Cumulative disease damage and anti-PM/Scl antibodies are associated with a heavy burden of calcinosis in systemic sclerosis.


Journal

Rheumatology (Oxford, England)
ISSN: 1462-0332
Titre abrégé: Rheumatology (Oxford)
Pays: England
ID NLM: 100883501

Informations de publication

Date de publication:
02 11 2023
Historique:
received: 20 05 2022
accepted: 27 11 2022
medline: 9 11 2023
pubmed: 6 12 2022
entrez: 5 12 2022
Statut: ppublish

Résumé

Ectopic calcification (calcinosis) is a common complication of SSc, but a subset of SSc patients has a heavy burden of calcinosis. We examined whether there are unique risk factors for a heavy burden of calcinosis, as compared with a light burden or no calcinosis. We reviewed the medical records of all patients in the Johns Hopkins Scleroderma Center Research Registry with calcinosis to quantify calcinosis burden using pre-specified definitions. We performed latent class analysis to identify SSc phenotypic classes. We used multinomial logistic regression to determine whether latent phenotypic classes and autoantibodies were independent risk factors for calcinosis burden. Of all patients, 29.4% (997/3388) had calcinosis, and 13.5% (130/963) of those with calcinosis had a heavy burden. The latent phenotypic class with predominantly diffuse skin disease and higher disease severity (characterized by pulmonary hypertension, interstitial lung disease, cardiomyopathy, severe RP, gastrointestinal involvement, renal crisis, myopathy and/or tendon friction rubs) was associated with an increased risk of both a heavy burden [odds ratio (OR) 6.92, 95% CI 3.66, 13.08; P < 0.001] and a light burden (OR 2.88, 95% CI 2.11, 3.95; P < 0.001) of calcinosis compared with the phenotypic class with predominantly limited skin disease. Autoantibodies to PM/Scl were strongly associated with a heavy burden of calcinosis (OR 17.31, 95% CI 7.72, 38.81; P < 0.001) and to a lesser degree a light burden of calcinosis (OR 3.59, 95% CI 1.84, 7.00; P < 0.001). Calcinosis burden is associated with cumulative SSc-related tissue damage. Independent of disease severity, autoantibodies to PM/Scl are also associated with a heavy burden of calcinosis.

Identifiants

pubmed: 36469337
pii: 6873735
doi: 10.1093/rheumatology/keac682
pmc: PMC10629791
doi:

Substances chimiques

Autoantibodies 0

Types de publication

Review Journal Article Research Support, Non-U.S. Gov't Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

3636-3643

Subventions

Organisme : NIAMS NIH HHS
ID : P30 AR070254
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR073208
Pays : United States
Organisme : NIAMS NIH HHS
ID : T32 AR048522
Pays : United States
Organisme : NIAMS NIH HHS
ID : K24 AR080217
Pays : United States

Informations de copyright

© The Author(s) 2022. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For permissions, please email: journals.permissions@oup.com.

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Auteurs

Carrie Richardson (C)

Department of Medicine (Rheumatology), Northwestern University, Chicago, IL, USA.

Jamie Perin (J)

Department of International Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.

Scott Zeger (S)

Departments of Biostatistics, Epidemiology and International Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.

Fredrick M Wigley (FM)

Department of Medicine (Rheumatology), Johns Hopkins University School of Medicine, Baltimore, MD, USA.

Laura K Hummers (LK)

Department of Medicine (Rheumatology), Johns Hopkins University School of Medicine, Baltimore, MD, USA.

Livia Casciola-Rosen (L)

Department of Medicine (Rheumatology), Johns Hopkins University School of Medicine, Baltimore, MD, USA.

Antony Rosen (A)

Department of Medicine (Rheumatology), Johns Hopkins University School of Medicine, Baltimore, MD, USA.

Ami A Shah (AA)

Department of Medicine (Rheumatology), Johns Hopkins University School of Medicine, Baltimore, MD, USA.

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