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AB0736 Myositis specific autoantibodies (msa) and myositis associated autoantibodies (maa). experience in a spanish cohort.
  1. M. J. Martinez Becerra on behalf of Multidisciplinary Group for Systemic Autoimmune Diseases1,
  2. F. Romero2,
  3. O. Sánchez2,
  4. C. Palacios1,
  5. P. Tramón1,
  6. M. J. Rodríguez1,
  7. C. Serrano1
  1. 1Immunology
  2. 2Rheumatology, Fundación Jiménez Díaz-CAPIO, Madrid, Spain


Background It has been suggested that MSA have a role in distinguishing subsets of IIM. Clinico-serological classifications have been proposed highlighting the importance of identifying the antibody profile.

Objectives Describe the prevalence of MSA and MAA. Study association of MSA with MAA, their levels and effects on muscle enzymes and serological markers of disease activity.

Methods We retrospectively evaluated sera postive for any MSA (Anti-PL7, PL12, SRP, Mi2, Jo1) or MAA (PmScl, Ku) from Jan. 2008-Jan. 2013. AntiRo (52/60 kDa), Creatin Kinase (CK), Aldolase, C Reactive Protein (CRP), Indirect ImmunoFluorescence (IIF) pattern and Eritrocyte Sedimentation Rate (ESR) were recorded. Statistical analysis was made by Wilcoxon test, Spearman correlation and Mc-Nemar test.

Results 81 out of 58,878 samples tested positive for a MSA or MAA corresponding to 33 patients. 84%Female. Female:Male ratio 5. Mean Age 51 years. Median 2 sample/patient. The specificities identified were: Jo1 (55%), PmScl (18%), PL7 (9%), PL12 (6%), Mi2 (6%), SRP (3%) and Ku (3%). 54.7% of sera with MSA of cytoplasmic localization (Jo1, SRP, PL7, PL12) exhibited no cytoplasm staining. Median CK: 126 UI/l, Aldolase: 5 U/l, ESR: 23 mm/h, CRP: 1 mg/dl. Results of the 81 sera were: Jo1 97 U/ml (CK 527 UI/l, Aldolase 11 U/l, ESR 33 mm/h, CRP 2 mg/dl); PmScl 34 U/ml (CK: 125, Aldolase: 7, ESR: 12, CRP: 1); PL7 (CK: 197, Aldolase: 34, ESR 28, CRP 2); PL12 (CK: 796, Aldolase: 16, ESR 62, CRP 3); Mi2 (CK: 733, Aldolase: 13, ESR 18, CRP 1); SRP (CK: 6510, Aldolase: 117, ESR 34, CRP 5) and Ku (CK: 69, Aldolase: 4, ESR 41, CRP 0). Jo1 positive sera showed reduced CK (ρ 0.0018) and Aldolase (ρ 0.0032) levels compared to the other positive MAA/MSA globally. The prevalence of antiRo was: Jo1 82%; PmScl 0%; PL7 33%; PL12 100%; Mi2 0%; SRP 100%; Ku 100%. Isolated Ro52 (28%) was the most prevalent, comparable to double positive Ro52/60 (27%) and higher than isolated Ro60 (7%) (ρ 0.0030). The coexistence of any subtype of Ro didn’t imply differences in CK, Aldolase, ESR or CRP levels (ρ≥0.0568). However sera with antiRo levels ≥240 showed higher ESR (ρ 0.0255) and CRP (ρ 0.0286) levels than Ro<240. Comparison between antiRo (<240) and antiJo1 levels showed no correlation (r -0.0648), nor did they correlate with CK, Aldolase, ESR or CRP levels (r range: -0.2696-0.3576).

Conclusions MSA have low prevalence and are mutually exclusive. Most prevalent MSAand MAAwere Jo1 and PmScl respectively. Though N wasn’t sufficient to establish comparisons, MAA show a trend to reduced CK and Aldolase. SRP showed the highest CK and Aldolase levels. We identify a high prevalence of Ro within all MSA. Nevertheless the proportion of double positive Ro52/60 is comparable to the well-known high prevalence of Ro52. Monitoring antiRo levels might be useful, with levels ≥240 representing a potential marker for clinical activity. Our data suggest reduced muscular involvement on Jo1 patients. These hypotheses must be confirmed through clinical data assessment. The absence of typical staining in a high proportion of our patients highlights the importance of a tight collaboration between Clinicians and Laboratory.


  • Betteridge et al. Arthritis Research & Therapy 2011 (13):209. McHugh et al. Rheumatology 2009;48:607–612

Disclosure of Interest None Declared

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