Informace o publikaci

Elevation of cardiac troponin T in patients with amyotrophic lateral sclerosis

Autoři	MACH Lukáš KONECNY Tomas HELÁNOVÁ Kateřina JAFFE Allan S. SORENSON Eric J. SOMERS Virend K. REEDER Guy S.
Rok publikování	2016
Druh	Článek v odborném periodiku
Časopis / Zdroj	Acta Neurologica Belgica
Fakulta / Pracoviště MU	Lékařská fakulta
Citace
www	http://link.springer.com/article/10.1007/s13760-015-0596-8
Doi	http://dx.doi.org/10.1007/s13760-015-0596-8
Obor	Kardiovaskulární nemoci včetně kardiochirurgie
Klíčová slova	Acute coronary syndrome; Neuromuscular disease; Amyotrophic lateral sclerosis; Troponin T
Popis	Limited evidence suggests that specificity of cardiac troponin T (cTnT), a highly sensitive biomarker of myocardial injury, is reduced in patients with skeletal myopathies. Whether amyotrophic lateral sclerosis (ALS) the most common motor neuron disease could be also associated with abnormal plasma or serum cTnT levels remains unclear. Our objective was to assess cTnT levels in patients with ALS without known cTnT elevating conditions. Among ALS patients seen at our institution until 2012 we identified those who had their cTnT measured. Patients who suffered from conditions known to elevate cTnT were excluded. A case–control analysis comparing cTnT levels of these ALS patients to matched non-ALS controls fulfilling the same inclusion criteria was performed. We included 40 ALS patients of whom 27 (68 %) patients had a positive cTnT. In the control group (n = 40), 2 (5 %) tested as cTnT positive. Among the ALS patients who underwent cTnT evaluation on more occasions (n = 7; median followup = 1.08 years), 2 (29 %) patients tested positive during the initial measurement while 6 (86 %) of them had positive cTnT at the subsequent evaluations. ALS patients with increased cTnT had been diagnosed with ALS significantly earlier than those without the elevation. Our findings raise the possibility that ALS may cause cTnT elevations. Further studies are needed to confirm these findings, clarify the pathophysiological mechanism, and establish the significance of cTnT elevations in patients with ALS.