Comprehensive arginine metabolomics and peripheral vasodilatory capacity in rheumatoid arthritis: A monocentric cross-sectional study.


Journal

Microvascular research
ISSN: 1095-9319
Titre abrégé: Microvasc Res
Pays: United States
ID NLM: 0165035

Informations de publication

Date de publication:
09 2020
Historique:
received: 19 03 2020
revised: 27 06 2020
accepted: 27 06 2020
pubmed: 6 7 2020
medline: 26 11 2020
entrez: 6 7 2020
Statut: ppublish

Résumé

The relationship between plasma arginine metabolites influencing vascular homeostasis and peripheral vasodilatory capacity in rheumatoid arthritis (RA) patients is not known. l-arginine (Arg), monomethyl-l-arginine (MMA), l-homoarginine (hArg), asymmetric dimethyl-l-arginine (ADMA), symmetric dimethyl-l-arginine, and l-citrulline (Cit) were measured by liquid chromatography tandem mass spectrometry (LC-MS/MS) in 164 RA patients and 100 age- and sex-matched healthy controls without previous cardiovascular events. Log-transformed reactive hyperemia index (Ln-RHI) evaluated by flow-mediated pulse amplitude tonometry (PAT, EndoPAT2000 device) was assessed as surrogate measure of peripheral vasodilatory capacity in RA patients. Ln-RHI values <0.51 indicated peripheral endothelial dysfunction (ED). The relationship between plasma arginine metabolite concentrations, RA descriptors and peripheral vasodilatory capacity was evaluated by bivariate correlation and regression analyses. Plasma ADMA concentrations were significantly higher, and plasma hArg concentrations significantly lower, in RA patients than in controls (0.53 ± 0.09 vs 0.465 ± 0.07 μmol/L and 1.50 ± 0.60 vs 1.924 ± 0.78 μmol/L, respectively; p < 0.001 for both comparisons). Bivariate correlation analysis demonstrated no significant correlation between arginine metabolites and disease descriptors. In regression analysis in RA patients, higher plasma ADMA concentrations were independently associated with presence of ED [OR(95% CI) = 77.3(1.478-4050.005), p = 0.031] and lower Ln-RHI [B coefficient(95% CI) = -0.57(-1.09 to -0.05), p = 0.032]. ADMA was significantly, albeit weakly, associated with impaired microcirculatory vasodilatory capacity and peripheral endothelial dysfunction in RA. This suggests an important pathophysiological role of this metabolite in the vascular alterations observed in this patient group.

Sections du résumé

BACKGROUND
The relationship between plasma arginine metabolites influencing vascular homeostasis and peripheral vasodilatory capacity in rheumatoid arthritis (RA) patients is not known.
METHODS
l-arginine (Arg), monomethyl-l-arginine (MMA), l-homoarginine (hArg), asymmetric dimethyl-l-arginine (ADMA), symmetric dimethyl-l-arginine, and l-citrulline (Cit) were measured by liquid chromatography tandem mass spectrometry (LC-MS/MS) in 164 RA patients and 100 age- and sex-matched healthy controls without previous cardiovascular events. Log-transformed reactive hyperemia index (Ln-RHI) evaluated by flow-mediated pulse amplitude tonometry (PAT, EndoPAT2000 device) was assessed as surrogate measure of peripheral vasodilatory capacity in RA patients. Ln-RHI values <0.51 indicated peripheral endothelial dysfunction (ED). The relationship between plasma arginine metabolite concentrations, RA descriptors and peripheral vasodilatory capacity was evaluated by bivariate correlation and regression analyses.
RESULTS
Plasma ADMA concentrations were significantly higher, and plasma hArg concentrations significantly lower, in RA patients than in controls (0.53 ± 0.09 vs 0.465 ± 0.07 μmol/L and 1.50 ± 0.60 vs 1.924 ± 0.78 μmol/L, respectively; p < 0.001 for both comparisons). Bivariate correlation analysis demonstrated no significant correlation between arginine metabolites and disease descriptors. In regression analysis in RA patients, higher plasma ADMA concentrations were independently associated with presence of ED [OR(95% CI) = 77.3(1.478-4050.005), p = 0.031] and lower Ln-RHI [B coefficient(95% CI) = -0.57(-1.09 to -0.05), p = 0.032].
CONCLUSIONS
ADMA was significantly, albeit weakly, associated with impaired microcirculatory vasodilatory capacity and peripheral endothelial dysfunction in RA. This suggests an important pathophysiological role of this metabolite in the vascular alterations observed in this patient group.

Identifiants

pubmed: 32622695
pii: S0026-2862(20)30098-4
doi: 10.1016/j.mvr.2020.104038
pii:
doi:

Substances chimiques

Biomarkers 0
Homoarginine 156-86-5
Citrulline 29VT07BGDA
symmetric dimethylarginine 49787G1ULV
N,N-dimethylarginine 63CV1GEK3Y
Arginine 94ZLA3W45F

Banques de données

ClinicalTrials.gov
['NCT02341066']

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

104038

Informations de copyright

Copyright © 2020. Published by Elsevier Inc.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Gian Luca Erre (GL)

Department of Clinical and Experimental Research, University of Sassari, Sassari, Italy; UOC di Reumatologia, Dipartimento di Specialità Mediche, Azienda Ospedaliero-Universitaria di Sassari, Sassari, Italy. Electronic address: gianluca.erre@aousassari.it.

Arduino Aleksander Mangoni (AA)

Discipline of Clinical Pharmacology, College of Medicine and Public Health, Flinders University and Flinders Medical Centre, Adelaide, Australia.

Giuseppe Passiu (G)

Department of Clinical and Experimental Research, University of Sassari, Sassari, Italy; UOC di Reumatologia, Dipartimento di Specialità Mediche, Azienda Ospedaliero-Universitaria di Sassari, Sassari, Italy.

Stefania Bassu (S)

UOC di Reumatologia, Dipartimento di Specialità Mediche, Azienda Ospedaliero-Universitaria di Sassari, Sassari, Italy.

Floriana Castagna (F)

UOC di Reumatologia, Dipartimento di Specialità Mediche, Azienda Ospedaliero-Universitaria di Sassari, Sassari, Italy.

Ciriaco Carru (C)

Departiment of Biomedical Sciences, University of Sassari, Sassari, Italy.

Matteo Piga (M)

UOC di Reumatologia, Policlinico Universitario e Università degli Studi di Cagliari, Italy.

Angelo Zinellu (A)

Departiment of Biomedical Sciences, University of Sassari, Sassari, Italy.

Salvatore Sotgia (S)

Departiment of Biomedical Sciences, University of Sassari, Sassari, Italy.

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Classifications MeSH