ABSTRACT
The use of statins has been increasing over the past decade for the primary and secondary prevention of cardiovascular disease worldwide. Subsequently, various side effects have also been unfolding. Muscle-related side effects secondary to statins range from myalgia to rhabdomyolysis and need close monitoring for early detection. Statin-induced necrotizing autoimmune myopathy (SINAM) in particular is unique given its pathophysiology, trigger factor, genetic predisposition, and aggressive management strategy. We present two cases of SINAM and discuss the clinical aspects of diagnosis, investigation, and management. Statin-induced necrotizing autoimmune myopathy usually presents with proximal myopathy along with increased creatinine kinase (CK) levels which do not resolve with only statin discontinuation. Diagnosis should be made with biopsy and 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) antibody detection. The investigation should also be directed to rule out other etiology of proximal myopathy. In most cases, rechallenge with a statin is unsuccessful and immunosuppressive treatment is essential.
ABSTRACT
5-Fluorouracil (5-FU) is a chemotherapeutic agent frequently used for the treatment of solid tumors. In a few cases, 5-FU can be associated with coronary vasospasm, cardiac ischemia, or life-threatening arrhythmias. Recognition of 5-FU cardiotoxicity is clinically important as after the rapid sensation of therapy, cardiotoxicity can be completely reversible, and on the other hand, readministration may lead to serious damage of the heart and even death. A 70-year-old male came to the emergency department (ED) with chest pain which started while receiving an infusion of 5-FU. The patient did not have a personal history or risk factors of coronary artery disease and his electrocardiogram (ECG) before starting chemotherapy was completely normal. In the ED, his ECG had ischemic changes, troponin was elevated, and echocardiogram showed anterior wall hypokinesis. However, emergent coronary angiogram did not reveal any acute coronary occlusion. 5-FU-induced cardiotoxicity was suspected; the patient was admitted to a progressive care unit for close monitoring and infusion of calcium channel blockers was initiated. The patient's symptoms and ECG findings gradually resolved, and two days later on discharge, patient was chest pain free and ECG was normal. This case supports the vasospastic hypothesis of 5-FU cardiac toxicity, describes its clinical course, and emphasizes the importance of better awareness and early recognition of the rare side effect as it may allow physicians to reduce the risk of life-threatening complications.
