Association of statin induced reduction in serum coenzyme Q10 level and conduction deficits in motor and sensory nerves: An observational cross-sectional study

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ObjectiveThe reduction of Coenzyme Q10 (CoQ10) levels following statin use has been linked to cause peripheral neuropathy. Hence, this study was planned to explore the effect of statin on the serum HMGCR (3-hydroxy-3-methyl-glutaryl-coenzyme A reductase), serum CoQ10 levels and nerve conduction and their correlation. Patients and MethodsIn an open labelled, cross-sectional, observational study, estimation of serum HMGCR and CoQ10 levels was performed in 50 atorvastatin/rosuvastatin users and 50 normal healthy volunteers (NHV). Statin users were also subjected to nerve conduction studies (NCS). ResultsMean serum HMGCR level in NHV was higher (73.58 ± 7.64 ng/ml; p = 0.003) than that in statin users (49.11 ± 1.98 ng/ml). Similarly, mean serum CoQ10 levels was also lower (30.54 ± 2.03 ng/ml, p < 0.0001) in statin users than in NHV (49.43 ± 3.23 ng/ml). Amongst the 50 statin users, 29 had impaired NCS in sural, tibial and common peroneal nerve with lower mean serum CoQ10 levels (24.05 ± 1.96 ng/ml; p < 0.0001). Significant negative correlation was observed between onset time of action potential (AP) of the sural nerve and serum CoQ10 (r=-0.32) and HMGCR (r=-0.43) levels. There was significant positive correlation of conduction velocity of sural (r = 0.38) and tibial (r = 0.31) nerves with serum CoQ10 level. While conduction velocity in sural (r = 0.37) and common peroneal (r = 0.34) nerves positively correlated with serum HMGCR levels. The amplitude of the AP of the common peroneal nerve positively correlated with both serum CoQ10 (r = 0.52) and HMGCR (r = 0.46) levels. ConclusionStatin users had lower serum CoQ10 and HMGCR levels associated with nerve conduction deficits suggesting a role of CoQ10 in the occurrence of the neurological adverse effects.