Depressed jejunal secretion of water and ions in response to prostaglandin E1 in adult celiac disease.
In order to test in man the concept that intestinal fluid secretion originates from the crypts of Lieberkühn, we assessed the jejunal secretory effect of intraluminal prostaglandin E1 (PGE1) (0.9 microgram/kg/min) in untreated adult celiac disease (ACD, N = 7), treated ACD (N = 4) and normal subjects using the intestinal perfusion technique. In untreated ACD (1) water and solutes were malabsorbed (or secreted) in the basal period; (2) fluid and ion secretion seen during PGE1 infusion and net secretory effect of PGE1 (difference in transport between basal and PGE1 periods) were reduced (P less than 0.01); (3) the effects of PGE1 inhibition of sodium insorption, and stimulation of sodium exsorption, were decreased and abolished, respectively. In treated patients PGE1-induced secretion returned towards normal values. Our finding of a depressed secretory response to PGE1 in the face of marked crypt hypertrophy do not support the concept that crypt cells are the major site of intestinal fluid secretion.
D000328:Adult; D002446:Celiac Disease / Q000178:diet therapy / Q000378:metabolism*; D004573:Electrolytes / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007419:Intestinal Secretions / Q000378:metabolism*; D007583:Jejunum / Q000187:drug effects* / Q000378:metabolism; D011458:Prostaglandins E / Q000494:pharmacology*; D012964:Sodium / Q000378:metabolism; D014867:Water / Q000378:metabolism*
D004573:Electrolytes; D011458:Prostaglandins E; D014867:Water; D012964:Sodium; D005947:Glucose