Medical management of patients with Zollinger-Ellison syndrome who have had previous gastric surgery: A prospective study

Maton, Paul N.; Frucht, Harold; Vinayek, Rakesh; Wank, S.A.; Gardner, Jerry D.; Jensen, Robert T.

doi:10.1016/0016-5085(88)90415-5

Cited by 98 publications

(52 citation statements)

References 18 publications

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“…If results remained uncertain from imaging studies, bone biopsy was performed 164 . Gastric acid hypersecretion was controlled in all patients using either histamine receptor antagonists (cimetidine, ranitidine, famotidine) alone or with an anticholinergic agent until 1983, then primarily with the use of proton pump inhibitors (omeprazole, lansoprazole) as described previously 203,207,264,277,[279][280][281][282]293,294 . Sufficient antisecretory drug was given to reduce acid secretion to <10 mEq/h in the hour before the next dose of medication or to <5 mEq/ h (or to the absence of symptoms) in patients with prior partial gastrectomy 264 or severe gastroesophageal reflux disease 264,277,279,281,282,294 .…”

Section: Methodsmentioning

confidence: 99%

Multiple Endocrine Neoplasia Type 1 and Zollinger-Ellison Syndrome

et al. 2004

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In patients with multiple endocrine neoplasia type 1 (MEN1), the most common functional pancreatic endocrine tumor (PET) syndrome is Zollinger-Ellison syndrome (ZES). ZES has been well studied in its sporadic form (that is, without MEN1); however, there are limited data on patients with MEN1 and ZES (MEN1/ZES), and the long-term natural history is largely unknown. To address this issue we report the results of a prospective long-term National Institutes of Health (NIH) study of 107 MEN1/ZES patients and compare our results with those of 1009 MEN1/ZES patients in 278 case reports and small series in the literature. Patients were clinically, radiologically, and biochemically evaluated yearly for all MEN1 manifestations (mean follow-up, 10 yr; range, 0.1-31 yr). Compared with patients from the literature, the NIH MEN1/ZES patients more frequently had pituitary (60%) and adrenal (45%) disease and carcinoid tumors (30%), but had equal frequency of hyperparathyroidism (94%), thyroid disease (6%), or lipomas (5%). Twenty-five percent of both the NIH and the literature patients lacked a family history of MEN1; ZES was the initial clinical manifestation of MEN1 in 40%. ZES onset preceded the diagnosis of hyperparathyroidism in 45%. However, ZES was rarely (8%) the only initial manifestation of MEN1 if careful testing was done. ZES occurred before age 40 years in 50%-60% of the current patients, in contrast to older studies. The diagnosis of ZES is delayed 3-5 years from its onset and is delayed as long as in sporadic ZES cases. Pituitary disease and carcinoid tumors (gastric > bronchial, thymic) are more frequent than generally reported, whereas a second functional PET is uncommon. In patients with MEN1/ZES without a family history of MEN1, the MEN1 manifestations are not as severe. This study shows that MEN1/ZES patients differ in many aspects from those commonly reported in older studies involving few MEN1/ZES patients. In this study we have identified a number of important clinical and laboratory features of MEN1/ZES that were not previously appreciated, which should contribute to earlier diagnosis and improve both short- and long-term management.

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Section: Methodsmentioning

confidence: 99%

Multiple Endocrine Neoplasia Type 1 and Zollinger-Ellison Syndrome

et al. 2004

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“…H2 blockers, to be effective, are usually required at higher doses than are those drugs used in conventional peptic disease (frequently up to 10 times the usual dose) and 4- to 6-hourly dosing is frequently needed [49,50,51,52]. Patients with complicated disease (presence of MEN1 with hypercalcemia, presence of severe GERD symptoms, presence of previous Billroth II resection) need higher doses of all antisecretory drugs and may need more frequent dosing even with PPIs [53,54,55,56]. Patients have been treated for up to 15 years with PPIs with no evidence of tachyphylaxis and no dose-related side effects.…”

Section: Medical Therapy (Gastric Acid Hypersecretion)mentioning

confidence: 99%

Gastrinoma (Duodenal and Pancreatic)

Jensen¹,

et al. 2006

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“…Symptoms have not been demonstrated to be reliable indicators of adequately controlled gastric acid secretion in patients with ZES [39]. If acid secretion is reduced to less than 10 mEq/hr before the next oral dose of drug in patients who have not had gastric surgery (or to <5 mEq/hr in patients with severe esophageal disease or previous gastric surgery), recurrent peptic ulcer disease will be prevented [3,14,15,43]. To convert from intravenous cimetidine to oral cimetidine, a close approximation of the oral dose required can be calculated by determining the total amount of cimetidine being administered intravenously over a 24-hour period; this value is then multiplied by 1.5 to adjust for the decreased potency of the oral form [44,46].…”

Section: Diagnosis Of Zes Should Be Established By Measur-mentioning

confidence: 99%

“…Studies with histamine H2-receptor antagonists have demonstrated that reducing acid secretion to less than 10 mEq/hr will not only allow healing of ulcers but also prevent the recurrence of the complications of gastric acid hypersecretion in most patients with ZES [4,5,8,14,[39][40][41][42]. In patients with severe esophageal disease or recurrent ulceration after a Billroth I or II gastric resection, gastric acid secretion must be reduced to less than 5 mEq/hr to allow healing [15,43]. Studies at the National Institutes of Health have shown that gastric acid secretion can be acutely controlled in all patients with ZES by a continuous intravenous infusion of cimetidine or ranitidine administered in the proper dose [44,45].…”

Section: Diagnosis Of Zes Should Be Established By Measur-mentioning

confidence: 99%

Zollinger-Ellison Syndrome in the Intensive Care Setting

London

Frucht

Doppman

et al. 1989

J Intensive Care Med

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drome in the intensive care setting. J Intensive Care Med 1989;4:272-283 Management of patients with Zollinger-Ellison syndrome differs markedly from management of patients with idiopathic gastric acid hypersecretion or routine peptic ulcer disease. Because of the possible complications arising from gastric acid hypersecretion or from complications caused by the gastrinoma itself, patients with these disorders frequently present to critical care physicians. It is important that critical care physicians be familiar with the acute presentation of patients with Zollinger-Ellison syndrome as well as the appropriate treatment. We review the important points pertaining to the recognition and treatment of Zollinger-Ellison syndrome in the acute care setting.In 1955, Zollinger and Ellison [1] described the clinical triad of fulminating ulcer diathesis, recurrent ulceration unresponsive to standard medical or surgical therapy, and the presence of non-beta islet cell tumors of the pancreas. The clinical symptoms of Zollinger-Ellison syndrome (ZES) are caused by gastric acid hypersecretion, which results from tumor-released, gastrin-stimulating acid secretion from gastric parietal cells [2,3]. With appropriate use of histamine Hz-receptor antagonists, it is now possible to inhibit gastric acid hypersecretion and to prevent severe, recurrent gastrointestinal ulcerations and their usual complications, such as bleeding and perforation [3][4][5][6][7][8]. Because of the severity of these complications when they are untreated or when the diagnosis is not yet established, patients with ZES will frequently require treatment in an intensive care unit.

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Medical management of patients with Zollinger-Ellison syndrome who have had previous gastric surgery: A prospective study

Cited by 98 publications

References 18 publications

Multiple Endocrine Neoplasia Type 1 and Zollinger-Ellison Syndrome

Multiple Endocrine Neoplasia Type 1 and Zollinger-Ellison Syndrome

Gastrinoma (Duodenal and Pancreatic)

Zollinger-Ellison Syndrome in the Intensive Care Setting

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