Watery diarrhoea andanislet cell tumour

EDITORIALSYNOPSISItissuggested thatthere aretwohormonal syndromes associated with noninsulin-secretin g islet cell tumoursandthis caseisan example ofthenon-gastrin-secreting type withwaterydiarrhoea andhypokalaemia. Thepatient hadhistamine-fast achlorhydria anda normal gastric biopsy andno gastrin was recovered fromthetumourtissue. Thewaterydiarrhoea was isosmotic withplasma andwas increased byanintravenous saline load. There was adramatic responsetosteroids. Since Zollinger andEllison (1955) first described thesyndrome ofrecurrent peptic ulceration, gastric hypersecretion, andanassociated adenomaofthe pancreatic islet cells, morethanonehundred cases havebeenreported. Shortly after their original paper itwasnoticed that anumberofthese patients also haddiarrhoea andthat thediarrhoea wassometimes thepresenting andoutstanding symptom. Maynard andPoint(1958) described onesuchpatient in whomthere wasagross excess offatinthestools. Theypostulated that thesteatorrhoea wastheresult oftheinactivation ofpancreatic enzymes atthelow pHcaused bytheexcessive gastric secretion andthis hypothesis hasreceived support fromtheworkof Summerskill (1959) andRawson, England, Gillam, French, andStammers (1960). Thereseemslittle doubtthatthegastric hypersecretion isduetothe formation ofagastrin-like substance bytheadenoma (Gregory, Tracy, French, andSircus, 1962). However, notall thepatients withdiarrhoea have hadsteatorrhoea (Priest andAlexander, 1957; Verner andMorrison, 1958) andrecently cases have beendescribed withhypochlorhydria andachlorhydria (Murray, Paton, andPope,1961; Parkins, 1961; Espiner andBeaven, 1962). Itisclear that in these circumstances someother mechanism mustbe thecauseofthediarrhoea. Inareview ofrecent literature SulmanandKirsner (1963), commenting onthereport byEspiner andBeaven, state: 'The hypokalaemia anddiarrhoea seemed attributable to anhumoral agent ofislet cell origin promoting the secretion ofsuccus entericus. Ifadditional cases ofthis typeareidentified, theentire concept ofan humoralagentspecifically stimulating gastric secretion willrequire modification toinclude a secretory stimulant also forthesmall intestine'. Thispaperdescribes another suchcase, together withsomeobservations onthefaecal excretion of sodiumandpotassium andtheresponse totreatmentwithsteroids. CASEREPORT