Abstract

The Verner-Morrison (1) or watery diarrhoea syndrome (WDS) results from islet-cell tumours of the pancreas or metastases from such tumours and is regularly associated with elevated levels of vasoactive intestinal peptide (VIP) (2, 3) and pancreatic polypeptide (PP) (3. 4). Since infusion of VIP results in severe watery diarrhoea, VIP elevations can be implicated in the pathogenesis of the disorder and be a useful tumour marker (2, 5, 6). The role of PP is less clear but, again, is a useful tumour marker because of the frequent elevations in WDS (4, 7). Somatostatin has been shown to palliate the WDS, presumably by a direct effect on the tumour, resulting in decreased circulating levels of VIP (8, 9). Since somatostatin has a short half-life, it is not practical for long-term management (10). Availability of the somatostatin analogue SMS 201-995 (11) and the report that its use suppressed the WDS in a patient with a VIP-secreting turnour (12) prompted its use in the management of this patient. This synthetic octapeptide is more potent than natural somatostatin and has a biologic half-life that is 20 times greater when given intravenously. This drug reaches peak plasma levels within 15-30 min after subcutaneous injection and has an elimination half-life of 113 min (13). The response to the SMS 201-995, chemotherapy, dexamethasone, and a combination of SMS 201-995 plus dexamethasone was assessed in a patient with WDS due to an islet-cell carcinoma that metastasized to the liver. Changes in the plasma levels of VIP and PP were related to measured circulating levels of SMS 201-995 during therapy.

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