Does hyperuricemia correlate with intervertebral disc degeneration?

Gout Intervertebral disc (IVD) Intervertebral disc degeneration (IDD) Uric acid

Journal

Medical hypotheses
ISSN: 1532-2777
Titre abrégé: Med Hypotheses
Pays: United States
ID NLM: 7505668

Informations de publication

Date de publication:
11 Mar 2020
Historique:
received: 26 02 2020
accepted: 10 03 2020
pubmed: 18 3 2020
medline: 18 3 2020
entrez: 18 3 2020
Statut: aheadofprint

Résumé

Gout is a form of crystal arthropathy associated with deposition of monosodium urate (MSU) crystals, and is directly related to hyperuricemia arising from abnormal purine metabolism and/or decreased uric acid excretion. Uric acid is the final oxidation product of purine metabolism and plays an important role as an in vivo antioxidant at physiological concentrations. Several case reports have described the presence of tophi in the intervertebral disc (IVD) or endplate of patients with hyperuricemia or gout, and these patients also exhibited severe intervertebral disc degeneration (IDD). We speculated that uric acid may have dual effects on an IVD. On the one hand, physiological concentrations of uric acid have powerful antioxidant activity and can effectively maintain the steady state of the IVD, while on the other hand, high concentrations of uric acid have strong oxidizing activity and the resulting high osmotic pressure can aggravate IDD. Moreover, when MSU crystals accumulate in the endplate and IVD, they lead to a series of mechanical damages and inflammatory reactions that further accelerate IDD. Further basic and clinical studies are needed to clarify the mechanism for the involvement of uric acid in the onset and development of IDD.

Identifiants

pubmed: 32182555
pii: S0306-9877(20)30303-0
doi: 10.1016/j.mehy.2020.109673
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

109673

Informations de copyright

Copyright © 2020 Elsevier Ltd. All rights reserved.

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

Yvang Chang (Y)

Department of Orthopaedics, First Affiliated Hospital of Dalian Medical University, Dalian, People's Republic of China; Key Laboratory of Molecular Mechanism for Repair and Remodeling of Orthopaedic Diseases, Liaoning Province, People's Republic of China.

Ming Yang (M)

Department of Orthopaedics, First Affiliated Hospital of Dalian Medical University, Dalian, People's Republic of China; Key Laboratory of Molecular Mechanism for Repair and Remodeling of Orthopaedic Diseases, Liaoning Province, People's Republic of China.

Yu Zhang (Y)

Department of Orthopaedics, First Affiliated Hospital of Dalian Medical University, Dalian, People's Republic of China; Key Laboratory of Molecular Mechanism for Repair and Remodeling of Orthopaedic Diseases, Liaoning Province, People's Republic of China.

Gang Xu (G)

Department of Orthopaedics, First Affiliated Hospital of Dalian Medical University, Dalian, People's Republic of China; Key Laboratory of Molecular Mechanism for Repair and Remodeling of Orthopaedic Diseases, Liaoning Province, People's Republic of China.

Zhonghai Li (Z)

Department of Orthopaedics, First Affiliated Hospital of Dalian Medical University, Dalian, People's Republic of China; Key Laboratory of Molecular Mechanism for Repair and Remodeling of Orthopaedic Diseases, Liaoning Province, People's Republic of China. Electronic address: lizhonghai@dmu.edu.cn.

Classifications MeSH