Pancreatic islet cell tumour with watery diarrhoea and hypokalaemia

Stoker, Dennis; Wynn, V.

doi:10.1136/gut.11.11.911

Cited by 20 publications

(3 citation statements)

References 44 publications

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“…The small intestine is able to secrete larger volumes of fluid which far exceed the maximal absorptive capacity of the colon if stimulated properly by intestinal secretagogues such as vasointestinal poly peptide (VIP) or cholera toxin. A patient with a VIP producing tumor of the pancreas (Vemer-Morrison syndrome or pancreatic cholera) lost up to 10 liters of fluid daily [23] and in fulminant cholera the weight of the diarrhoeal stool may almost equal the body weight of the patient, when adequately rehydrated. In these cases the co lon is not able to compensate the fluid loss and overflow explains this type of diar rhoea.…”

Section: Intestinal Electrolyte and Water Balancementioning

confidence: 99%

Intestinal Transport in Constipation and Diarrhoea

K¹

1988

Pharmacology

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Approximatively 10 liters of fluid enter the gastrointestinal tract with food and endogenous secretions, and only less than 100 ml or 1 % leave it with the faeces. Minor changes of this equilibrium in the intestinal transport may cause diarrhoea or constipation. Functions of small and large intestine differ markedly in transport of electrolytes and water. The relatively leaky epithelium of the small intestine allows for rapid equilibrium of osmolality in both directions while the tight epithelium of the colon preserves electrolytes and water once they have been absorbed. It may compensate secretory diarrhoea of the small intestine for instance caused by bacterial toxins to a certain degree unless it is overwhelmed leading to an overflow type of diarrhoea. On the other hand, small changes of net fluid transport in the colon in either direction will lead to diarrhoea or constipation since there is no compensating mechanism behind it. Mechanisms involved in the regulation of transintestinal electrolyte and water movements are the energy providing Na⁺, K⁺-ATPase, the mediators of membrane permeability and active Cl^– secretion such as cAMP and Ca²⁺ and substances affecting the tight junctions. Various substances may affect one or more of these regulatory mechanisms. Laxatives are one of those.

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Section: Intestinal Electrolyte and Water Balancementioning

confidence: 99%

Intestinal Transport in Constipation and Diarrhoea

K¹

1988

Pharmacology

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“…Das V.-M.-Syndrom ist somit kein Endstadium des Zollinger-Ellison-Syndroms mit ,,ausgebrannten" Belegzellen. Eine Dilatation der Schlingen wird bei vielen F/illen yon V.-M.-Syndrom beschrieben[68,110,127], die Passagezeit ist jedoch bei den meisten F/illen nicht beschleunigt[34,108]. Andersson u. Mitarb [1].…”

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“…Andersson u. Mitarb [1]. und Stoker und Wynn[110] eine erh6hte Passagezeit. Selten findet sich eine Steatorrhoe (vgl.…”

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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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