Nonbeta Islet-cell Carcinoma of the Pancreas Presenting as Diarrhea

Shafer, William H.

doi:10.7326/0003-4819-61-3-539

Cited by 8 publications

(2 citation statements)

References 12 publications

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“…On the other hand, it has been shown by repeated observations in ZES that increased fecal water and electrolyte losses cease as soon as no, or only normal, quantities of acid gastric juice are allowed to enter the intestine. This has been noted during constant gastric aspiration [7] and after total gastrectomy [19], despite persistently elevated plasma and urinary gastrin levels [24]. Moreover, the fact that the diarrhea in ZES can be cured by total gastrectomy indicates that gastric acid is an essential factor in producing diarrhea.…”

Section: Discussionmentioning

confidence: 99%

Synthetic human gastrin I and gastrin-like pentapeptide in studies of intestinal absorption in man

et al. 1982

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The effects of synthetic human gastric I (SHG I) and gastrin-like pentapeptide (PG) on jejunal water, electrolyte, and glucose absorption were studied in 11 normal subjects. The i.v. administration of graded doses of SHG I increased plasma gastrin levels similar to those after food intake and in the Zollinger-Ellison syndrome. SHG I and PG caused no significant changes in the net movement of water and solute. The findings indicate that gastrin has no direct effect on intestinal absorption in normal man, and does not account for the mechanism of diarrhea in the Zollinger-Ellison syndrome.

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Section: Discussionmentioning

confidence: 99%

Synthetic human gastrin I and gastrin-like pentapeptide in studies of intestinal absorption in man

et al. 1982

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“…Ebensowenig erscheint es gerechtfertigt, anzunehmen, dal3 die Diarrhoen ein Vorstadium des Zollinger-Ellison-Syndroms wfiren, wie dies diskutiert wurde[21,77,79,105,116,125], auch, wenn in wenigen Ffillen ein Wechsel der Anaciditgt zur Hypersekretion beobachtet wurde[71]. Das V.-M.-Syndrom ist somit kein Endstadium des Zollinger-Ellison-Syndroms mit ,,ausgebrannten" Belegzellen.…”

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Das Verner-Morrison-Syndrom

Burkhardt

1976

Klin Wochenschr

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The Verner-Morrison Syndrome is a clinically defined entity caused by an islet cell tumor of the pancreas. More than 60 cases have been described so long. The syndrome is characterized by diarrhea, hypokalemia and hypochlorhydria. In addition to a diabetic disposition, raised calcium levels and skin alterations may be present. The diagnosis is a clinical one. A pancreatic tumor should be searched for and removed. Morphologically a benign and a maligne islet cell tumor or a diffuse hyperplasia of the islets of Langerhans can be found. Until now identification of the tumor cells has not been possible. There seems no doubt that the tumor cells produce a peptide hormone. Secretin, gastric inhibitory polypeptide, vasoactive intestinal polypeptide and combinations of hormones are discussed. The results are contradictory. Theories concerning the formal and causal pathogenesis are only incomplete and unproved up to now.

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Radiologic evaluation of pancreatic diseases in children

Singleton

Gray

1968

Seminars in Roentgenology

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Nonbeta Islet-cell Carcinoma of the Pancreas Presenting as Diarrhea

Cited by 8 publications

References 12 publications

Synthetic human gastrin I and gastrin-like pentapeptide in studies of intestinal absorption in man

Synthetic human gastrin I and gastrin-like pentapeptide in studies of intestinal absorption in man

Das Verner-Morrison-Syndrom

Radiologic evaluation of pancreatic diseases in children

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