The measurement of serum creatine kinase (CK), which is used widely in the diagnosis and management of polymyositis and dermatomyositis lacks both sensitivity1-7 and specificity,7-9 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.6 ,10 ,11This often results in an increase in the CKMB/total CK ratio by more than the 3% threshold commonly used to imply myocardial damage.6 ,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 athletes13 ,14 and to be increased in a small series of patients with polymyositis13 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 injury15 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 …