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NSAID acyl glucuronides and enteropathy.

Urs A Boelsterli1, Veronica Ramirez-Alcantara

  • 1Mechanistic Toxicology Lab, Department of Pharmaceutical Sciences, University of Connecticut School of Pharmacy, 69 North Eagleville Road Unit 3092, Storrs, CT 06269-3092, USA. urs.boelsterli@uconn.edu

Current Drug Metabolism
|March 15, 2011
PubMed
Summary

Nonsteroidal anti-inflammatory drugs (NSAIDs) form acyl glucuronides, which can cause small intestinal injury by releasing high concentrations of the parent drug in the lower intestine. This highlights a potential safety concern in drug development.

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Area of Science:

  • Pharmacology
  • Toxicology
  • Gastroenterology

Background:

  • Nonsteroidal anti-inflammatory drugs (NSAIDs) are linked to gastric and small intestinal injury (enteropathy).
  • The precise mechanisms underlying NSAID enteropathy remain unclear, with proposed factors including topical effects, COX inhibition, and inflammatory responses.
  • NSAID metabolism involves conjugation to acyl glucuronides, which are excreted into bile.

Purpose of the Study:

  • To elucidate the role of NSAID acyl glucuronides in the pathogenesis of NSAID-induced enteropathy.
  • To investigate the toxicokinetic properties of NSAID acyl glucuronides as a potential mechanism for small intestinal injury.

Main Methods:

  • Analysis of NSAID metabolism and excretion pathways.
  • Investigation of NSAID acyl glucuronide interactions with intestinal tissues.
  • Assessment of local drug concentrations following glucuronide cleavage in the small intestine.

Main Results:

  • NSAID acyl glucuronides are transported via bile to the distal small intestine (jejunum/ileum).
  • Higher local pH and bacterial β-glucuronidase activity cleave the glucuronic acid moiety, releasing the parent NSAID.
  • This process can lead to high local concentrations of the parent NSAID, potentially causing tissue injury.

Conclusions:

  • NSAID acyl glucuronides may act as a transport form, delivering parent NSAID to distal intestinal sites.
  • The release of parent NSAID from acyl glucuronides in the jejunum/ileum is a plausible mechanism for NSAID enteropathy.
  • High biliary excretion rates of NSAID acyl glucuronides warrant consideration as a potential red flag in drug development due to localized toxicity risks.