INTRODUCTION: Some reports in the literature suggest that cardiac troponin-I (cTnI) is falsely elevated in patients with seropositive rheumatoid arthritis (RA) because of the presence of rheumatoid factor (RF). But, there are no reports in the literature on cTnI concentrations in other autoimmune diseases. We therefore decided to measure the serum concentrations of cTnI in patients with seropositive and seronegative RA, systemic lupus erythematosus (SLE), primary Sjogren's syndrome (pSS) and Graves' disease (GD), in order to find out if this cardiac marker is falsely elevated or not. METHODS: Serum samples were drawn from 50 patients with seropositive RA, 50 patients with seronegative RA, 50 patients with SLE, 20 patients with pSS and 15 patients with GD. We measured cTnI levels using the Beckman Access Immunoassay System in these serum samples. RESULTS: Of the 50 patients with seropositive RA, five had cTnI levels higher than 0.1 ng per ml (the diagnostic value for myocardial infarction in our hospital laboratory), while none of the patients with seronegative RA, SLE, pSS, or GD had levels above this value. Furthermore, univariate regression analysis showed a positive association (r equals 0.35, p-value equals 0.02) between cTnI and RF in patients with seropositive RA. CONCLUSION: Using the Beckman Access Immunoassay System for cTnI quantification, it was found that some patients with seropositive RA had falsely-elevated cTnI, while none of the patients with seronegative RA, SLE, pSS, or GD had falsely-elevated cTnl.
INTRODUCTION: Some reports in the literature suggest that cardiac troponin-I (cTnI) is falsely elevated in patients with seropositive rheumatoid arthritis (RA) because of the presence of rheumatoid factor (RF). But, there are no reports in the literature on cTnI concentrations in other autoimmune diseases. We therefore decided to measure the serum concentrations of cTnI in patients with seropositive and seronegative RA, systemic lupus erythematosus (SLE), primary Sjogren's syndrome (pSS) and Graves' disease (GD), in order to find out if this cardiac marker is falsely elevated or not. METHODS: Serum samples were drawn from 50 patients with seropositive RA, 50 patients with seronegative RA, 50 patients with SLE, 20 patients with pSS and 15 patients with GD. We measured cTnI levels using the Beckman Access Immunoassay System in these serum samples. RESULTS: Of the 50 patients with seropositive RA, five had cTnI levels higher than 0.1 ng per ml (the diagnostic value for myocardial infarction in our hospital laboratory), while none of the patients with seronegative RA, SLE, pSS, or GD had levels above this value. Furthermore, univariate regression analysis showed a positive association (r equals 0.35, p-value equals 0.02) between cTnI and RF in patients with seropositive RA. CONCLUSION: Using the Beckman Access Immunoassay System for cTnI quantification, it was found that some patients with seropositive RA had falsely-elevated cTnI, while none of the patients with seronegative RA, SLE, pSS, or GD had falsely-elevated cTnl.