AB0736 Myositis specific autoantibodies (msa) and myositis associated autoantibodies (maa). experience in a spanish cohort.
Authors: M. J. Martinez Becerra, F. Romero, O. Sánchez, C. Palacios, P. Tramón, M. J. Rodríguez, C. Serrano
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> 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. <h3>Objectives</h3> 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. <h3>Methods</h3> 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. <h3>Results</h3> 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&lt;240. Comparison between antiRo (&lt;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). <h3>Conclusions</h3> 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. <h3>References</h3> Betteridge et al. Arthritis Research &amp; Therapy 2011 (13):209. McHugh et al. Rheumatology 2009;48:607–612 <h3>Disclosure of Interest</h3> None Declared