Ta. Winter et al., Impaired pancreatic secretion in severely malnourished patients is a consequence of primary pancreatic dysfunction, NUTRITION, 17(3), 2001, pp. 230-235
Severe undernutrition has been associated with reduced secretions of gastri
c acid and pancreatic enzymes. This may be the result of an impaired gut mu
cosal response to food and primary gastric parietal and pancreatic acinar c
ell secretory dysfunction as a consequence of the poor nutritional state. T
o investigate the relative contributions of these factors, severely underno
urished patients underwent enteral-meal-stimulated (ES; n = 7) or intraveno
us hormone (pentagastrin and cholecystokinin-8)-stimulated (HS; n = 12) gas
tric acid and pancreatic enzyme secretion before and after a period of nutr
itional support. Results were evaluated in comparison with normal healthy c
ontrol subjects (ES = 7, HS = 10). In the control subjects, enteral-meal an
d cholecystokinin-8 stimulation resulted in similar outputs of the pancreat
ic 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 significantl
y 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 amyl
ase (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-X stimulation was comparable. Gast
ric acid was similarly reduced in the undernourished patients (ES = 4.39 mE
q/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) impr
oved 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 unde
rnutrition was associated with primary gastric parietal and pancreatic acin
ar cell dysfunction, which, at least in the case of pancreatic enzymes, app
eared to be the determining factor controlling secretion in these patients,
Nutrition 2001:17:230-235. (C) Elsevier Science Inc. 2001.