title: Subclinical exocrine pancreatic dysfunction resulting from decreased cholecystokinin secretion in the presence of intestinal villous atrophy.
abstract: The aim of this study was to evaluate the concept that pancreatic dysfunction in patients having gluten sensitivity (celiac disease [CD]) or cow's milk protein enteropathy (CMPE) may result from the lack of pancreatic enzyme stimulation in the absence or decrease of cholecystokinin (CCK) secretion caused by villous atrophy.
  
  
  METHODS
  The following parameters were measured: plasma CCK in response to a fatty meal and human pancreatic fecal elastase in 24 patients with CD while on gluten-free diet and after gluten provocation and in 12 patients with CMPE at diagnosis and after a 6-month period of cow's milk-free diet. Intestinal mucosa morphology was examined by small bowel biopsy. Sixty-three controls having no organic gastrointestinal problems were investigated once at the time of diagnostic evaluation.
  
  
  RESULTS
  Fasting CCK, obtained at a time when patients with CD or CMPE had normal intestinal mucosa, was significantly different from postprandial and comparable to that of the control group. Fasting CCK obtained from patients with villous atrophy was also statistically different, but not significantly, from the postprandial. Fasting and postprandial plasma CCK and fecal pancreatic elastase values from patients having normal intestinal mucosa were significantly higher than those obtained from patients with villous atrophy. Significant correlation of intestinal mucosa morphology and CCK with fecal elastase concentration was documented.
  
  
  CONCLUSIONS
  Exocrine pancreatic dysfunction in individuals having villous atrophy may be the consequence of decreased CCK secretion. Cholecystokinin and pancreatic secretion is restored to normal, with intestinal mucosa regeneration.
authors.affiliation: 4th Pediatric Department, Aristotle University of Thessaloniki, Thessaloniki, Greece. sarvanit@med.auth.gr
authors.forename: Sanda
authors.initials: S
authors.lastname: Nousia-Arvanitakis
authors.forename: Maria
authors.initials: M
authors.lastname: Fotoulaki
authors.forename: Kyriaki
authors.initials: K
authors.lastname: Tendzidou
authors.forename: Constantina
authors.initials: C
authors.lastname: Vassilaki
authors.forename: Christina
authors.initials: C
authors.lastname: Agguridaki
authors.forename: Michael
authors.initials: M
authors.lastname: Karamouzis
mesh_terms: D000293:Adolescent; D001284:Atrophy; D001706:Biopsy; D002446:Celiac Disease / Q000473:pathology / Q000503:physiopathology*; D002648:Child; D002675:Child, Preschool; D002766:Cholecystokinin / Q000378:metabolism*; D004041:Dietary Fats / Q000008:administration & dosage; D005243:Feces / Q000201:enzymology; D005260:Female; D006801:Humans; D007223:Infant; D007413:Intestinal Mucosa / Q000473:pathology; D007422:Intestines / Q000473:pathology*; D008297:Male; D016269:Milk Hypersensitivity / Q000473:pathology / Q000503:physiopathology*; D008894:Milk Proteins; D010179:Pancreas / Q000503:physiopathology*; D010196:Pancreatic Elastase / Q000032:analysis; D012844:Sincalide / Q000097:blood
chemical_list: D004041:Dietary Fats; D008894:Milk Proteins; D002766:Cholecystokinin; D010196:Pancreatic Elastase; D012844:Sincalide