Correlation of intestinal lactulose permeability with exocrine pancreatic dysfunction

David R. Mack, Jonathan A. Flick, Peter R. Durie, Beryl J. Rosenstein, Lynda E. Ellis, Jay A. Perman

Research output: Contribution to journalArticlepeer-review

Abstract

Increased intestinal permeability to lactulose has been reported in patients with cystic fibrosis (CF). To determine whether this finding is unique to CF or whether it is related to accompanying exocrine pancreatic dysfunction, we evaluated 31 patients with CF and 10 with Shwachman syndrome who had variable degrees of pancreatic dysfunction, together with 17 healthy control subjects. There was no significant difference in the mean urinary lactulose excretion, expressed as the percentage of dose recovered, between CF and non-CF patients with pancreatic insufficiency (2.1%±1.2% and 1.9%±0.8%, respectively) or between CF and non-CF patients with pancreatic sufficiency (0.6%±0.5% and 0.6%±0.3%, respectively). However, there was a significant difference in mean lactulose excretion between the pancreatic-insufficient and the pancreatic-sufficient patients (both CF and non-CF groups; p<0.001 and p<0.013, respectively). We further analyzed the results from 26 of the 41 patients (16 patients with CF and 10 non-CF patients) with pancreatic dysfunction who had previously undergone quantitative pancreatic function testing. A nonlinear, inverse relationship was found between urinary lactulose excretion and exocrine pancreatic function determined by duodenal trypsin output. These data confirm a direct relationship between intestinal lactulose permeability and the degree of exocrine pancreatic dysfunction, unrelated to the cause of the pancreatic disease.

Original languageEnglish (US)
Pages (from-to)696-701
Number of pages6
JournalThe Journal of pediatrics
Volume120
Issue number5
DOIs
StatePublished - May 1992

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health

Fingerprint Dive into the research topics of 'Correlation of intestinal lactulose permeability with exocrine pancreatic dysfunction'. Together they form a unique fingerprint.

Cite this