Drug-Induced Rhabdomyolysis with Elevated Cardiac Troponin T

Abstract

The essential role of cardiac troponin in the diagnosis of acute myocardial infarction has led to the development of high-sensitivity assays, which are able to detect very small amounts of myocardial necrosis. The high-sensitivity cardiac troponin T assay, however, is not entirely specific for myocardial injury. This case report describes a 48-year-old woman, who, two years after cardiac transplantation, presented with rhabdomyolysis. During the course of the disease, her troponin T level was elevated on repeated occasions, but other definitive evidence of myocardial injury was not found. Asymptomatic cardiac troponin T elevations during rhabdomyolysis may be due to either cardiac involvement or false positive results stemming from skeletal muscle injury.

Value of the high-sensitivity troponin T assay for diagnosis of acute myocardial infarction in patients with and without renal insufficiency

“…Troponin-T is also released from cells other than myocardial cells. One clinical study shows that troponin-T is expressed in the skeletal muscle of dialysis patients [ 19 ], and this expression could explain the mechanism of elevated troponin-T in patients with seizure or rhabdomyolysis [ 17 , 20 ]. Although elevation of cardiac troponins in the blood usually reflects injury leading to necrosis of the myocardium, such levels do not indicate the mechanism of ischemia-induced myocardial necrosis [ 1 ].…”

<p>Comparison of Lipid Profile, Liver Enzymes, Creatine Kinase and Lactate Dehydrogenase Among Type II Diabetes Mellitus Patients on Statin Therapy</p>

“…45 Statin drugs can disrupt the normal cardiac myocyte membrane integrity leading to release of intracellular components including structural proteins and enzymes such as CK-MB isotype in serum. 41 Similarly, CK-MB isotype among T2DM patients who were on 40 mg statin was higher as compared to T2DM patients who were on 20 mg statin therapy (Table 7). A study done by Auer et al 46 showed as the doses of statins administered for patients increase muscle-related side effects will become more prevalent.…”

“…Creatine kinase-MB can also be used as a secondary marker to aid in the diagnosis and measurement of the degree of myocardial necrosis as a result of drug toxicity. 41 Out of the total CK isotypes found in the serum, CK-MB accounts for 6-25%. The finding of this study indicated that the mean serum level of CK-MB isotype was within normal reference range (Table 5) among T2DM patients who were on statin for greater than 18 months as compared to other study groups.…”

False-Positive Causes in Serum Cardiac Troponin Levels

“…Most often, such false-positive reactions occurred with first and second generation troponin immunoassays with weakly specific antibodies that could interact with skeletal troponin molecules [46][47][48][49]. However, subsequently, a considerable number of cases of false-positive increases in cTns were registered when using more specific third and fourth generation troponin immunoassays [24][25][26][27]. The specific cause and mechanism of increase in cTns in patients with skeletal myopathies has not been unraveled yet, and cases of false-positive increases in cTns have been described even with the use of modern highly sensitive immunoassays [49].…”

“…However, in some cases, elevated (positive) troponin concentrations cannot be explained, even after careful clinical examination and exclusion of all possible pathologies that may cause cardiomyocyte damage. Such cases are called falsepositive and are most often associated with the following reasons: fibrin clots, heterophile antibodies, alkaline phosphatase, rheumatoid factor, and cross-reactions of diagnostic (anti-cTn) antibodies with troponin molecules released from skeletal muscle [16][17][18][19][20][21][22][23][24][25][26][27][28]. Knowledge of the main causes and mechanisms of a false-positive increase in cTn concentrations is important in clinical practice, since many physicians may make incorrect diagnoses and prescribe unnecessary treatment based on laboratory results, which can be harmful to the patient and lead to unnecessary economic costs.…”