06 November 2023
: Case report
[In Press] Unveiling the Rare Complication: Statin-Induced Immune-Mediated Necrotizing Myopathy
Unknown etiology, Challenging differential diagnosis, Rare disease, Adverse events of drug therapy , Educational Purpose (only if useful for a systematic review or synthesis)
Farheen Hussain Chowdhury1BCDEFG, Olena Mahneva2ABCDEF, Maniekha Maharaj1BE, Werther Marciales1CGAm J Case Rep In Press; DOI: :: ID: 941387
Available online: 2023-11-06, In Press, Corrected Proof
Publication in the "In-Press" formula aims at speeding up the public availability of the pending manuscript while waiting for the final publication. The assigned DOI number is active and citable. The availability of the article in the Medline, PubMed and PMC databases as well as Web of Science will be obtained after the final publication according to the journal schedule
Abstract
BACKGROUND
Statin-induced necrotizing autoimmune myopathy is an exceptionally rare yet severe complication of statin therapy that may develop in individuals at any time during their exposure to statins. The development of proximal muscle weakness, muscle pain, and elevated creatine kinase (CK) levels in patients while taking statins should prompt clinical consideration of statin-induced myopathy. The pathophysiology arises from the production of auto-antibodies, which target the 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA reductase) enzyme, leading to the aggressive breakdown of myofibrils.
CASE REPORT
Here, we present a case of a 59-year-old woman with a medical history of dyslipidemia who developed anti-HMG-CoA reductase antibodies after taking atorvastatin. She came to the emergency department with complaints of severe proximal muscle weakness. The laboratory workup showed an elevated CK level up to 12 000 IU/L. Despite discontinuing atorvastatin, the patient’s elevated CK levels persisted. The patient underwent a muscle biopsy, demonstrating myofibril necrosis. Serological analysis showed anti-HMG-CoA reductase antibodies in the patient’s serum, which led to the diagnosis of immune-mediated necrotizing myopathy due to statins. The patient’s statin therapy was promptly discontinued, and she was treated with a high dose of IV corticosteroids. After the patient’s discharge, brief discontinuation of the corticosteroids resulted in CK elevation and a return of symptoms. This led to the second re-admission and restarting of corticosteroids until stabilization and discharge.
CONCLUSIONS
This case represents an important reminder for clinicians to recognize the possibility of statin-induced immune-mediated necrotizing myopathy in patients presenting with proximal muscle weakness while taking a statin, notwithstanding the rarity of this condition.
Keywords: Myositis; Myotoxicity; Anti-HMG-CoA Reductase-Induced Myopathy; Statin-Induced Myopathy; Statins; Myonecrosis; HMG-CoA Reductase Enzyme
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