Elevated cardiac troponin I can occur in patients with cardiac injury or sepsis. However, extreme elevations of serum cardiac troponin I in pediatric patients without myocardial injury are rare. We present a case of a 14-year-old girl involved in a motor vehicle accident with muscle injury, who was readmitted with sepsis and severely elevated serum cardiac troponin I level in the absence of myocardial injury.
[Show abstract][Hide abstract] ABSTRACT: The measurement of cardiac troponins (cTn) is of considerable usefulness in the diagnosis of acute coronary syndrome. Abnormal levels of serum cTn are occasionally found in patients who are not suffering a myocardial infarction. This may be observed in several well-known situations including pulmonary embolism, pericarditis, myocarditis, coronary vasospasm, sepsis, congestive heart failure, supraventricular tachycardia with hemodynamic compromise, re-nal insufficiency, and prolonged strenuous endurance exercise. Endogenous antibodies such as heterophile antibodies, rheumatoid factor, and other autoantibodies are known to interfere with the immunoassay measurements of many different analytes, including the widely used Abbot AxSYM™ cTnI analyzer. Other sources of circulating antibodies include immunotherapies, vaccinations, or blood transfusions that may interfere with these immunoassays as well. We examine the case of a 48-year-old man with a history of hypercholesterolemia and obesity who presented with chest pain and was found to have elevated Tn I levels on two separate occasions. Further work-up revealed that the Tn I levels were spuriously elevated because the patient's blood revealed a normal cTnI level when mixed with polyethylene glycol to inactivate any antibodies interfering with the cTnI assay.
[Show abstract][Hide abstract] ABSTRACT: 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.
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.
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.
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.
Singapore medical journal 10/2007; 48(9):847-9. · 0.60 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Debate surrounds the interpretation of troponin assays for the diagnosis and prognosis of cardiac disease in patients with renal failure.
To systematically review the diagnostic and prognostic test characteristics of quantitative serum cardiac troponin I (cTnI) and T (cTnT) in renal failure patients without acute coronary syndrome (ACS) symptoms.
English-language literature was identified through searching MEDLINE from 1966 to August 2003 and reviewing reference lists. Studies were excluded if they did not meet research objectives, had fewer than 10 patients or focused primarily on nonrenal patients. Of 119 potential studies, 39 articles with over 349 patients with chronic kidney disease (CKD) and 3899 hemodialysis patients were selected for abstraction.
Among CKD and hemodialysis patients without ACS symptoms, cTnI had a mean specificity of 97% (95% CI 93% to 99%) and 96% (95% CI 94% to 98%), respectively, using the myocardial infarction cut-off threshold. The mean specificity of cTnT compared less favourably at 85% (95% CI 75% to 93%) and 71% (95% CI 64% to 77%) for CKD and hemodialysis patients, respectively. In hemodialysis patients without ACS symptoms, positive and negative likelihood ratios for all-cause mortality over 12 to 24 months for cTnT were 4.5 (95% CI 2.9 to 7.1) and 0.6 (95% CI 0.4 to 0.8), and for cTnI were 1.6 (95% CI 0.9 to 2.9) and 1.0 (95% CI 0.9 to 1.1), respectively.
In CKD and hemodialysis patients without ACS symptoms, troponin I, at the myocardial infarction cut-off threshold, is unlikely to be falsely elevated. Among hemodialysis patients without ACS symptoms, a positive troponin T helps predict all-cause mortality.
The Canadian journal of cardiology 11/2004; 20(12):1212-8. · 3.71 Impact Factor
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