Fast skeletal troponin I, but not the slow isoform, is increased in patients under statin therapy: a pilot study

被引:5
作者
Trentini, Alessandro [1 ]
Spadaro, Savino [2 ]
Rosta, Valentina [1 ]
Manfrinato, Maria C. [1 ]
Cervellati, Carlo [1 ]
Dalla Cortez, Francesca [2 ]
Hanau, Stefania [1 ]
Volta, Carlo A. [2 ]
Bellini, Tiziana [1 ]
机构
[1] Univ Ferrara, Dept Biomed & Specialist Surg Sci, Sect Med Biochem Mol Biol & Genet, Ferrara, Italy
[2] Univ Ferrara, Dept Morphol Surg & Expt Med, Sect Anesthesia & Intens Care, Ferrara, Italy
关键词
statin; fast skeletal troponin; slow skeletal troponin; muscle damage; creatine kinase; CREATINE-KINASE; MUSCLE; SERUM; BIOMARKERS; TOXICITY; MARKERS; INJURY;
D O I
10.11613/BM.2019.010703
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Introduction: Statin therapy is often associated with muscle complaints and increased serum creatine kinase (CK). However, although essential in determining muscle damage, this marker is not specific for skeletal muscle. Recent studies on animal models have shown that slow and fast isoforms of skeletal troponin I (ssTnI and fsTnI, respectively) can be useful markers of skeletal muscle injury. The aim of this study was to evaluate the utility of ssTnI and fsTnI as markers to monitor the statin-induced skeletal muscle damage. Materials and methods: A total of 51 patients (14 using and 37 not using statins) admitted to the intensive care unit of the University of Ferrara Academic Hospital were included in this observational study. Serum activities of CK, aldolase, alanine aminotransferase and myoglobin were determined by spectrophotometric assays or routine laboratory analysis. Isoforms ssTnI and fsTnI were determined by commercially available ELISAs. The creatine kinase MB isoform (CK-MB) and cardiac troponin I (cTnI) were evaluated as biomarkers of cardiac muscle damage by automatic analysers. Results: Among the non-specific markers, only CK was significantly higher in statin users (P = 0.027). Isoform fsTnI, but not ssTnI, was specifically increased in those patients using statins (P = 0.009) evidencing the major susceptibility of fast-twitch fibres towards statins. Sub-clinical increase in fsTnI, but not CK, was more frequent in statin users (P = 0.007). Cardiac markers were not significantly altered by statins confirming the selectivity of the effect on skeletal muscle. Conclusions: Serum fsTnI could be a good marker for monitoring statin-associated muscular damage outperforming traditional markers.
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页数:9
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