Anti-ribosomal P protein antibodies in patients with systemic lupus erythematosus is associated with hyperferritinemia.


Journal

International journal of rheumatic diseases
ISSN: 1756-185X
Titre abrégé: Int J Rheum Dis
Pays: England
ID NLM: 101474930

Informations de publication

Date de publication:
Jan 2022
Historique:
revised: 28 09 2021
received: 27 07 2021
accepted: 07 11 2021
pubmed: 20 11 2021
medline: 16 3 2022
entrez: 19 11 2021
Statut: ppublish

Résumé

Anti-ribosomal P protein antibodies (anti-ribo P) have been reported as one of the specific autoantibodies in patients with systemic lupus erythematosus (SLE) and has been demonstrated to bind and activate macrophages in vitro. Clinically, hyperferritinemia has been known to be a biomarker for macrophage activation. The aim of this study is to clarify the relationship of anti-ribo P and clinical characteristics and biomarkers including serum ferritin in patients with SLE. Clinical parameters and laboratory data were measured in patients with active SLE (N = 127) in our university hospital. The risk factors affected by anti-ribo P were retrospectively calculated by logistic regression analysis, and the correlation of anti-ribo P and clinical factors was demonstrated. Anti-ribo P was significantly elevated in active SLE compared to non-SLE diseases (P < .0001). Sensitivity and the specificity of anti-ribo P in patients with SLE were 32.0% and 99.3%, respectively. Patients positive for anti-ribo P had the highest risk for elevated serum ferritin (odds ratio: 8.432). Accordingly, anti-ribo P positive patients had significantly elevated serum ferritin compared to negative patients (P = .024). A significant positive correlation was observed between the anti-ribo P titer and the serum ferritin level (r The presence of anti-ribo P is a risk factor for higher ferritin levels that is independent of systemic inflammation regulated by IL-6. We speculate that anti-ribo P could be directly associated with macrophage activation leading to hyperferritinemia in patients with SLE.

Identifiants

pubmed: 34796669
doi: 10.1111/1756-185X.14245
doi:

Substances chimiques

Anti-ribosomal P protein autoantibodies 0
Antibodies, Antinuclear 0
Biomarkers 0
Ferritins 9007-73-2

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

70-75

Informations de copyright

© 2021 Asia Pacific League of Associations for Rheumatology and John Wiley & Sons Australia, Ltd.

Références

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Auteurs

Yoshiyuki Arinuma (Y)

Department of Rheumatology and Infectious Diseases, Kitasato University School of Medicine, Kanagawa, Japan.

Shunsei Hirohata (S)

Department of Rheumatology and Infectious Diseases, Kitasato University School of Medicine, Kanagawa, Japan.
Department of Rheumatology, Nobuhara Hospital, Hyogo, Japan.

Takuya Isayama (T)

Medical and Biological Laboratories CO., LTD., Tokyo, Japan.

Yasuhiro Hasegawa (Y)

Department of Rheumatology and Infectious Diseases, Kitasato University School of Medicine, Kanagawa, Japan.

Takumi Muramatsu (T)

Department of Rheumatology and Infectious Diseases, Kitasato University School of Medicine, Kanagawa, Japan.

Junichi Kondo (J)

Department of Rheumatology and Infectious Diseases, Kitasato University School of Medicine, Kanagawa, Japan.

Yoshiro Kanayama (Y)

Department of Rheumatology and Infectious Diseases, Kitasato University School of Medicine, Kanagawa, Japan.

Kazuma Ino (K)

Department of Rheumatology and Infectious Diseases, Kitasato University School of Medicine, Kanagawa, Japan.

Yu Matsueda (Y)

Department of Rheumatology and Infectious Diseases, Kitasato University School of Medicine, Kanagawa, Japan.

Kenji Oku (K)

Department of Rheumatology and Infectious Diseases, Kitasato University School of Medicine, Kanagawa, Japan.

Kunihiro Yamaoka (K)

Department of Rheumatology and Infectious Diseases, Kitasato University School of Medicine, Kanagawa, Japan.

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