LETTERS TO THE EDITOR Serum skeletal troponin I in inflammatory muscle disease: relation to creatine kinase, CKMB and cardiac troponin I

The measurement of serum creatine kinase (CK), which is used widely in the diagnosis and management of polymyositis and dermatomyositis lacks both sensitivity and specificity, leading to potential problems if the serum total CK concentration is interpreted as a direct measure of muscle disease activity. Furthermore, in those cases where the total CK is raised reliance on an analysis of the CK isoforms is an unreliable means of determining the presence of myocardial involvement. This is because in chronic inflammatory muscle diseases, regenerating striated muscle contains up to 50% of the CKMB isoform. 10 11 This often results in an increase in the CKMB/total CK ratio by more than the 3% threshold commonly used to imply myocardial damage. 8 9 11 12 The need for more sensitive and specific serum markers of striated and myocardial inflammation has led us to a study of the troponins. Skeletal troponin I (sTnI) has been found to correlate with total CK in exercising athletes 14 and to be increased in a small series of patients with polymyositis but has not previously been studied in detail in relation to total CK in inflammatory muscle disease. Cardiac troponin I (cTnI) is a highly specific marker of myocardial injury in contrast with CKMB, which is expressed both in myocardial and striated muscle. The behaviour of cTnI has not been reported in the inflammatory muscle diseases. We report the relation between serum sTnI and total CK in patients with polymyositis and dermatomyositis. In the assessment of myocardial disease the use of serum cTnI has been compared with serum CKMB and the CKMB/total CK ratio. Serum samples were collected from 43 healthy control subjects (23 female) and 16 patients with polymyositis or dermatomyositis. Patients with inflammatory muscle disease were recruited from the Muscle Clinic at St George’s Hospital between 1994 and 1997. Table 1 gives details of the patients. Diagnoses were established according to the criteria of Bohan and Peter from clinical features of proximal muscle weakness with or without rash, serum total CK, EMG, muscle histology and in addition muscle magnetic resonance imaging. Evidence of myocardial involvement was assessed from clinical examination, ECG and echocardiography. Patients were treated with standard immunosuppressants including prednisolone, azathioprine, cyclosporin A and IV immunoglobulin according to clinical and biochemical assessment of disease activity, including serial muscle strength of deltoid and hip abductors using a hand held myometer and serum total CK. In the myositis group between one and six samples were collected per patient Table 1 Demographic details and CK, CKMB, skeletal and cardiac Troponin I values in patients with polymyositis and dermatoyositis