A Case of Statin-Associated Autoimmune Myopathy: Management and Treatment

Abstract

Elevated lipid panels are associated with an increased risk of cardiovascular disease. Management of heart disease with lipid lowering agents play a vital role in medicine. Statins are one group of medications that are widely utilized in the medical field to decrease the risk of atherosclerotic disease. Statins work by inhibiting the hepatic enzyme 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR). Although statins are one of the most effective drugs for secondary and primary prevention of heart disease, they are not without risks and side effects such as hepatotoxicity and myopathy. We present a case of a male patient who developed progressively worsening muscle weakness and elevated muscle enzyme markers upon initiation of a statin. His symptoms persisted despite a trial of an alternative statin and subsequent discontinuation of all statin medications. A multitude of possible etiologies were considered and ranged from infectious, autoimmune, cancerous, to congenital in nature. Environmental factors, such as exposure to medications or toxins, were also considered as one of the possible precipitating factors. The association between his statin consumption and muscle weakness were not easily apparent at first. He required further workup including physical examination, electromyography, panel of myositis antibodies, and muscle biopsy. After clinical suspicion and elevated antibodies to HMGCR beyond the normal limit, he was discovered to have statin-associated autoimmune myopathy. The patient improved with the treatment of immunosuppressive agent’s prednisone and methotrexate.

Statin-Associated Myalgia, Myopathy, and Myositis

“…17 These patients are often younger at the age of symptom onset, have more severe disease, possess a higher serum CK level, and respond less well to treatment. 18 In contrast with patients who only have myalgia, those with autoimmune necrotizing myositis usually present with symmetrical proximal upper and lower limb muscle weakness that can develop over days or weeks, and the onset of symptoms develops on average 3 years after initiation of treatment. The limb weakness, dysphagia, and myalgia are found more commonly in patients with statin-induced myopathy as compared with patients with dermatomyositis and polymyositis.…”

“…17 In addition, some reports describe an ascending pattern of weakness that is similar to the presentation of Guillain-Barre syndrome, with normal reflexes and normal findings on lumbar puncture. 18 Unfortunately, the symptoms can progress even after cessation of the statin because the presence of the autoantibodies that recognize HMGCR, the pharmacologic enzyme target of statin therapies, is triggered into a self-sustaining cycle of attacking muscle cells that express HMGCR. For this reason, patients with statininduced autoimmune myopathy and anti-HMGCR autoantibodies often require chronic immunosuppression to control the disease and prevent flares.…”

“…However, to make matters more complex, a history of statin exposure is sometimes lacking in patients with the presence of HMGCR antibodies but who present with symptoms consistent with autoimmune myositis 17. These patients are often younger at the age of symptom onset, have more severe disease, possess a higher serum CK level, and respond less well to treatment 18…”

“…The limb weakness, dysphagia, and myalgia are found more commonly in patients with statin-induced myopathy as compared with patients with dermatomyositis and polymyositis 17. In addition, some reports describe an ascending pattern of weakness that is similar to the presentation of Guillain-Barre syndrome, with normal reflexes and normal findings on lumbar puncture 18. Unfortunately, the symptoms can progress even after cessation of the statin because the presence of the autoantibodies that recognize HMGCR, the pharmacologic enzyme target of statin therapies, is triggered into a self-sustaining cycle of attacking muscle cells that express HMGCR.…”

Molecular Mechanisms and Mediators of Hepatotoxicity Resulting from an Excess of Lipids and Non-Alcoholic Fatty Liver Disease

“…If the high quantities of AST/ALT persist, the statin must be stopped, while switching to another statin or rechallenge may also be possible [143]. Transaminase levels that were overall high and higher than the ULN were present in only 2% of patients receiving statin monotherapy [144].…”