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Low fecal elastase: potentially related to transient small bowel damage resulting from enteric pathogens.
UNLABELLED: Fecal elastase is considered to be a highly sensitive and specific non-invasive exocrine pancreatic function test. However, enteropathy may theoretically cause decreased exocrine pancreatic enzyme secretion through alteration of enteric hormone release.
OBJECTIVE: The aim of this study was to evaluate the possible influence of transient small bowel damage on pancreatic elastase secretion.
METHODS: We studied 166 children (aged 4 months to 14 years, mean 2 years); 114 of these children had acute enteritis and 52 children were control subjects (with gastro-intestinal symptoms or extra-intestinal diseases). Feces were collected from each patient 3 days after the onset of diarrhea and then tested for fecal elastase, bacterial pathogens, Rotavirus, and Adenovirus. Liquid fecal samples were not considered eligible for elastase measurement. Pancreatic elastase was measured using an ELISA method (Sche.Bo.Tech, Germany). We classified the results, expressed in microg/g stool, as: severe pancreatic insufficiency (<100 microg/g), moderate pancreatic insufficiency (100 to 200 microg/g), and normal (>200 microg/g).
RESULTS: In the acute enteritis group we found severe levels in 14 (12%) children, moderate levels in 18 children (16%), and normal levels in 82 children (72%). In contrast, 52 of 52 (100%) control subjects demonstrated normal results. Statistical analysis (Wilcoxon rank test) demonstrated a significant difference between the enteritis and control groups (P < 0.01). Serial measurement of fecal elastase performed in 10 patients with enteritis showed a progressive increase of levels in 6 patients and an early decline with subsequent increases in the other 4 patients.
CONCLUSIONS: Transient exocrine pancreatic insufficiency may be present in transient small bowel disease, caused by both bacterial and viral infections, possibly related to reduced enteric CCK secretion.
OBJECTIVE: The aim of this study was to evaluate the possible influence of transient small bowel damage on pancreatic elastase secretion.
METHODS: We studied 166 children (aged 4 months to 14 years, mean 2 years); 114 of these children had acute enteritis and 52 children were control subjects (with gastro-intestinal symptoms or extra-intestinal diseases). Feces were collected from each patient 3 days after the onset of diarrhea and then tested for fecal elastase, bacterial pathogens, Rotavirus, and Adenovirus. Liquid fecal samples were not considered eligible for elastase measurement. Pancreatic elastase was measured using an ELISA method (Sche.Bo.Tech, Germany). We classified the results, expressed in microg/g stool, as: severe pancreatic insufficiency (<100 microg/g), moderate pancreatic insufficiency (100 to 200 microg/g), and normal (>200 microg/g).
RESULTS: In the acute enteritis group we found severe levels in 14 (12%) children, moderate levels in 18 children (16%), and normal levels in 82 children (72%). In contrast, 52 of 52 (100%) control subjects demonstrated normal results. Statistical analysis (Wilcoxon rank test) demonstrated a significant difference between the enteritis and control groups (P < 0.01). Serial measurement of fecal elastase performed in 10 patients with enteritis showed a progressive increase of levels in 6 patients and an early decline with subsequent increases in the other 4 patients.
CONCLUSIONS: Transient exocrine pancreatic insufficiency may be present in transient small bowel disease, caused by both bacterial and viral infections, possibly related to reduced enteric CCK secretion.
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