Low Fecal Elastase: Potentially Related to Transient Small Bowel Damage Resulting from Enteric Pathogens

Abstract

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 g/g stool, as: severe pancreatic insufficiency (<100 g/g), moderate pancreatic insufficiency (100 to 200 g/g), and normal (>200 g/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.

Fecal calprotectin and alpha-1 antitrypsin predict severity and response to corticosteroids in gastrointestinal graft-versus-host disease

“…As such, a low concentration of elastase can reflect either primary pancreatic insufficiency and/or the lack of pancreatic enzyme stimulation in patients with transient intestinal damage (as revealed by abnormal calprotectin and/or ␣ 1 -AT), regardless of the cause. 28 Consequently, elastase levels may be interpreted only in patients with normal concentrations of calprotectin and ␣ 1 -AT, who represent a minority of patients. For this reason, fecal elastase did not appear to be a reliable marker.…”

Transient exocrine pancreatic insufficiency as a possible complication of an enterovirus infection

“…The pancreatic insufficiency in this boy was very important as reflected by the fat excretion of 20 g/day, a MTG breath test with a cPDR of 4% and FE-1 of <15 lg/g stool and lasted at least 1.5 months after the initial infection. In the literature, the decrease in pancreatic activity due to SPI is not as pronounced as in this boy [10] and that following gastroenteritis resolves within 15 days [7].…”

“…Secondary pancreatic insufficiency (SPI) due to mucosal damage cannot be excluded since we have no data on the intestinal architecture [7,10]. The decreased release of cholecystokinin by damaged mucosa and consequent insufficient stimulation of the pancreas is supposed to be the cause of SPI [6,9].…”

Exercise Intolerance, Malnutrition, Abnormal Sweat Chloride Levels, and Two CFTR Mutations: Is It Cystic Fibrosis?

“…Our patient presented with malnutrition, and his first FE1 was in the intermediate category (100 to 200 mg/g). However, he did not have infectious diarrhea, severe enteropathy, celiac disease, or short bowel syndrome that could explain a falsely low FE1 level (Salvatore et al, 2003;Sch€ appi, Smith, Cubitt, Milla, & Lindley, 2002;Walkowiak & Herzig, 2001). Because we did not perform a 72-hour fecal fat analysis, we could not confirm mild pancreatic insufficiency or fat malabsorption in our patient.…”