Effectiveness of omeprazole in seven patients with Zollinger-Ellison syndrome resistant to histamine H2-receptor antagonists

Delchier, Jean‐Charles; Soulé, Jean–Claude; Mignon, M; Goldfain, D; Cortot, Antoine; Travers, B.; Isal, J P; Bader, J P

doi:10.1007/bf01296445

Cited by 52 publications

(11 citation statements)

References 26 publications

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“…Literature BAO data are from 129 patients 11,14,35,[39][40][41]67,92,95,96,100,103,117,122,144,146,153,154,170,175,177,185,189,191,192,216,220,228,230,236,254,257,270,284,289,292,331,343,355,[369][370][371][372]378,401,439,443,446,474,491 ; and literature MAO data are from 55 patients 11,…”

Section: Discussionmentioning

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: Discussionmentioning

confidence: 99%

Multiple Endocrine Neoplasia Type 1 and Zollinger-Ellison Syndrome

et al. 2004

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“…Omeprazole is a very potent antisecretory drug [12][13][14] which has been successfully administered in duodenal [17,18] and gas tric [ 19,20] ulcer and reflux esophagitis [21 -25] and proved effective even in H2-receptor antagonist resistant ulcers and reflux esopha gitis [26][27][28][29][30][31][32][33], and Zollinger-Ellison syn drome [34][35][36][37],…”

Section: Discussionmentioning

confidence: 99%

Effect of Omeprazole on Nocturnal Intragastric pH in Cirrhotics with Inadequate Antisecretory Response to Ranitidine

Walker

Klotz²,

Sarem-Aslani

et al. 1991

Digestion

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Failure of acid suppression by H₂-receptor antagonists has been observed, and recently we have found a higher frequency of patients with inadequate antisecretory response among patients with cirrhosis of the liver. In the present study comprising 16 cirrhotics with inadequate antisecretory response to 300 mg of ranitidine, we tested the effect of 40 mg omeprazole. Nighttime intragastric pH was continuously monitored, and a rise in the intragastric pH above 4.0 for more than 6 h following the oral dose at 18.00 h was considered as response. The median pH profile during the omeprazole treatment was significantly higher than with ranitidine (p ≤ 0.001). In contrast to 300 mg ranitidine, which despite sufficient plasma levels 2 and 4 h after intake (762 ± 431 and 802 ± 668 ng/ml) resulted in a rise in the nighttime intragastric pH above 4 only for 1.8 ± 1.7 h, after omeprazole for at least 5 days, the intragastric pH was for 10.1 ± 2.4 of 12 h above 4 during the night (p < 0.001). The omeprazole plasma levels were 611 ± 323 and 881 ± 533 ng/ml after 2 and 4 h. The data obtained with intragastric pH monitoring indicate that the H⁺K⁺-ATPase inhibitor omeprazole is able to overcome the H₂-blocker resistance in cirrhotics.

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“…Recently a new class of potent antisecretory agents, the substituted benzimidazoles such as omeprazole, which function as H+-K+-adenosine triphosphatase inhibitors [49,50], have been used in treatment of ZES [42,[51][52][53][54]. Although omeprazole…”

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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Effectiveness of omeprazole in seven patients with Zollinger-Ellison syndrome resistant to histamine H2-receptor antagonists

Cited by 52 publications

References 26 publications

Multiple Endocrine Neoplasia Type 1 and Zollinger-Ellison Syndrome

Multiple Endocrine Neoplasia Type 1 and Zollinger-Ellison Syndrome

Effect of Omeprazole on Nocturnal Intragastric pH in Cirrhotics with Inadequate Antisecretory Response to Ranitidine

Zollinger-Ellison Syndrome in the Intensive Care Setting

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