M N Meriggioli1, A C Barboi, J Rowin, E J Cochran. 1. Section of Neuromuscular Disease Department of Neurological Sciences, Neurological Rush University, Chicago, Illnois, USA.
Abstract
OBJECTIVES: To define the clinical, electrophysiological, and pathologic features of the myopathy associated with the use of HMG CoA reductase inhibitors. METHODS: Five patients with myopathy associated with HMG CoA reductase inhibitors were evaluated. Complete histories, physical examinations, manual muscle testing, serum creatine kinase, urine myoglobin measurements, electrodiagnostic studies, and muscle biopsy were performed. RESULTS: Consistent features in our patients included a subacute onset of myalgias and weakness, electromyography demonstrating electrical myotonia, elevated creatine kinase levels, and in some patients myoglobinuria despite a relative lack of muscle necrosis on muscle biopsy and preserved myofibrillatory architecture by electron microscopy. All patients experienced resolution of symptoms within 3 weeks of drug discontinuation. CONCLUSIONS: We postulate that the constellation of clinical, electrophysiological, and pathologic findings among our patients with HMG CoA reductase inhibitor myopathy may be explained by the early toxic effects of HMG CoA reductase inhibitors on muscle membrane organelles and sarcolemmal function. Patients on concurrent therapy with cyclosporine, gemfibrozil, and antifungal agents of the azole groups are at an increased risk of developing this toxic myopathy.
OBJECTIVES: To define the clinical, electrophysiological, and pathologic features of the myopathy associated with the use of HMG CoA reductase inhibitors. METHODS: Five patients with myopathy associated with HMG CoA reductase inhibitors were evaluated. Complete histories, physical examinations, manual muscle testing, serum creatine kinase, urine myoglobin measurements, electrodiagnostic studies, and muscle biopsy were performed. RESULTS: Consistent features in our patients included a subacute onset of myalgias and weakness, electromyography demonstrating electrical myotonia, elevated creatine kinase levels, and in some patientsmyoglobinuria despite a relative lack of muscle necrosis on muscle biopsy and preserved myofibrillatory architecture by electron microscopy. All patients experienced resolution of symptoms within 3 weeks of drug discontinuation. CONCLUSIONS: We postulate that the constellation of clinical, electrophysiological, and pathologic findings among our patients with HMG CoA reductase inhibitor myopathy may be explained by the early toxic effects of HMG CoA reductase inhibitors on muscle membrane organelles and sarcolemmal function. Patients on concurrent therapy with cyclosporine, gemfibrozil, and antifungal agents of the azole groups are at an increased risk of developing this toxic myopathy.
Authors: James D Triplett; Shahar Shelly; Guy Livne; Margherita Milone; Charles D Kassardjian; Teerin Liewluck; Cecilia Kelly; Elie Naddaf; Ruple S Laughlin; Christopher J Lamb; Devon Rubin; Elliot L Dimberg; Divanshu Dubey; John R Mills; Jay Mandrekar; Christopher J Klein Journal: Brain Commun Date: 2020-12-13
Authors: A Alfirevic; D Neely; J Armitage; H Chinoy; R G Cooper; R Laaksonen; D F Carr; K M Bloch; J Fahy; A Hanson; Q-Y Yue; M Wadelius; A H Maitland-van Der Zee; D Voora; B M Psaty; C N A Palmer; M Pirmohamed Journal: Clin Pharmacol Ther Date: 2014-06-04 Impact factor: 6.875