Urinary concentrations of physiological markers of intestinal barrier dysfunction do not increase with acute aspirin use (LB749)

Abstract

Previous studies have shown that acute aspirin use causes increased intestinal permeability to ingested permeability probes. The purpose of the present studies was to determine whether acute aspirin use also increases concentrations of urinary physiological markers of intestinal barrier dysfunction. The urinary markers were: 1) D‐lactate (produced by intestinal bacteria; a marker of intestinal barrier dysfunction if increased in the plasma or urine), 2) intestinal fatty acid binding protein (I‐FABP; a marker of small intestinal enterocyte damage), and 3) claudin‐3 (an intestinal tight junction protein). Two studies were conducted and involved ingestion of aspirin (975 mg) or placebo the night before and the morning of an experiment. Eight healthy subjects participated in each study. Six hours after the morning dose of aspirin or placebo, subjects provided a urine sample. In the first study, the urine was assayed for D‐lactate. In the second study, the urine was assayed for I‐FABP and claudin‐3. No significant differences were found between aspirin and placebo experiments for D‐lactate in study 1, or for I‐FABP or claudin‐3 in study 2. These results indicate that urinary concentrations of D‐lactate, I‐FABP, and claudin‐3 do not increase with acute aspirin use.