Divergent PGD2 and leukotriene C4 metabolite excretion following aspirin therapy: Ten patients with systemic mastocytosis

Joseph H. Butterfield, Ravinder J. Singh

Research output: Contribution to journalArticlepeer-review

Abstract

Aspirin-exacerbated respiratory disease and some cases of chronic idiopathic urticaria are disorders in which increased baseline urinary excretion of leukotriene(LT)E4 further increases following aspirin administration. Increased urinary excretion of the metabolites of prostaglandin D2, 11β-prostaglandin(PG)F2α and (2,3-dinor)-11β-PGF2α, have been documented in systemic mastocytosis (SM) and in mast cell activation syndrome (MCAS). Symptoms due to increased baseline and/or episodic release of PGD2 can be prevented with aspirin, an inhibitor of cyclooxygenase (COX)1 and COX2. Here by retrospective chart review we discovered 8 of 10 patients with SM in whom normalization of an elevated urinary (2,3-dinor)-11β-PGF2α occurred with aspirin therapy also had a parallel increased excretion of LTE4 by an average of nearly 13-fold. How widespread this phenomenon occurs in SM is unknown; however, this occurrence needs to be considered when interpreting changes in these urinary mast cell mediator metabolites during aspirin therapy.

Original languageEnglish (US)
Article number106563
JournalProstaglandins and Other Lipid Mediators
Volume155
DOIs
StatePublished - Aug 2021

Keywords

  • Aspirin
  • Cyclooxygenase
  • Leukotriene E4
  • Mast cell activation syndrome
  • Prostaglandin D2
  • Systemic mastocytosis

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Pharmacology
  • Cell Biology

Fingerprint

Dive into the research topics of 'Divergent PGD<sub>2</sub> and leukotriene C<sub>4</sub> metabolite excretion following aspirin therapy: Ten patients with systemic mastocytosis'. Together they form a unique fingerprint.

Cite this