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Brief Paper

 

Choline metabolite, trimethylamine N-oxide (TMAO), is associated with inflammation in psoriatic arthritis

1, 2, 3, 4, 5, 6, 7, 8, 9

 

  1. Department of Medicine, School of Medicine, University of California, San Diego, USA; and Department of Medicine, Autonomous University of Barcelona, Spain.
  2. Department of Medicine, School of Medicine, University of California, San Diego, USA.
  3. Department of Medicine, School of Medicine, University of California, San Diego, USA.
  4. Department of Medicine, School of Medicine, University of California, San Diego, USA.
  5. Department of Medicine, School of Medicine, University of California, San Diego, USA.
  6. Department of Medicine, School of Medicine, University of California, San Diego, USA.
  7. Center for Computational Biology and Bioinformatics, University of California, San Diego, USA.
  8. Department of Medicine, School of Medicine, University of California, San Diego, USA.
  9. Department of Medicine, School of Medicine, University of California, San Diego, USA; and Department of Medicine, Autonomous University of Barcelona, Spain. mguma@ucsd.edu

CER11469
2019 Vol.37, N°3
PI 0481, PF 0484
Brief Paper

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PMID: 30620278 [PubMed]

Received: 20/06/2018
Accepted : 09/10/2018
In Press: 04/01/2019
Published: 10/05/2019

Abstract

OBJECTIVES:
Dietary intake of choline has been linked to systemic inflammation through the microbial production of two metabolites, trimethylamine (TMA) and trimethylamine-N-oxide (TMAO). Herein we explore the association between choline metabolites and inflammation in psoriatic arthritis (PsA) patients.
METHODS:
Thirty-eight patients with PsA, all of whom satisfied the CASPAR classification criteria for PsA, were studied. Outcomes reflecting the activity of peripheral arthritis as well as skin psoriasis, Disease Activity Score (DAS)28, Clinical Disease Index (CDAI) and Body Surface Area (BSA) were assessed. Serum concentration of choline metabolites (choline, TMA, TMAO, betaine and carnitine) were determined by LC-MS, and metabolite levels associated with disease scores.
RESULTS:
Among the 38 PsA patients included, the mean DAS28PCR was 2.74±1.29. Twenty-seven patients had active skin disease, with an average BSA of 7.2±16.22. TMAO, but not TMA or choline, significantly correlated with measures of disease activity for both skin and peripheral joints.
CONCLUSIONS:
In our cohort, only TMAO, but not TMA, choline, betaine or carnitine, was associated with inflammation in PsA patients, establishing a mechanistic link between TMAO and PsA phenotypes. Future studies will explore the modulation of TMAO and disease severity in PsA.

Rheumatology Article