Impaired pancreatic secretion in severely malnourished patients is a consequence of primary pancreatic dysfunction.
Severe undernutrition has been associated with reduced secretions of gastric acid and pancreatic enzymes. This may be the result of an impaired gut mucosal response to food and primary gastric parietal and pancreatic acinar cell secretory dysfunction as a consequence of the poor nutritional state. To investigate the relative contributions of these factors, severely undernourished patients underwent enteral-meal-stimulated (ES; n = 7) or intravenous hormone (pentagastrin and cholecystokinin-8)-stimulated (HS; n = 12) gastric acid and pancreatic enzyme secretion before and after a period of nutritional support. Results were evaluated in comparison with normal healthy control subjects (ES = 7, HS = 10). In the control subjects, enteral-meal and cholecystokinin-8 stimulation resulted in similar outputs of the pancreatic enzymes amylase (2213 versus 2305 U/h), lipase (84.93 versus 118.6 U/h), and trypsin (498.9 versus 341.4 U/h), whereas acid output was significantly lower in the ES group (10.90 versus 25.53 mEq/h; P < 0.01). Compared with controls, malnourished groups had significantly reduced secretions of amylase (ES = 870.1 U/h, HS = 686.5 U/h; P < 0.02), lipase (ES = 30.68 U/h, HS = 25.96 U/h; P < 0.02), and trypsin (ES = 175.6 U/h, HS = 109.3 U/h; P < 0.01). The response to enteral-meal or CCK-8 stimulation was comparable. Gastric acid was similarly reduced in the undernourished patients (ES = 4.39 mEq/h, HS = 5.04 mEq/h; P < 0.01). After refeeding, secretion of amylase (ES = 2351 U/h, HS = 2228 U/h) and lipase (ES = 58.83 U/h, HS = 84.91 U/h) improved to levels not significantly different from controls, whereas trypsin (ES = 226.4 U/h, HS = 213.1 U/h; P < 0.03) and acid secretion (ES = 3.52 mEq/h, HS = 11.85 mEq/h; P < 0.01) remained significantly impaired. Severe undernutrition was associated with primary gastric parietal and pancreatic acinar cell dysfunction, which, at least in the case of pancreatic enzymes, appeared to be the determining factor controlling secretion in these patients.
Winter
T A
TA
From the Gastrointestinal Clinic, Groote Schuur Hospital, Cape Town, South Africa. winter@curie.uct.ac.za
Marks
T
T
Callanan
M
M
O'Keefe
S J
SJ
Bridger
S
S
D000328:Adult; D016022:Case-Control Studies; D004750:Enteral Nutrition; D005744:Gastric Acid / Q000378:metabolism*; D006801:Humans; D007408:Intestinal Absorption; D007413:Intestinal Mucosa / Q000503:physiopathology; D009748:Nutrition Disorders / Q000503:physiopathology*; D018529:Nutritional Support; D010179:Pancreas / Q000201:enzymology / Q000378:metabolism*; D010418:Pentagastrin / Q000008:administration & dosage; D012844:Sincalide / Q000008:administration & dosage
D010418:Pentagastrin; D012844:Sincalide