gms | German Medical Science

60th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN)

German Society for Neuropathology and Neuroanatomy

26. - 28.08.2015, Berlin

Two patients with Statin-induced necrotizing myopathy with similar histology but different clinical behaviour: a diagnostic challenge

Meeting Abstract

  • corresponding author presenting/speaker Clara Frydrychowicz - Universitätsklinikum Leipzig, Neuropathologie, Leipzig, Germany; University, Neuropathology, Leipzig, Germany
  • Lorenz Weidhase - University, ICU, Leipzig, Germany
  • Stefan Merkelbach - Heinrich Braun, Neurology, Zwickau, Germany
  • Wolf Müller - Universitätsklinikum Leipzig, Neuropathologie, Leipzig, Germany

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie. 60th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN). Berlin, 26.-28.08.2015. Düsseldorf: German Medical Science GMS Publishing House; 2015. Doc15dgnnP41

doi: 10.3205/15dgnn65, urn:nbn:de:0183-15dgnn654

Published: August 25, 2015

© 2015 Frydrychowicz et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at



Statins are the most common group of cholesterol lowering medications with more than 100 million prescriptions per year. Statin induced muscular adverse effects occur in 10-25% of patients. We present two cases with Statin- induced necrotizing myopathy. A 70 year old man presented with acute kidney failure due to severe rhabdomyolysis and high creatine kinase (CK) levels. He had a six year history of low dose Statin therapy. Stopping Statin medication led to a fast recovery of muscle related symptoms and CK normalized quickly. A 63 year old woman presented with muscle pain, proximal muscle weakness and mild tetraparesis. She also had been on Statin medication. However, symptoms persisted after Statin had been withdrawn for a period of six months. The two clinical presentations with similar histopathology but different clinical behaviour after Statin- arrest suggest a different pathogenesis. The exact mechanism of Statin-associated myopathies (SAM) still remains elusive. However, a self- limiting Statin induced primarily toxic necrotizing myopathy is now distinguished from a persisting autoimmune mediated Statin- induced necrotizing myopathy. In the latter Anti-HMG- CoA- Reductase- Antibodies can be detected in the serum and muscle of affected patients. Statin-induced autoimmune mediated myopathy was confirmed in the second patient. Neuropathologists should be aware of the possibility of autoimmune mediated Statin- induced necrotizing myopathy and should recommend Anti-HMG-CoA-reductase- Antibody testing in all patients with persistent muscle pathology after Statin-arrest.