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      Necrotizing Autoimmune Myopathy: A Case Report on Statin-Induced Rhabdomyolysis

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          Abstract

          Statin-induced necrotizing myopathy (SINM) is an uncommon but severe complication associated with statin medication. SINM can develop at any point after a person starts taking steroids. It is now being acknowledged as a component of the broader category of "statin-induced myopathy." Like other immune-mediated necrotizing muscle diseases, statin-induced myositis is identified by weakness in proximal muscles, increased serum creatine kinase (CK) levels, and, in some cases, dysphagia and respiratory distress. In addition, there is evidence of muscle cell damage when examined under a microscope, occurring with minimal or no infiltration of inflammatory cells. Diagnosing SINM promptly is frequently challenging due to its unpredictable development over time, with symptoms sometimes emerging many years after the initial exposure to statins. One distinctive characteristic of SINM is the continued presence of muscle inflammation and elevated CK levels even after discontinuing statin treatment. Currently, no clinical trials are available to guide how to manage statin-induced immune-mediated necrotizing myopathy (IMNM). Here, we present a case of a 42-year-old woman diagnosed with SINM and was found to have persistently elevated CPK despite discontinuation of statins. Our case also suggests that intravenous (IV) immunoglobins and steroids are an effective and well-tolerated alternative to immunosuppressants.

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            A novel autoantibody recognizing 200-kd and 100-kd proteins is associated with an immune-mediated necrotizing myopathy.

            Myofiber necrosis without prominent inflammation is a nonspecific finding in patients with dystrophies and toxic or immune-mediated myopathies. However, the etiology of a necrotizing myopathy is often obscure, and the question of which patients would benefit from immunosuppression remains unanswered. The aim of this study was to identify novel autoantibodies in patients with necrotizing myopathy. Muscle biopsy specimens and serum samples were available for 225 patients with myopathy. Antibody specificities were determined by performing immunoprecipitations from (35)S-methionine-labeled HeLa cell lysates. Selected biopsy specimens were stained for membrane attack complex, class I major histocompatibility complex (MHC), and endothelial cell marker CD31. Muscle biopsy specimens from 38 of 225 patients showed predominantly myofiber necrosis. Twelve of these patients had a known autoantibody association with or other etiology for their myopathy. Sixteen of the remaining 26 sera immunoprecipitated 200-kd and 100-kd proteins; this specificity was observed in only 1 of 187 patients without necrotizing myopathy. Patients with the anti-200/100 autoantibody specificity had proximal weakness (100%), high creatine kinase levels (mean maximum 10,333 IU/liter), and an irritable myopathy on electromyography (88%). Sixty-three percent of these patients had been exposed to statins prior to the onset of weakness. All patients responded to immunosuppressive therapy, and many experienced a relapse of weakness when the medication was tapered. Immunohistochemical studies showed membrane attack complex on small blood vessels in 6 of 8 patients and on the surface of non-necrotic myofibers in 4 of 8 patients. Five of 8 patients had abnormal capillary morphology, and 4 of 8 patients expressed class I MHC on the surface of non-necrotic myofibers. An anti-200/100-kd specificity defines a subgroup of patients with necrotizing myopathy who previously were considered to be autoantibody negative. We propose that these patients have an immune-mediated myopathy that is frequently associated with prior statin use and should be treated with immunosuppressive therapy.
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              Statin-Associated Autoimmune Myopathy

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                Author and article information

                Journal
                Cureus
                Cureus
                2168-8184
                Cureus
                Cureus (Palo Alto (CA) )
                2168-8184
                19 November 2023
                November 2023
                : 15
                : 11
                : e49065
                Affiliations
                [1 ] Department of Internal Medicine, Continental Medical College, Lahore, PAK
                [2 ] Department of Internal Medicine, BronxCare Health System, New York, USA
                [3 ] Department of Internal Medicine, The Frank H. Netter M.D. School of Medicine at Quinnipiac University, Bridgeport, USA
                [4 ] Department of Internal Medicine, St. Vincent's Medical Center, Bridgeport, USA
                [5 ] Department of Internal Medicine, American University of the Caribbean School of Medicine, Cupecoy, SXM
                [6 ] Department of Neurology, BronxCare Health System, New York, USA
                Author notes
                Article
                10.7759/cureus.49065
                10660882
                9195f592-e222-4428-8e1d-5a0061cda8b9
                Copyright © 2023, Altaf et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 19 November 2023
                Categories
                Internal Medicine
                Rheumatology
                Allergy/Immunology

                general internal medicine,medicine,atorvastatin,statin,rheumatology,creatinine kinase,rhabdomyolysis,myopathy,anti-hmg coa antibody,necrotizing autoimmune

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