DEC 09, 2014 7:00 AM PST

Statin Myopathy: When might it be autoimmune?

Speaker
  • Director of the Johns Hopkins Myositis Center
    Biography
      Dr. Christopher-Stine is currently Director of the Johns Hopkins Myositis Center. She is an Associate Professor of Medicine and Neurology. She also serves as one of the Johns Hopkins University School of Medicine College Advisors, and is a Board Member of the Johns Hopkins Institutional Review Board (IRB 5). Dr. Christopher-Stine graduated Cum Laude with a B.A. in chemistry from Franklin and Marshall College; was elected to Alpha Omega Alpha at Hahnemann University School of Medicine, where she received her MD degree , and she attained her Master of Public Health degree from the Johns Hopkins Bloomberg School of Public Health. Her internship and residency training were completed at MCP Hahnemann University, where she also served as Chief Resident, after which she pursued rheumatology fellowship training at Johns Hopkins.
      Dr. Christopher-Stine's primary research focus is clinical research pertaining to inflammatory myopathies - specifically describing unique phenotypes, novel therapeutic approaches, and novel disease subsets among patients with inflammatory myopathies who are part of the growing cohort of over 1500 patients evaluated clinically for confirmed or suspected muscle disease at the Myositis Center who agree to be part of the Johns Hopkins Myositis database. Dr. Christopher-Stine and her colleagues made the novel discovery of an autoimmune myopathy closely linked to statins. She has a continued interest in statins and their toxicities toward muscle, both as a direct muscle toxin as well as its contribution to autoimmune muscle injury.

    Abstract

     

    Statins are among the most commonly prescribed medications that significantly reduce cardiovascular risk in selected individuals. However, these drugs can also be associated with muscle symptoms ranging from mild myalgias to severe rhabdomyolysis.

    While statin myotoxicity is usually self-limited, in some instances statin-exposed subjects can develop an autoimmune myopathy typically characterized by progressive weakness, muscle enzyme elevations, a necrotizing myopathy on muscle biopsy, and autoantibodies that recognize 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), the pharmacologic target of statins.

    These antibodies are also found in some autoimmune myopathy patients without statin exposure. Importantly, anti-HMGCR antibodies are not found in the vast majority of statin-exposed subjects without autoimmune myopathy, including those with self-limited statin intolerance.

    Thus, testing for these antibodies may help differentiate those with self-limited statin myopathy who recover after statin discontinuation from those with a progressive statin-associated autoimmune myopathy who typically require immunosuppressive therapy.


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