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Department of Medical Chemistry and Biochemistry, Division of Clinical Biochemistry, University of Innsbruck, Fritz-Pregl-Strasse 3, A-6020 Innsbruck, Austria.
2
Department of Anatomy 3, University of Vienna, A-1010
Vienna, Austria.
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Department of Pediatrics, University of Freiburg,
D-79106 Freiburg, Germany.
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Department of Pediatrics, University of Innsbruck,
A-6020 Innsbruck, Austria.
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Department of Internal Medicine, Division of Pneumology,
University of Freiburg, D-79106 Freiburg, Germany.
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Department of Internal Medicine, Division of Cardiology,
University of Innsbruck, A-6020 Innsbruck, Austria.
a Address correspondence to this author at: Department of Medical Chemistry and Biochemistry, Division of Clinical Biochemistry, University of Innsbruck, Fritz-Pregl-Strasse 3, A-6020 Innsbruck, Austria. Fax 43-512-507-2876; e-mail
Angelika.Lercher{at}uibk.ac.at.
Background: Because of controversial earlier studies, the purpose of this study was to provide novel experimental and additional clinical data regarding the possible reexpression of cardiac troponin T (cTnT) in regenerating skeletal muscle in Duchenne muscular dystrophy (DMD).
Methods: Plasma from 14 patients (mean age, 7.5 years; range, 5.7–19.4 years) with DMD was investigated for creatine kinase (CK), the CK MB isoenzyme (CKMB), cTnT and cardiac troponin I (cTnI), and myoglobin. cTnT concentrations were measured by an ELISA (second-generation assay; Roche) using the ES 300 Analyzer. cTnI, myoglobin, and CKMB were measured by an ELISA using the ACCESS System (Beckman Diagnostics). Troponin isoform expression was studied by Western blot analysis in remnants of skeletal muscle biopsies of three patients with DMD and in an animal model of DMD (mdx mice; n = 6).
Results: There was no relation of cTnT and cTnI to clinical evidence for cardiac failure. cTnI concentrations remained below the upper reference limit in all patients. cTnT was increased (median, 0.11 µg/L; range, 0.06–0.16 µg/L) in 50% of patients. The only significant correlation was found for CK (median, 3938 U/L; range, 2763–5030 U/L) with age (median, 7.5 years; range, 6.8–10.9 years; r = -0.762; P = 0.042). Western blot analysis of human or mouse homogenized muscle specimens showed no evidence for cardiac TnT and cTnI expression, despite strong signals for skeletal muscle troponin isoforms.
Conclusions: We found no evidence for cTnT reexpression in human early-stage DMD and in mdx mouse skeletal muscle biopsies. Discrepancies of cTnT and cTnI in plasma samples of DMD patients were found, but neither cTnT nor cTnI plasma concentrations were related with other clinical evidence for cardiac involvement.
The following articles in journals at HighWire Press have cited this article:
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  J S Hamilton and P C Sharpe Two cases of inflammatory muscle disease presenting with raised serum concentrations of troponin T J. Clin. Pathol., December 1, 2005; 58(12): 1323 - 1324. [Abstract] [Full Text] [PDF]
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 B. J. Freda, W. H. W. Tang, F. Van Lente, W. F. Peacock, and G. S. Francis Cardiac troponins in renal insufficiency: Review and clinical implications J. Am. Coll. Cardiol., December 18, 2002; 40(12): 2065 - 2071. [Abstract] [Full Text] [PDF]
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 S. Fredericks, J. F. Murray, N. D. Carter, A. M.S. Chesser, S. Papachristou, M. M. Yaqoob, P. O. Collinson, D. Gaze, and D. W. Holt Cardiac Troponin T and Creatine Kinase MB Content in Skeletal Muscle of the Uremic Rat Clin. Chem., June 1, 2002; 48(6): 859 - 868. [Abstract] [Full Text] [PDF]
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