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. 2025 Sep 10;161(11):1184–1186. doi: 10.1001/jamadermatol.2025.3143

Autoantibody Positivity Rates in Classic and Clinically Amyopathic Dermatomyositis

Xiwei Yang 1,2, Shae Chambers 1,2, Aretha On 1,2, Hammad Ali 1,2, Touraj Khosravi-Hafshejani 1,2, Lais Lopes Almeida Gomes 1,2, Rui Feng 3, Victoria P Werth 1,2,
PMCID: PMC12423947  PMID: 40928802

Abstract

This cross-sectional study compares the positivity rates of all commonly tested myositis-specific autoantibodies, myositis-associated autoantibodies, and antinuclear antibody in classic dermatomyositis vs clinically amyopathic dermatomyositis.


Dermatomyositis (DM) is an idiopathic inflammatory myopathy (IIM) subclassified as classic DM (CDM) and clinically amyopathic DM (CADM) based on the presence or absence of clinically evident muscle disease. It can involve myositis-associated autoantibodies (MAA) and myositis-specific autoantibodies (MSA). The associations between MSA and specific DM phenotypes have been well studied but might not be fully captured by commercial autoantibody panels in clinical settings.1,2 To better understand the utility of autoantibody status in DM phenotyping, we compared the positivity rates of all commonly tested MSA, MAA, and antinuclear antibodies (ANA) in CDM vs CADM.

Methods

This cross-sectional study assessing the association between DM subtype and autoantibody positivity rate included adult patients with CDM and CADM seen at the University of Pennsylvania rheumatology-dermatology clinic who had myositis autoantibody testing between 2016 and 2024. This study followed the STROBE reporting guideline and was approved by the University of Pennsylvania Institutional Review Board. Participants provided written informed consent. We evaluated the presence of MAA, MSA, and ANA. An antibody was considered present if ever positive. Details on study dates, software used for analysis, and statistical assessment and significance are available in eMethods of Supplement 1.

Results

We identified 320 patients with DM (mean [SD] age of 53 [14] years; 276 female [86%], 44 male [14%]). Sixteen types of panels from 5 laboratories were recorded (Table 1).

Table 1. Testing Laboratories, Tested Antibodies, and Detection Assays of Myositis Autoantibody Panels Performed in the Study Cohort.

Laboratory/panel name No. (%) performed (n = 373) Tested antibodies Tested antibodies (for No. of tested antibodies <10) Untested antibodies (for No. of tested antibodies ≥10) Assay
Type No.
ARUP 191 (51) Immunoblot, IP, multiplex bead assaya
Myositis extended panel 170 (46) MSA, MAA 16 NA Anti-U2-RNP
Myositis antibody comprehensive 11 (3) MSA, MAA 14 NA Antibodies to TIF-1γ, MDA-5, NXP-2, SAE
Myositis-specific antibody 5 (1) MSA 11 NA Antibodies to SSA, Pm-Scl, Ku, U1-RNP, U2-RNP, U3-RNP
Polymyositis and dermatomyositis panel 5 (1) MSA 11 NA Antibodies to SSA, Pm-Scl, Ku, U1-RNP, U2-RNP, U3-RNP
Labcorp 97 (26) ELISA, RIPA gel radiographyb
Myomarker 3 plus profile 67 (18) MSA, MAA 17 NA NA
Myositis panel III 13 (3) MSA, MAA 11 NA Antibodies to TIF-1γ, MDA5, NXP-2, SAE, U2-RNP, U3-RNP
Myositis panel VI 7 (2) MSA, MAA 17 NA NA
Myositis panel I 4 (1) MSA, MAA 7 Antibodies to Mi-2, SRP, PL-7, PL-12, EJ, OJ, Ku NA
Myositis panel II 3 (1) MSA, MAA 7 Antibodies to Mi-2, SRP, PL-7, PL-12, EJ, OJ, Ku NA
Myositis panel IV 3 (1) MSA, MAA 8 Antibodies to Mi-2, SRP, PL-7, PL-12, EJ, OJ, Ku, U1-RNP NA
Quest 68 (18) Chemiluminescence, ELISA, line blot
Myositis-specific 11 antibody panel 29 (8) MSA 10 NA Antibodies to SAE, SSA, Pm-Scl, Ku, U1-RNP, U2-RNP, U3-RNP
Myositis panel comprehensive 25 (7) MSA 6 Antibodies to PL-7, PL-12, Mi-2, Jo-1, EJ, OJ NA
Extended myositis-specific antibody panel 9 (2) MSA 12 NA (includes anti-HMGCR, anti-cN-1A) Antibodies to SAE, SSA, Pm-Scl, Ku, U1-RNP, U2-RNP, U3-RNP
Myositis AssessR plus JO-1 5 (1) MSA, MAA 8 Antibodies to Mi-2, SRP, PL-7, PL-12, EJ, OJ, Jo-1, Ku NA
OMRF
Myositis panel 12 (3) MSA, MAA 12 NA Antibodies to TIF-1γ, MDA-5, NXP-2, SAE, U3-RNP IP, ID, IF
Mayo
Myomarker panel 3 5 (1) MSA, MAA 10 NA Antibodies to TIF-1γ, MDA-5, NXP-2, Jo-1, SAE, Pm-Scl, SSA ELISA, RIPA gel radiography

Abbreviations: ARUP, Associated Regional and University Pathologists Inc; ELISA, enzyme-linked immunosorbent assay; ID, immunodiffusion; IF, immunofluorescence; IP, immunoprecipitation; MAA, myositis-associated autoantibodies; MDA-5, melanoma differentiation-associated protein 5; MSA, myositis-specific autoantibodies; NA, not applicable; NXP-2, nuclear matrix protein 2; OMRF, Oklahoma Medical Research Foundation; RIPA, radioimmunoprecipitation assay; SAE, small ubiquitin-like modifier activating enzyme; SRP, signal recognition particle; TIF-1γ, transcription intermediary factor 1 γ.

a

ARUP uses qualitative immunoblot for anti-MDA-5, anti-NXP-2, anti-SAE, anti-TIF-1γ, anti-PM/Scl-100, anti-RNPs; qualitative IP for anti-Mi-2, anti-TIF-1γ, anti-EJ, anti-OJ, anti-PL-7, anti-PL1-2, anti-SRP; and semiquantitative multiplex bead assay for anti-Jo-1, anti-SSA.

b

Labcorp uses ELISA for anti-MDA-5, anti-NXP-2, anti-SAE, anti-TIF-1γ, anti-PM/Scl-100, anti-Ku, anti-SSA, anti-U1-RNP, anti-Jo-1, anti-EJ, anti-OJ, anti-PL-7, anti-PL-12; and RIPA gel radiography for anti-Mi-2, anti-Jo-1, anti-EJ, anti-OJ, anti-PL-7, anti-PL-12, anti-SRP, anti-U2-RNP, anti-U3-RNP.

This cohort consisted of 198 (62%) patients with CDM and 122 (38%) patients with CADM, with a mean (SD) of 1.2 (0.5) panels performed per patient. MSA were positive in 47% of patients with CDM and 40% of patients with CADM (P = .20); MAA were positive in 29% of patients with CDM and 26% of patients with CADM (P = .65) (Table 2). Similar results were found in patients tested by the most comprehensive panels that assessed 17 autoantibodies (MSA: CDM 14/35 [40%], CADM 8/25 [32%]; P = .53; MAA: CDM 8/35 [23%], CADM 5/25 [20%]; P = .80). Within each laboratory, no statistically significant difference in MSA and MAA positivity rates was found between panels performed in patients with CDM and patients with CADM. In both subtypes, anti-TIF-1γ was the most common MSA and anti-SSA the most common MAA. ANA were positive in 63% of patients with CDM vs 49% of patients with CADM (P = .045). Among those with both negative MSA and MAA results, ANA were positive in 49% of patients with CDM and 36% of patients with CADM (P = .20).

Table 2. Positivity Rates of MSA, MAA, and ANA by DM Subtype.

Positivity status DM subtype, No./total No. (%) P value
Classic (n = 198) Clinically amyopathic (n = 122)
Any MSA positive 94/198 (47) 49/122 (40) .20
Any MAA positive 48/168 (29) 26/100 (26) .65
Any ANA positive 90/143 (63) 42/85 (49) .045
Either MSA or MAA positive 118/198 (60) 63/122 (52) .16
Both MSA and MAA negative 80/198 (40) 59/122 (48) .16
Both MSA and MAA negative but ANA positive 26/53 (49) 13/36 (36) .23
MSA
Anti-TIF-1γ 29/169 (17) 21/97 (22) .37
Anti-MDA-5 13/166 (8) 10/97 (10) .49
Anti-NXP-2 16/162 (10) 5/94 (5) .20
Anti-SAE 10/137 (7) 7/79 (9) .68
Anti-Mi-2 12/197 (6) 6/119 (5) .70
Anti-PL-7 10/197 (5) 2/119 (2) .22
Anti-Jo-1 9/192 (5) 1/118 (1) .10
Anti-SRP 3/187 (2) 3/109 (3) .67
Anti-PL-12 2/197 (1) 1/119 (1) >.99
Anti-OJ 1/197 (1) 1/119 (1) >.99
Anti-EJ 0 0 >.99
MAA
Anti-SSA 33/159 (21) 18/94 (19) .76
Anti-SSA-52 26/159 (16) 15/94 (16) .93
Anti-SSA-60 11/159 (7) 6/94 (6) .89
Anti-SSA-52 positive with CT-proven ILDa 11/26 (42) 5/15 (33) .57
Anti-Pm-Scl 13/160 (8) 5/94 (5) .40
Anti-U1-RNP 12/160 (8) 3/93 (3) .27
Anti-Ku 1/166 (1) 3/100 (3) >.99
Anti-U2-RNP 0 1/57 (2) .39
Anti-U3-RNP 2/139 (1) 1/84 (1) >.99
ANA
Anti-RNP 5/42 (12) 1/20 (5) .65
Anti-Smith 0 0 >.99

Abbreviations: ANA, anti-nuclear autoantibodies; DM, dermatomyositis; ILD, interstitial lung disease; MAA, myositis-associated autoantibodies; MDA-5, melanoma differentiation-associated protein 5; MSA, myositis-specific autoantibodies; NXP-2, nuclear matrix protein 2; SAE, small ubiquitin-like modifier activating enzyme; SRP, signal recognition particle; TIF-1γ, transcription intermediary factor 1 γ.

a

Consistent with the known association between anti-SSA-52 and higher frequency of interstitial lung disease (ILD), 39% anti-SSA-52-positive patients vs 19% anti-SSA-52-negative patients developed CT-proven ILD; P = .005.

Discussion

We observed no significant difference in MSA and MAA prevalence between CDM and CADM on commercial autoantibody testing. MSA were previously reported in over 50% patients with IIM,3 slightly higher than the prevalence in this DM-only cohort. MAA prevalence reached 35% to 40% in other cohorts compared with 26% to 29% in ours.4 Besides population characteristics, such discrepancies might be due to the inconsistency of detection methods and tested autoantibodies.

In this cohort study, ANA were significantly more common in patients with CDM, which suggests a potential association between ANA positivity and DM muscle involvement that merits further investigation. More than one-third of patients with negative results for MSA and MAA had positive results for ANA, suggesting the presence of undiscovered DM-related autoantibodies.

Although DM autoantibody profile may be a helpful tool in prognosis when positive, its utility is limited by the variability in detection methods and tested antibodies. Hence, we need to refine and standardize myositis-related autoantibody testing in DM, which remains a clinical diagnosis.

Supplement 1.

eMethods. Study Dates, Software Used for Analysis, and Statistical Assessment and Significance

Supplement 2.

Data Sharing Statement

References

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Associated Data

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Supplementary Materials

Supplement 1.

eMethods. Study Dates, Software Used for Analysis, and Statistical Assessment and Significance

Supplement 2.

Data Sharing Statement


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