Author + information
- Kosit Sribhen, MD,
- Nilrat Wannasilp, MD⁎ ( and )
- Rewat Phankingthongkum, MD
- ↵⁎Clinical Pathology, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok 10600, Thailand
We thank Drs. Giannitis and Katus for their interest in our paper (1) concerning the clinical specificity of cardiac troponin T (cTnT) in skeletal muscle disease. Because several parts of their letter also referred to the article by Jaffe et al. (2), which is beyond the scope of our discussion, we will respond only to the parts addressing the results of our study.
Drs. Giannitis and Katus have stated that the re-elevations of cTnT found in the subacute phase (2 to 4 weeks) of rhabdomyolysis in our patient could be due to post-operative myocardial infarction or pulmonary embolism. However, the patterns of cTnT release that showed chronic elevations, and not acute rise and fall, over several weeks are not typical of acute ischemic events. They also stated that the negative cardiac troponin I (cTnI) results observed in our study might occur as a result of interference by certain factors present in the blood samples. In this regard, it is true that analytic interferences by hemolysis or heterophilic antibodies may cause false-negative troponin I results (2). Nevertheless, these interferences can occur in both cardiac troponin assays. In addition, it is unlikely that hemolysis caused negative troponin I results in all 5 blood samples that were measured in the subacute phase of rhabdomyolysis. Furthermore, why should the interfering effects of heterophilic antibodies occur only in the subacute phase and not in the acute phase in blood samples obtained from the same person?
To substantiate the significance of our findings, we report another patient with chronic renal failure who was receiving maintenance hemodialysis and developed rhabdomyolysis after limb ischemia. As in the first index case, there were significant increases in both creatine kinase myocardial band and cTnT (third-generation immunoassay; Roche Diagnostics, Basel, Switzerland) from elevated baseline concentrations during the second to fourth weeks of the acute event, with peak values of approximately 7-fold the upper limit of reference ranges (personal observation). During this period, no increase in cTnI (first-generation immunoassay; Ortho Clinical Diagnostics, Raritan, New Jersey) serum concentration was observed. Of interest was the observation by Visvanathan and Visvanathan (3), who reported a female patient with sepsis-associated rhabdomyolysis exhibiting persistent elevations of cTnT and creatine kinase myocardial band serum concentrations throughout her stay in the rehabilitation unit of more than 2 months. Unfortunately, measurement of cTnI was not performed. Nonetheless, the authors theorized that the prolonged elevations of cTnT were most likely due to reexpression of the cTnT isoform in regenerating skeletal muscle.
In this context, it should be noted that we did not intend to provide evidence for the reexpression phenomenon with data from our case study. Rather, the results are hypothesis generating and, in agreement with Drs. Giannitis and Katus, require thorough scientific evaluation and confirmation from large studies.
- American College of Cardiology Foundation