Résumé :
|
Communication n° 368. Statins ( HMG CoA reductase) reduce colesterol by reducing the sythesis of mevalonate, a intermediary in the cholesterol pathway. This therapy can be associated with different degrees of skeletal muscle disorders varying from severe myositis with rhabdomyolysis, to mild muscle weakness and muscle cramps. Usually serum CK are elevated in all these conditions. Moreover myalgias and high serum CK levels often persist after statin withdrawal. CoQ 10, is a lipophilic component of the electron-transport chain, which transfers electrons from complex I-II to complex III . It plays a role as antioxidant and as membrane stabilizer, and it is synthetized from mevalonate. Rundek T et al. described a depletion of CoQ10 in plasma of patient treated with Atorvastatin . Johnson et al, studying human myotube cultures, postulated the statin related myopathy is related to apoptosis but no to Co Q 10 deficiency, To better understand the correlations between statins and myopathy and to investigate the role of Co Q 10 in the pathogenesis of this condition, we studied muscle biopsies from 20 patients with statins related myalgias and high CK level. Evidence of apoptosis was investigated using tunnel reaction and antibodies against cas 3, bax and bcl2. Furthermore we dose either the Co Q10 level and the Complex III activity in muscle tissues. We found that in all patients the muscle biopsy was normal or with mild myopathic changes. No tunnel positivity was found in all muscle sections examined. The Co Q10 level was mildly decrease in 9/20 of our patients being half of normal range in 2 of them. The complex III activity was normal in all patients. Our results suggest that a secondary Co Q10 deficiency present in some patients may correlated with clinical presentations of cramps and myalgias in statins related myopathy.
|