MetzAbstract:Abstract BACKGROUND & AIMS: The interrelation between Helicobacter pylori infection and proton pump inhibitor therapy in patients with Zollinger- Ellison Syndrome is unknown. The aim of this study was to evaluate the influence of these factors on parameters of Zollinger-Ellison Syndrome. METHODS: Prevalence of H. pylori was determined by biopsy and antibody testing in 84 patients. The influence of H. pylori status on clinical and laboratory parameters of Zollinger-Ellison Syndrome was evaluated. Seroconversion after surgery was assessed retrospectively in infected patients. RESULTS: The prevalence of H. pylori exposure was 23% (10% with active infection). Acid output was higher in H. pylori-negative patients, but other clinical and biochemical parameters did not differ. Parameters were also similar for patients determined to be H. pylori positive by histology or antibody testing alone. Seroconversion rates did not differ between those rendered or not rendered disease free despite a significant reduction in acid output. CONCLUSIONS: H. pylori infection is not a risk factor for peptic ulceration in patients with Zollinger-Ellison Syndrome. The prevalence is lower than in the general population and much lower than for patients with idiopathic peptic ulcer disease. Long-term omeprazole therapy in H. pylori-positive patients with Zollinger-Ellison Syndrome may-lead to a reduction in parietal cell mass. (Gastroenterology 1997 Jan;112(1):84-91)
M. M. Haber - One of the best experts on this subject based on the ideXlab platform.
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Helicobacter pylori effects on gastritis, gastrin and enterochromaffin‐like cells in Zollinger–Ellison Syndrome and non‐Zollinger–Ellison Syndrome acid hypersecretors treated long‐term with lansoprazole
Alimentary Pharmacology & Therapeutics, 2001Co-Authors: Basil I. Hirschowitz, M. M. HaberAbstract:Background: Helicobacter pylori is said to cause atrophy of the gastric corpus and enterochromaffin-like cell proliferation in gastro-oesophageal reflux disease (GERD) patients treated long-term with a proton pump inhibitor. Aims: To determine the effect of H. pylori infection on gastritis, enterochromaffin-like cell density and hyperplasia, mucosal atrophy and serum gastrin in patients with gastric hypersecretion (basal acid output gt; 15 mmol/h) with either hypergastrinemia (Zollinger–Ellison Syndrome) or normal gastrin (non-Zollinger–Ellison Syndrome) before and during long-term treatment with lansoprazole. Methods: Lansoprazole was individually titrated to reduce basal acid output to
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helicobacter pylori effects on gastritis gastrin and enterochromaffin like cells in Zollinger Ellison Syndrome and non Zollinger Ellison Syndrome acid hypersecretors treated long term with lansoprazole
Alimentary Pharmacology & Therapeutics, 2001Co-Authors: B I Hirschowitz, M. M. HaberAbstract:Background: Helicobacter pylori is said to cause atrophy of the gastric corpus and enterochromaffin-like cell proliferation in gastro-oesophageal reflux disease (GERD) patients treated long-term with a proton pump inhibitor. Aims: To determine the effect of H. pylori infection on gastritis, enterochromaffin-like cell density and hyperplasia, mucosal atrophy and serum gastrin in patients with gastric hypersecretion (basal acid output gt; 15 mmol/h) with either hypergastrinemia (Zollinger–Ellison Syndrome) or normal gastrin (non-Zollinger–Ellison Syndrome) before and during long-term treatment with lansoprazole. Methods: Lansoprazole was individually titrated to reduce basal acid output to < 5 mmol/h (< 1 mmol/h in post-surgical Zollinger–Ellison Syndrome). Gastric corpus biopsies were obtained every 6 months before treatment and up to 8 years later. Results: H. pylori was present in corpus biopsies in ≈ 50%, causing active gastritis which resolved rapidly in 15 subjects after elimination of H. pylori. Patchy mild/moderate corpus atrophy was present at entry in two and at the end in four out of 60 patients, one being H. pylori-positive. Intestinal metaplasia (< 10%) was seen in six isolated biopsies (1% of total). H. pylori did not affect serum gastrin, enterochromaffin-like cell density or hyperplasia. Enterochromaffin-like cell density was twice as high in Zollinger–Ellison Syndrome as in non-Zollinger–Ellison Syndrome patients (241 vs. 126 cells/mm2, P < 0.001). Enterochromaffin-like cells remained normal in the non-Zollinger–Ellison Syndrome hypersecretors regardless of H. pylori status. Conclusion: Corpus enterochromaffin-like cell increases were related to serum gastrin elevation, but neither H. pylori nor long-term treatment with lansoprazole alone or together had any effect on enterochromaffin-like cell density or hyperplasia. Corpus acute gastritis resulted from H. pylori infection, but did not result in mucosal atrophy despite long-term proton pump inhibitor treatment and promptly resolved with loss of H. pylori.
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Helicobacter pylori effects on gastritis, gastrin and enterochromaffin-like cells in Zollinger-Ellison Syndrome and non-Zollinger-Ellison Syndrome acid hypersecretors treated long-term with lansoprazole.
Alimentary pharmacology & therapeutics, 2001Co-Authors: B I Hirschowitz, M. M. HaberAbstract:Background: Helicobacter pylori is said to cause atrophy of the gastric corpus and enterochromaffin-like cell proliferation in gastro-oesophageal reflux disease (GERD) patients treated long-term with a proton pump inhibitor. Aims: To determine the effect of H. pylori infection on gastritis, enterochromaffin-like cell density and hyperplasia, mucosal atrophy and serum gastrin in patients with gastric hypersecretion (basal acid output gt; 15 mmol/h) with either hypergastrinemia (Zollinger–Ellison Syndrome) or normal gastrin (non-Zollinger–Ellison Syndrome) before and during long-term treatment with lansoprazole. Methods: Lansoprazole was individually titrated to reduce basal acid output to
Basil I. Hirschowitz - One of the best experts on this subject based on the ideXlab platform.
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Zollinger-Ellison Syndrome: presentation, response to therapy, and outcome.
Digestive and Liver Disease, 2010Co-Authors: C. Mel Wilcox, Toni Seay, Justin Arcury, Jean Mohnen, Basil I. HirschowitzAbstract:Abstract Background Recent series describing the clinical presentation, response to therapy, and long-term outcome of Zollinger–Ellison Syndrome are limited. Aims To assess the clinical characteristics and long-term outcome of patients with Zollinger–Ellison Syndrome. Methods Over a 20-year period, patients with Zollinger–Ellison Syndrome were enrolled in a prospective trial evaluating the efficacy of lansoprazole. Following dose stabilization, patients were followed on a 6-monthly basis with interval history, physical examination, endoscopy with gastric biopsies, gastric acid analysis and laboratory studies. Results 72 patients (mean age 54 ± 12 years, % male 58%, % Caucasian 69%) were prospectively enrolled. The clinical presentation was stereotypical for Zollinger–Ellison Syndrome. Symptoms had been reported for a median of 9 years prior to diagnosis. Cross-sectional abdominal imaging was often negative for demonstrable tumour. All patients had gastric acid hypersecretion controlled with variable doses of lansoprazole (median dose 60 mg/day, range 15–480 mg/day). The median survival from the time of diagnosis was 6.6 years; only two of 19 deaths were due to metastatic gastrinoma. Conclusions The clinical presentation of Zollinger–Ellison Syndrome was similar to prior reports. Acid hypersecretion was controlled in all patients with variable doses of lansoprazole. Long-term survival was principally related to underlying co-morbidity.
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Zollinger–Ellison Syndrome: Presentation, response to therapy, and outcome
Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver, 2010Co-Authors: C. Mel Wilcox, Toni Seay, Justin Arcury, Jean Mohnen, Basil I. HirschowitzAbstract:Abstract Background Recent series describing the clinical presentation, response to therapy, and long-term outcome of Zollinger–Ellison Syndrome are limited. Aims To assess the clinical characteristics and long-term outcome of patients with Zollinger–Ellison Syndrome. Methods Over a 20-year period, patients with Zollinger–Ellison Syndrome were enrolled in a prospective trial evaluating the efficacy of lansoprazole. Following dose stabilization, patients were followed on a 6-monthly basis with interval history, physical examination, endoscopy with gastric biopsies, gastric acid analysis and laboratory studies. Results 72 patients (mean age 54 ± 12 years, % male 58%, % Caucasian 69%) were prospectively enrolled. The clinical presentation was stereotypical for Zollinger–Ellison Syndrome. Symptoms had been reported for a median of 9 years prior to diagnosis. Cross-sectional abdominal imaging was often negative for demonstrable tumour. All patients had gastric acid hypersecretion controlled with variable doses of lansoprazole (median dose 60 mg/day, range 15–480 mg/day). The median survival from the time of diagnosis was 6.6 years; only two of 19 deaths were due to metastatic gastrinoma. Conclusions The clinical presentation of Zollinger–Ellison Syndrome was similar to prior reports. Acid hypersecretion was controlled in all patients with variable doses of lansoprazole. Long-term survival was principally related to underlying co-morbidity.
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treatment strategies for Zollinger Ellison Syndrome
Expert Opinion on Pharmacotherapy, 2009Co-Authors: Mel C Wilcox, Basil I. HirschowitzAbstract:Background Zollinger-Ellison Syndrome (ZES) is a rare disorder caused by tumor secretion of the hormone gastrin, which results in gastric acid hypersecretion and secondarily complicated peptic ulcer and diarrhea. Until the development of H(2)-receptor antagonists and later proton pump inhibitors (PPIs), the disease was virulent, often associated with ulcer-related mortality, and the mainstay of treatment was total gastrectomy. Objective To evaluate current approaches to diagnosis and therapy, focusing on the role of PPIs. Methods An extensive literature search through PubMed using the search term 'Zollinger-Ellison Syndrome' from 1964 to the present was performed. Primary articles were identified, and pertinent articles obtained from the reference lists were also examined. Results/conclusions The clinical manifestations of ZES are well described, but overlaps with other more common disorders delay diagnosis. The use of abdominal imaging with somatostatin receptor scintigraphy and endoscopic ultrasound has improved tumor staging. PPI therapy is remarkably effective in controlling gastric acid hypersecretion, thereby reducing morbidity and potential mortality of this Syndrome. The dose of drug necessary to control symptoms is highly variable but, even when used in high doses for prolonged periods of time, the disease remained controlled with very few drug-related side effects.
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Treatment strategies for Zollinger–Ellison Syndrome
Expert Opinion on Pharmacotherapy, 2009Co-Authors: C. Mel Wilcox, Basil I. HirschowitzAbstract:Background: Zollinger–Ellison Syndrome (ZES) is a rare disorder caused by tumor secretion of the hormone gastrin, which results in gastric acid hypersecretion and secondarily complicated peptic ulcer and diarrhea. Until the development of H2-receptor antagonists and later proton pump inhibitors (PPIs), the disease was virulent, often associated with ulcer-related mortality, and the mainstay of treatment was total gastrectomy. Objective: To evaluate current approaches to diagnosis and therapy, focusing on the role of PPIs. Methods: An extensive literature search through PubMed using the search term ‘Zollinger–Ellison Syndrome’ from 1964 to the present was performed. Primary articles were identified, and pertinent articles obtained from the reference lists were also examined. Results/conclusions: The clinical manifestations of ZES are well described, but overlaps with other more common disorders delay diagnosis. The use of abdominal imaging with somatostatin receptor scintigraphy and endoscopic ultrasound h...
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Helicobacter pylori effects on gastritis, gastrin and enterochromaffin‐like cells in Zollinger–Ellison Syndrome and non‐Zollinger–Ellison Syndrome acid hypersecretors treated long‐term with lansoprazole
Alimentary Pharmacology & Therapeutics, 2001Co-Authors: Basil I. Hirschowitz, M. M. HaberAbstract:Background: Helicobacter pylori is said to cause atrophy of the gastric corpus and enterochromaffin-like cell proliferation in gastro-oesophageal reflux disease (GERD) patients treated long-term with a proton pump inhibitor. Aims: To determine the effect of H. pylori infection on gastritis, enterochromaffin-like cell density and hyperplasia, mucosal atrophy and serum gastrin in patients with gastric hypersecretion (basal acid output gt; 15 mmol/h) with either hypergastrinemia (Zollinger–Ellison Syndrome) or normal gastrin (non-Zollinger–Ellison Syndrome) before and during long-term treatment with lansoprazole. Methods: Lansoprazole was individually titrated to reduce basal acid output to
Paul N Maton - One of the best experts on this subject based on the ideXlab platform.
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Secretin and Calcium Provocative Tests in the Zollinger-Ellison Syndrome
Annals of Internal Medicine, 2020Co-Authors: Harold Frucht, Rakesh Vinayek, J M Howard, Jerry D. Gardner, Stephen A Wank, Paul N Maton, Denis M. Mccarthy, James I. Slaff, Robert T JensenAbstract:Abstract Study Objective:To evaluate criteria of positivity for and usefulness of both the secretin and calcium gastrin-provocative tests in patients with the Zollinger-Ellison Syndrome. Design:Pro...
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Role of acid suppressants in patients with Zollinger-Ellison Syndrome.
Alimentary Pharmacology & Therapeutics, 2007Co-Authors: Paul N MatonAbstract:SUMMARY Virtually all symptoms in patients with Zollinger-Ellison Syndrome are due to acid hypersecretion, thus the control of acid secretion is the first and most important step in the management of patients with this Syndrome. Antisecretory medication is prescribed as soon as the diagnosis of Zollinger-Ellison Syndrome is made, as patients may bleed or perforate with little warning. Acid output is reduced to < 10 mmol/h to heal mucosal lesions, but in patients with a Billroth I or II gastrectomy and those with severe oesophagitis and stricture formation, acid output is reduced to < 5 or < 1 mmol/h. Acid output and not symptomatic response is a reliable guide of the adequacy of therapy. In sufficient doses, all H2-receptor antagonists are useful; however, side effects associated with cimetidine therapy limit its use. The ratio of potencies of cimetidine: ranitidine: famotidine is 1:4:32. Ranitidine given as a 50-mg intravenous bolus, followed by a continuous infusion of 0.5 mg. kg/h, controls acid hypersecretion acutely in patients with Zollinger-Ellison Syndrome. Acid output is checked after 4 h, and the dose increased until acid output is < 10 mmol/h. In 70% of patients with Zollinger-Ellison Syndrome, 1 mg. kg/h reduces acid output to < 10 mmol/h; however, doses up to 4 mg. kg/h have been used. When patients are switched to oral ranitidine, a useful dosage conversion is to administer 1.5 times the total daily intravenous dose in four equal doses every 6 h. Four doses of oral drug are given before the infusion is stopped. Six hours after the first/last oral dose, acid output is checked. In our patients, the mean dose of ranitidine was 2100 mg/day (range, 450–9200 mg/day). No serious toxicity was observed. Omeprazole, which has a long duration of action and is a potent inhibitor of gastric acid secretion, has simplified management. Once-daily dosing is sufficient in most patients, and a reasonable starting dose is 60 mg daily. The dose may be increased to 120 mg once daily; if this dosage fails to control acid secretion, 60 mg is administered every 12 h. In our studies, the median dose was 90 mg/day (range, 20–120 mg/day). Omeprazole was more effective than H2-receptor antagonists in providing symptom relief and mucosal healing and did not cause significant toxicity. In particular, no gastric carcinoid tumours developed during four years of use. Omeprazole is, therefore, the treatment of choice for control of acid secretion in patients with Zollinger-Ellison Syndrome. Surgery plays a minor role in the control of acid hypersecretion. Parathyroidectomy in patients with Zollinger-Ellison Syndrome as part of multiple endocrine neoplasia type I, or highly selective vagotomy decrease gastric acid output and lower drug requirements but do not cure the patient. Except when resection of gastrinoma is curative, lifelong medical therapy for control of acid secretion in patients with Zollinger-Ellison Syndrome is required.
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Helicobacter pylori and Zollinger-Ellison Syndrome
Digestive Diseases and Sciences, 1991Co-Authors: Z. A. Saeed, Dolores G. Evans, M. J. Cornelius, Paul N Maton, Robert T Jensen, Doyle J. Evans, Davidy . GrahamAbstract:Helicobacter pylori (previouslyCampylobacter pylori) is almost invariably associated with chronic duodenal ulcer disease. The relationship betweenH. pylori infection and duodenal ulcer in Zollinger-Ellison Syndrome is unknown. We investigated the frequency ofH. pylori infection in Zollinger-Ellison Syndrome and also what effectH. pylori infection had on gastric function in patients with Zollinger-Ellison Syndrome.H. pylori infection was diagnosed based on a specific serologic (ELISA) assay based on high-molecular-weight cell-associated proteins ofH. pylori. We studied 20 patients with Zollinger-Ellison Syndrome; 15 men and 5 women ranging in age from 24 to 71 years, median age 51. Six Zollinger-Ellison Syndrome patients hadH. pylori infection compared to 100 consecutive patients with chronic recurrent duodenal ulcer disease (P
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Peptic ulcer perforation as the presentation of Zollinger-Ellison Syndrome.
Digestive Diseases and Sciences, 1991Co-Authors: Irving Waxman, Jerry D. Gardner, Robert T Jensen, Paul N MatonAbstract:We examined the characteristics of patients with Zollinger-Ellison Syndrome who developed a perforation prior to diagnosis to determine whether any clinical features were useful markers of the Syndrome. Of 160 patients with Zollinger-Ellison Syndrome, perforation occurred prior to the diagnosis being made in 11 (7%). At surgery, perforations were found in the duodenum in six cases and in the jejunum in five. In no case was tumor identified at emergency surgery, and the diagnosis of Zollinger-Ellison Syndrome was made only in the postoperative period when excessive gastric secretions were noted. Neither acid output nor serum gastrin concentration were useful predictors for perforation. The patients, six men and five women, were 27–61 years old (median 48) and one had MEN-1. Three patients had no symptoms prior to the perforation. The other eight had symptoms for 1–15 years, with diarrhea occurring in 45% of the cases. Following the diagnosis of Zollinger-Ellison Syndrome, patients were given medication to control gastric acid hypersecretion. Eight patients remained well, but the three patients who had had a partial gastrectomy had a complicated course despite medical therapy. Although features of perforation in Zollinger-Ellison Syndrome are not specific, jejunal perforation or perforation associated with a history of diarrhea is suggestive of the diagnosis. Serum gastrin should be measured in every case and a partial gastrectomy avoided.
B I Hirschowitz - One of the best experts on this subject based on the ideXlab platform.
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helicobacter pylori effects on gastritis gastrin and enterochromaffin like cells in Zollinger Ellison Syndrome and non Zollinger Ellison Syndrome acid hypersecretors treated long term with lansoprazole
Alimentary Pharmacology & Therapeutics, 2001Co-Authors: B I Hirschowitz, M. M. HaberAbstract:Background: Helicobacter pylori is said to cause atrophy of the gastric corpus and enterochromaffin-like cell proliferation in gastro-oesophageal reflux disease (GERD) patients treated long-term with a proton pump inhibitor. Aims: To determine the effect of H. pylori infection on gastritis, enterochromaffin-like cell density and hyperplasia, mucosal atrophy and serum gastrin in patients with gastric hypersecretion (basal acid output gt; 15 mmol/h) with either hypergastrinemia (Zollinger–Ellison Syndrome) or normal gastrin (non-Zollinger–Ellison Syndrome) before and during long-term treatment with lansoprazole. Methods: Lansoprazole was individually titrated to reduce basal acid output to < 5 mmol/h (< 1 mmol/h in post-surgical Zollinger–Ellison Syndrome). Gastric corpus biopsies were obtained every 6 months before treatment and up to 8 years later. Results: H. pylori was present in corpus biopsies in ≈ 50%, causing active gastritis which resolved rapidly in 15 subjects after elimination of H. pylori. Patchy mild/moderate corpus atrophy was present at entry in two and at the end in four out of 60 patients, one being H. pylori-positive. Intestinal metaplasia (< 10%) was seen in six isolated biopsies (1% of total). H. pylori did not affect serum gastrin, enterochromaffin-like cell density or hyperplasia. Enterochromaffin-like cell density was twice as high in Zollinger–Ellison Syndrome as in non-Zollinger–Ellison Syndrome patients (241 vs. 126 cells/mm2, P < 0.001). Enterochromaffin-like cells remained normal in the non-Zollinger–Ellison Syndrome hypersecretors regardless of H. pylori status. Conclusion: Corpus enterochromaffin-like cell increases were related to serum gastrin elevation, but neither H. pylori nor long-term treatment with lansoprazole alone or together had any effect on enterochromaffin-like cell density or hyperplasia. Corpus acute gastritis resulted from H. pylori infection, but did not result in mucosal atrophy despite long-term proton pump inhibitor treatment and promptly resolved with loss of H. pylori.
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Helicobacter pylori effects on gastritis, gastrin and enterochromaffin-like cells in Zollinger-Ellison Syndrome and non-Zollinger-Ellison Syndrome acid hypersecretors treated long-term with lansoprazole.
Alimentary pharmacology & therapeutics, 2001Co-Authors: B I Hirschowitz, M. M. HaberAbstract:Background: Helicobacter pylori is said to cause atrophy of the gastric corpus and enterochromaffin-like cell proliferation in gastro-oesophageal reflux disease (GERD) patients treated long-term with a proton pump inhibitor. Aims: To determine the effect of H. pylori infection on gastritis, enterochromaffin-like cell density and hyperplasia, mucosal atrophy and serum gastrin in patients with gastric hypersecretion (basal acid output gt; 15 mmol/h) with either hypergastrinemia (Zollinger–Ellison Syndrome) or normal gastrin (non-Zollinger–Ellison Syndrome) before and during long-term treatment with lansoprazole. Methods: Lansoprazole was individually titrated to reduce basal acid output to
