Studies on the interrelation between Zollinger-Ellison syndrome, Helicobacter pylori, and proton pump inhibitor therapy

Weber, H. Christian; Venzon, DJ; Rt, Jensen; Metz, DC

doi:10.1016/s0016-5085(97)70222-1

Cited by 38 publications

(34 citation statements)

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“…These values are clearly less than those in patients with ordinary chronic peptic ulcer in Japan. [19][20][21] In agreement with our data, Saeed et al 12 found a [12][13][14] These results strongly suggest that H. pylori infection decreases gastric acid secretion, even in patients with ZES. Several possible mechanisms may be responsible for the decrease of gastric acid secretion with H. pylori infection in patients with ZES.…”

Section: Discussionsupporting

confidence: 92%

“…A similar result was observed by Weber et al, 14 who found the seroprevalence of the infection to be 22%, but the rate of active infection to be 10%. In this study, we found that both the serum PG I level and the PG I/II ratio in patients positive only by serology were between the values in patients with active H. pylori infection and those without infection.…”

Section: Discussionsupporting

confidence: 88%

“…10,11 Thus, it appears reasonable to speculate that H. pylori infection could also modulate acid secretion in ZES. Indeed, it has already been reported that, in patients with ZES, acid secretion in H. pylori-positive subjects is lower than that in H. pylori-negative subjects, [12][13][14] but the pathophysiological significance of H. pylori infection in ZES remains unknown.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Helicobacter pylori infection on Zollinger-Ellison syndrome

Watanabe

Matsushima

Nakase

et al. 2000

Journal of Gastroenterology

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Both Zollinger-Ellison syndrome (ZES) and Helicobacter pylori infection are major etiologic factors for peptic ulcer. The aim of this study was to investigate the effect of H. pylori infection on ZES with special reference to acid secretion. Sixteen patients with ZES were selected (median age, 59 years; range, 39-66 years; M/F, 9/7), and H. pylori status, ulcer location, gastric acid secretion, serum pepsinogen (PG) I and II concentrations, and PG I/II ratio were determined. The seroprevalence of H. pylori infection was 50%, whereas active H. pylori infection was seen in only 25% of the patients. Thirteen patients had duodenal ulcer (DU), 1 had gastric ulcer (GU), and 2 had both GU and DU. DU was seen in both H. pylori-positive and H. pylori-negative patients, whereas GU was found only in H. pylori-positive patients. Both basal and maximal acid outputs were significantly lower in H. pylori-positive patients than in H. pylori-negative patients (P< 0.05). Moreover, both serum PG I and the PG I/II ratio were significantly lower in H. pylori-positive patients than in H. pylori-negative patients. These results indicate that ZES is an independent risk factor for DU, but H. pylori infection may play some role in the development of GU in ZES. In patients with ZES, H. pylori infection may reduce both hypersecretion from parietal cells and PG I secretion from chief cells, and hyperacidity of the stomach in ZES may have eradicated H. pylori in some patients.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

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Effects of Helicobacter pylori infection on Zollinger-Ellison syndrome

Watanabe

Matsushima

Nakase

et al. 2000

Journal of Gastroenterology

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“…Therefore, lack of H. pylori should lead to a suspicion of ZES in a patient with recurrent peptic ulcer disease [30]. …”

Section: Diagnostic Procedures For Zes and Men1: Laboratory Tests Immentioning

confidence: 99%

Gastrinoma (Duodenal and Pancreatic)

Jensen¹,

et al. 2006

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“…A diagnosis of ZES is dependent upon the presence of hypergastrinemia (>100 pg/ml) in the absence of achlorhydria, with levels > 900 pg/ml almost diagnostic of the disease. In patients with borderline elevated gastrin values (e.g., 200 to 500 pg/ml), a secretin provocative test may be required to make a diagnosis of ZES [19]. Following the administration of secretin (2 units/kg intravenously as a bolus), a rise in the fasting serum gastrin of >200 pg/ml within 10 minutes is highly sensitive and specific for the diagnosis of ZES [20,21].…”

Section: Opinion Statementmentioning

confidence: 99%

Zollinger-Ellison syndrome

Pisegna

1999

Curr Treat Options Gastro

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The first goal of therapy is the control of gastric acid hypersecretion using PPIs or high-dose H2R antagonists. The diagnosis of Multiple Endocrine Neoplasia (MEN I) should be established early in the disease. Localization of gastrinoma tumor should be performed using a combination of endoscopic ultrasonography (EUS), somatostatin receptor scintigraphy (SRS), and computerized tomography (CT), or Magnetic Resonance Imaging (MRI). Surgical resection in sporadic ZES should be performed to attempt cure of tumor. Surgery, hormonal, chemotherapy, embolization therapy or therapeutic OctreoScan should be considered in patients with metastatic tumor.

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Studies on the interrelation between Zollinger-Ellison syndrome, Helicobacter pylori, and proton pump inhibitor therapy

Cited by 38 publications

References 0 publications

Effects of Helicobacter pylori infection on Zollinger-Ellison syndrome

Effects of Helicobacter pylori infection on Zollinger-Ellison syndrome

Gastrinoma (Duodenal and Pancreatic)

Zollinger-Ellison syndrome

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