Omeprazole: Effective, Convenient Therapy for Zollinger—Ellison Syndrome

McArthur, K E; Collen, Martin J.; Maron, Paul N.; Cherner, Jay A.; Howard, John M.; Ciarleglio, Cecelia A.; Cornelius, Mary Jo; Jensen, Robert T.; Gardner, Jerry D.

doi:10.1016/s0016-5085(85)80011-1

Cited by 137 publications

(46 citation statements)

References 18 publications

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“…In 11 patients studied for periods of up to 9 months in the USA the mean daily dose was 70 mg (range 20-160 mg). Doses were usually constant, but 1 patient required ome prazole twice daily [7]. These results were confirmed in a multicenter study on 31 pa tients from the USA [17], In a European study on 9 patients treated for periods up to 27 months, treatment with 20-80 mg ome prazole daily reduced BAO by 77-100%.…”

Section: Omeprazole In Zollinger-ellison Syndromementioning

confidence: 73%

“…In single-dose studies as well as during long-term treatment omeprazole did not af fect fasting serum gastrin concentrations in Zollinger-Ellison patients [7,16,19,27], In refractory ulcer disease serum gastrin con centration rose to about 4 times the normal level during the first months of omeprazole therapy, while thereafter no further increase was observed for periods up to 4 years [24,27,28]. No pronounced changes were ob served in volume density of antral G and D cells and ECL cells in the oxyntic mucosa.…”

Section: Effect O F Omeprazole On Serum Gastrin and Gastric Endocrinementioning

confidence: 78%

“…The clinical symptoms were completely abolished for at least 48 h. When a single 80-mg dose of enteric-coated omeprazole was given inhibition was 26-100% after 6 h and 76-100% after 24 h [6]. McArthur et al [7] showed in a study on 11 patients with Zollinger-Ellison syndrome that a single oral dose of 60 mg entericcoated omeprazole induced maximal inhibi tion of gastric acid within 4 h (range 3-7 h). The inhibition persisted for at least 48 h, amounting to more than 50% at that time.…”

Section: Omeprazole In Zollinger-ellison Syndromementioning

confidence: 99%

“…Even high doses of omeprazole were well tolerated [21], Only a few minor and transient side effects have been noticed, but no major drug-related ad verse events have been reported [6,7,10,16,19,21,24,26],…”

Section: Other Side Effects O F Omeprazolementioning

confidence: 99%

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Omeprazole in the Treatment of Zollinger-Ellison Syndrome and Histamine H<sub>2</sub>-Antagonist Refractory Ulcers

Meijer

Jansen²,

Lamers³

1989

Digestion

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Omeprazole is a very potent and long-acting inhibitor of gastric acid secretion. These characteristics make the drug very suitable for the management of gastric acid hyper-secretion and symptom relief in patients with the Zollinger-Ellison syndrome, and in the treatment of patients with ulcers resistant to histamine H₂-receptor antagonists. Most patients require only a once-daily dose, whereas in about 30% of patients with Zollinger-Ellison syndrome the dose has to be split. During long-term treatment the required dose of omeprazole is usually rather stable. Up until now neither in patients with Zollinger-Ellison syndrome nor in those with resistant ulcers have convincing reports of resistance to omeprazole been published. However, a relative disadvantage of omeprazole is the observation that symptom-free Zollinger-Ellison syndrome patients are less inclined to undergo the work-up for surgery, which is the only possible curative treatment for these patients. Omeprazole therapy has been well tolerated and no side effects, significant changes in laboratory variables or toxicity have been noted.

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Section: Omeprazole In Zollinger-ellison Syndromementioning

confidence: 73%

Section: Effect O F Omeprazole On Serum Gastrin and Gastric Endocrinementioning

confidence: 78%

Section: Omeprazole In Zollinger-ellison Syndromementioning

confidence: 99%

Section: Other Side Effects O F Omeprazolementioning

confidence: 99%

See 2 more Smart Citations

Omeprazole in the Treatment of Zollinger-Ellison Syndrome and Histamine H<sub>2</sub>-Antagonist Refractory Ulcers

Meijer

Jansen²,

Lamers³

1989

Digestion

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“…Ranitidine treatment was discontinued 48 h before assessment. Ranitidine dosage was decreased if the patient was symptom-free, presented without any mucosal lesions at endoscopy and with BAO below 10 mmol h-' [2,12].…”

Section: Methodsmentioning

confidence: 99%

Long‐term treatment with octreotide in patients with the Zollinger‐ElIison syndrome

Ruszniewski

Ramdani

Cadiot

et al. 1993

Eur J Clin Investigation

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Abstract. This study reports the effects of 4 and 5-year treatment with octreotide (200 pg sc bid) in the Zollinger-Ellison syndrome (ZES). No symptoms related to acid hypersecretion were observed in the four patients throughout the study, and upper GI endoscopy was normal. Basal acid output (BAO) measured 12 h after injection, was below 10 mmol h-' in three to four patients and previous ranitidine treatment was discontinued. In the fourth case (pretreatment BAO value: 11 5 mmol h-I), BAO progressively decreased to 42 mmol h-' after 5 years of octreotide treatment. At the end of the study, serum gastrin levels were 58.5% (30-68) of the pretreatment values and two patients had normal gastrin levels. Peak acid output (PAO) decreased markedly after 2,4 and 5 years, by 68% (35-89) suggesting that octreotide had exerted an antitrophic effect on parietal cell mass. Diffuse hyperplasia of fundic argyrophil cells present in two patients before octreotide, decreased during the treatment. Mean argyrophil cell density for all patients was not significantly modified. Antral gastrin-cell density was in the normal range. No long-term side effect of octreotide treatment was observed. Although octreotide may not be considered as a substitute for benzimidazoles in the treatment of ZES, its specific properties may be of therapeutic benefit in some ZES patients.

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