4.1 Article

Dysphagia: A Case Report of an Atypical Presentation of Statin-Induced Necrotizing Myositis

Journal

CUREUS JOURNAL OF MEDICAL SCIENCE
Volume 15, Issue 8, Pages -

Publisher

SPRINGERNATURE
DOI: 10.7759/cureus.43587

Keywords

statin use; proximal weakness; elevated creatine phosphokinase (cpk); statin-induced necrotizing autoimmune myositis; rare cause of dysphagia

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The author discussed a serious side effect - he found that his patient, although no longer taking the statin medication that was harmful to his muscles, still exhibited symptoms of necrotizing autoimmune myositis with positive antibodies. It is important to be vigilant for adverse reactions that may occur with therapeutic medications when assessing patients with this condition.
Statin medications act by inhibiting the enzyme hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (HMGCR), thus decreasing hepatic cholesterol synthesis. They are considered the mainstay treatment of hypercholesterolemia due to their tremendous efficacy and mortality benefit. Although generally well tolerated, statins may adversely affect skeletal muscle resulting in side effects ranging from mild myalgia to life-threatening necrotizing myositis. Statin-induced necrotizing autoimmune myositis is a rare yet devastating adverse effect that may occur shortly after initiation of therapy or after several years of use. Unfortunately, medication discontinuation has shown no impact on prevention or alleviation of symptoms. Though there is currently no definitive guidance for the treatment of this condition, corticosteroids are generally considered to be first line, via high-dose oral prednisone or intravenous methylprednisolone. In this case report, we discuss the case of a 72-year-old male with an unusual presentation of statin-induced necrotizing autoimmune myositis: dysphagia, weakness, and weight loss. His diagnosis was confirmed by muscle biopsy indicating necrotizing myositis and his serum was found to be strongly positive for anti-HMG-CoA reductase antibodies. This patient had a very brief history of statin use, but his primary care provider discontinued the medication a couple of months prior to symptom onset due to elevated liver function tests. He was treated with aggressive intravenous fluid hydration and intravenous corticosteroids during an extended inpatient hospital stay. He was discharged to a rehabilitation facility. This report demonstrates the importance of creating a wide differential for patients who present with fatigue, generalized weakness, and dysphagia. It is essential to always consider statin-induced necrotizing myositis if a patient has a history of statin use, even if the statin has been discontinued. Necrotizing myositis demands timely diagnosis and management to improve mortality.

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