THU0331 SKELETAL TROPONIN I A POSSIBLE NOVEL BIOMARKER FOR MANAGEMENT OF PATIENTS WITH IDIOPATHIC INFLAMMATORY MYOPATHIES
Authors: Katriina Bamberg, Laura Mehtälä, Olli Arola, Seppo Laitinen, Pauliina Nordling, Marjatta Strandberg, Niko Strandberg, Johanna Paltta, Markku Mali, Fabricio Espinosa-Ortega, Laura Pirilä, Ingrid E. Lundberg, Tanja Savukoski, Kim Pettersson
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Background</h3> The current biomarkers for the diagnosis and monitoring of diseased and injured skeletal muscles, such as creatine kinase (CK), have limited tissue specificity and incapability to differentiate between pathological and physiological changes. Thus, new biomarkers with improved diagnostic certainty are needed. Skeletal troponin I (skTnI) is a promising new biomarker for injured and diseased skeletal muscle tissue. Although studies have reported that circulating skTnI levels are elevated in response to trauma, exercise and various muscular diseases (1), its clinical utility to serve as a diagnostic indicator has largely been unexplored. <h3>Objectives</h3> Our aim was to develop and validate a novel assay for skTnI, and to assess its clinical performance with idiopathic inflammatory myopathy (IIM) patients. <h3>Methods</h3> A two-step fluoroimmunoassay was used to analyze the levels of skTnI in samples from healthy reference individuals (n=125), trauma patients (n=151), and patients with IIM (n=94). Later, skTnI and CK levels in patients with IIM were compared according to their disease activity status (active, pre-active or stable). <h3>Results</h3> The limit of detection was 1.2 ng/ml, and the upper reference limit (90th percentile) was 5.4 ng/ml. The median skTnI concentrations were &lt;LoD, 2.7 ng/ml, and 9.8 ng/ml in reference, trauma, and IIM cohorts, respectively. Differences in measured skTnI levels were statistically significant between all three study cohorts (Mann-Whitney p&lt;0.001 for all). skTnI and CK had a strong positive correlation (Spearman's r=0.848, p&lt;0.001). With skTnI, patients in both pre-active and active IIM were differentiated from stable phase patients (33.9 and 34.5 ng/ml vs 5.1 ng/ml, p&lt;0.001 for both). This was not possible with CK as significantly elevated CK levels were mainly present in active IIM (median 16.5 µkat/L) and the medians of pre-active and stable phase patients (4.8 µkat/L vs 1.7 µkat/L, p=0.060) remained close to normal reference ranges. The area under the receiver operator characteristic curve was 0.87, 0.84, and 0.87 for skTnI and CK individually and combined, respectively. <h3>Conclusion</h3> With the developed skTnI assay, IIM patients were identified from healthy individuals and from patients with traumatic muscular injuries. Also, skTnI was shown to outperform CK in detecting IIM patients in different disease activity statuses. <h3>Reference</h3> [1] Kiely PDW, Bruckner FE. Serum skeletal troponin I in inflammatory muscle disease: Relation to creatine kinase, CKMB and cardiac troponin I. Ann Rheum Dis 2000;59:750–1. <h3>Disclosure of Interests</h3> Katriina Bamberg: None declared, Laura Mehtälä: None declared, Olli Arola: None declared, Seppo Laitinen: None declared, Pauliina Nordling: None declared, Marjatta Strandberg: None declared, Niko Strandberg: None declared, Johanna Paltta: None declared, Markku Mali: None declared, Fabricio Espinosa-Ortega: None declared, Laura Pirilä Consultant for: Abbvie, Novartis, Eli Lilly, MSD Finland, Pfizer, UCB, Roche, Jansen- Cilag, Sandoz, Speakers bureau: Pfizer, Ingrid E. Lundberg Grant/research support from: Dr. Lundberg has received honoraria from Bristol Myers Squibb and MedImmune and is currently receiving a research grant from Bristol Myers Squibb and from Astra Zeneca., Consultant for: She is a scientific advisor for Bristol Myers Squibb, and aTyr, Tanja Savukoski: None declared, Kim Pettersson: None declared