More prominent muscle involvement in patients with dermatomyositis with anti-Mi2 autoantibodies.
Adult
Aged
Autoantibodies
/ immunology
Calcinosis
/ epidemiology
Case-Control Studies
Cohort Studies
Creatine Kinase
/ blood
Dermatomyositis
/ blood
Female
Fever
/ epidemiology
Humans
Longitudinal Studies
Lung Diseases, Interstitial
/ epidemiology
Male
Mi-2 Nucleosome Remodeling and Deacetylase Complex
/ immunology
Middle Aged
Muscle Weakness
/ epidemiology
Myositis
/ immunology
Necrosis
Phenotype
Prevalence
Severity of Illness Index
Journal
Neurology
ISSN: 1526-632X
Titre abrégé: Neurology
Pays: United States
ID NLM: 0401060
Informations de publication
Date de publication:
05 11 2019
05 11 2019
Historique:
received:
14
03
2019
accepted:
29
05
2019
pubmed:
9
10
2019
medline:
6
2
2020
entrez:
10
10
2019
Statut:
ppublish
Résumé
To define the clinical phenotype of dermatomyositis (DM) with anti-Mi2 autoantibodies. In this longitudinal cohort study, the prevalence and severity of clinical features at disease onset and during follow-up in patients with anti-Mi2-positive DM were compared to patients with anti-Mi2-negative DM, antisynthetase syndrome (AS), and immune-mediated necrotizing myopathy (IMNM). Longitudinal anti-Mi2 autoantibody titers were assessed. A total of 58 patients with anti-Mi2-positive DM, 143 patients with anti-Mi2-negative DM, 162 patients with AS, and 170 patients with IMNM were included. Among patients with anti-Mi2-positive DM, muscle weakness was present in 60% at disease onset and occurred in 98% during longitudinal follow-up; fewer patients with anti-Mi2-negative DM developed weakness (85%; Patients with anti-Mi2-positive DM have more severe muscle disease than patients with anti-Mi2-negative DM or patients with AS. Anti-Mi2 autoantibody levels correlate with disease severity and may normalize in patients who enter remission.
Identifiants
pubmed: 31594859
pii: WNL.0000000000008443
doi: 10.1212/WNL.0000000000008443
pmc: PMC6946486
doi:
Substances chimiques
Autoantibodies
0
CHD4 protein, human
0
Creatine Kinase
EC 2.7.3.2
Mi-2 Nucleosome Remodeling and Deacetylase Complex
EC 3.5.1.98
Types de publication
Journal Article
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e1768-e1777Informations de copyright
© 2019 American Academy of Neurology.
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