Zollinger-Ellison Syndrome

Isenberg, Jon I.; Walsh, John H.; Grossman, Morton I.

doi:10.1016/s0016-5085(19)33157-9

Cited by 255 publications

(30 citation statements)

References 180 publications

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“…The preoperative diagnosis of Zollinger-Ellison (ZE) syndrome is based on the combination of basal gastric acid hypersecretion and hypergastrinaemia (Isenberg et al, 1973). The criteria of acid secretion as proposed for the ZE syndrome, however, give both false positive and false negative results (Aoyagi and Summerskill, 1966;Kaye et al, 1970;Lewin et al, 1972).…”

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confidence: 99%

“…The criteria of acid secretion as proposed for the ZE syndrome, however, give both false positive and false negative results (Aoyagi and Summerskill, 1966;Kaye et al, 1970;Lewin et al, 1972). The serum gastrin level, as measured by radioimmunoassay, is a valuable tool for the diagnosis of ZE syndrome (Thompson et al, 1972a;Isenberg et al, 1973;Walsh and Grossman, 1975). In some ZE patients, however, the serum gastrin level may at times be only slightly raised and an overlap with non-ZE patients may be present (Thompson et al, 1972a;Isenberg et al, 1973;Walsh and Grossman, 1975).…”

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confidence: 99%

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Comparative study of the value of the calcium, secretin, and meal stimulated increase in serum gastrin to the diagnosis of the Zollinger-Ellison syndrome.

Lamers¹,

Tongeren²

1977

Gut

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SUMMARY To evaluate the usefulness of provocation tests in the diagnosis of the Zollinger-Ellison (ZE) syndrome stimulation tests with calcium, 15 mg/kg.3 h, and secretin GIH, 1 U/kg.30 s, were performed in 15 patients with histologically proven or suspected ZE syndrome. Nine of these 15 patients were without previous gastric surgery and in them meal stimulated serum gastrin levels were measured as well. These tests were also performed in normal subjects and in patients with duodenal ulcer, antrectomy, total gastrectomy, and achlorhydria. All tests were considered to be positive if a more than a 50 % increase in serum gastrin was found. The results indicate that secretin stimulation is the provocation test of first choice in the diagnosis of this syndrome. This test is most valuable for the following reasons: (1) there were few (two out of 15) false-negative test results in ZE patients; (2) there were no false-positive tests in 69 patients without gastrinoma; (3) it was easy and quick to perform; and (4) there were no adverse reactions. The two ZE patientswithnegativesecretinstimulation tests had negative calcium provocation tests as well, in spite of histologically proven gastrinoma. In 11 patients with suspected or proven ZE syndrome and basal serum gastrin levels of less than 1000 pg/ml a rather good correlation (r = 0-841; p < 0 01) was found between the percental increase in serum gastrin after stimulation by calcium and secretin. Meal stimulated serum gastrin levels are helpful only in patients without previous gastric surgery.

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confidence: 99%

Comparative study of the value of the calcium, secretin, and meal stimulated increase in serum gastrin to the diagnosis of the Zollinger-Ellison syndrome.

Lamers¹,

Tongeren²

1977

Gut

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“…This "prestimulation" is best expressed as the ratio of basal versus maximal acid output. When the ratio of BAO / MAO exceeds 0.6, the diagnosis of ZES is highly suggestive [15]. It is important to note that hypergastrinemia in a patient will almost never be related to a gastrinproducing tumor if the gastric pH is > 2 [6].…”

Section: Diagnosismentioning

confidence: 99%

Diagnosis and treatment of gastrinoma in the era of proton pump inhibitors

Banasch

Schmitz

2007

Wien Klin Wochenschr

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The Zollinger-Ellison syndrome is characterized pathophysiologically by a significant hypergastrinemia derived from a gastrin-secreting neuroendocrine tumor with a primary location in the pancreas or duodenum. Chronic hypergastrinemia in turn triggers gastric acid hypersecretion yielding in chronic or recurrent or refractory peptic ulcer disease and/or chronic diarrhea. One half of patients with ZES will have distant metastases in the liver by the time the diagnosis is established and one half of all patients with ZES will experience chronic diarrhea as chief complaint rather than peptic ulcer-related symptoms and signs. Gastrinomas have been reported to either manifest sporadically or to occur in conjunction with the genetic background of the MEN-I syndrome. Diagnosis is based on the patients history which is typically characterized by recurrent episodes of peptic ulcer disease or by severe reflux esophagitis and/or diarrhea or by acid-related symptoms which fail to respond to standard treatment regimens. Upper gastrointestinal tract endoscopy will provide evidence for peptic ulcer disease in anatomical regions located aborally the duodenal bulb within the descending part of the duodenum or even farther distally within the jejunum. Peptic ulcers frequently occur in groups indicating some substantial acid hypersecretion. A gastric pH > 2 is mutually exclusive for ZES. Increased serum gastrin levels confirm the diagnosis biochemically. Gastrin secretion can be determined in the basal state or following stimulation with secretin or calcium. High sensitivity and specificity for the diagnosis of ZES is provided by determining the ratio of basal versus pentagastrin-stimulated gastric acid secretion: The ratio of BAO / MAO > 0.6 is highly specific for gastrinoma. To localize the gastrin-secreting tumor computer-assisted tomography, endoscopic ultrasound, and somatostatin receptor scintigraphy provide useful help but most recently, endoscopic ultrasound with high resolution transducers appear to improve preoperative site localization. If modern imaging techniques fail to elucidate the site of the tumor, intraoperative diaphany may help to detect gastrinomas within the duodenal wall. Definitive treatment will only be achieved by total surgical resection of the gastrin-producing tumor in the pancreas or duodenum including dissection of the regional lymph nodes. Control of symptoms will have to be achieved by administration of highly potent proton pump inhibitors in up to 2-3-fold increased standard doses to inhibit gastric acid hypersecretion. Elevation of gastric pH > 4 will be the therapeutic target to protect the mucosa of the upper gastrointestinal tract. Basal acid output should be reduced to less than 10 mEq H(+) per hour which requires administration of highly potent proton pump inhibitors with a recommended starting dose of 60 mg omeprazole equivalents per day.

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“…It has been proposed that a maximal acid output (MAO) after pentagastrin stimulation and a BAO/ MAO ratio greater than 0.6 is suggestive of ZES [38].…”

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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Zollinger-Ellison Syndrome

Cited by 255 publications

References 180 publications

Comparative study of the value of the calcium, secretin, and meal stimulated increase in serum gastrin to the diagnosis of the Zollinger-Ellison syndrome.

Comparative study of the value of the calcium, secretin, and meal stimulated increase in serum gastrin to the diagnosis of the Zollinger-Ellison syndrome.

Diagnosis and treatment of gastrinoma in the era of proton pump inhibitors

Zollinger-Ellison Syndrome in the Intensive Care Setting

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