Abstract

For patients who qualify, statins are among the most frequently prescribed drugs for the primary and secondary prevention of cardiovascular disease. A wide range of clinical manifestations, from generalized muscle aches to severe necrotizing myositis, are present in statin-induced myopathy. Here, we present a case of a 49-year-old woman with Vitamin D deficiency who developed statin-induced myopathy 45 days after starting rosuvastatin. A 49-year-old female was admitted to the hospital with a history of lower back pain and bilateral lower limb pain for 7 days. Her ongoing medications include ticagrelor 90 mg BD, metoprolol 25 mg OD, nicorandil 5 mg BD, telmisartan 20 mg OD, dapagliflozin 10 mg OD, metformin 1000 mg OD, vildagliptin 100 mg OD, pantoprazole 40 mg OD, and rosuvastatin 40 mg OD, which were started 45 days back when she was diagnosed with ischemic heart disease. On neurological evaluation, muscle weakness was present in the lower extremities with proximal muscle involvement more than the distal muscle, power at the hip was 2/5, knee and ankle joint were 4/5, knee and ankle reflex were 2/5, and the plantar reflex was normal, with no upper limb involvement. Laboratory investigation on the day of admission revealed elevated creatine phosphokinase (9873.00 U/L) and serum creatinine (2.45 mg/dl). Arterial blood gas analysis revealed a high anion gap with increased lactate levels. Vitamin D levels were found to be insufficient, and serum calcium was in the low normal range. Magnetic resonance imaging of the bilateral lower limb revealed bilaterally symmetrical abnormal edematous signal in muscles of the gluteal region, extensor, adductor, and flexor compartment indicative of myopathy. Volitional testing revealed the presence of spontaneous activity, and an electromyography study revealed that the interference pattern was complete with early recruitment, similar to what is seen in inflammatory myopathy. The motor unit action potential was polyphasic with short duration and amplitude. She was diagnosed with statin-induced myopathy with acute kidney injury. In this case, initiation of rosuvastatin and Vitamin D deficiency were the only positive associated factors that were responsible for myopathy and acute kidney injury and liver injury. Despite the reported incidence of myopathy and renal toxicity by rosuvastatin in the present era, rosuvastatin holds a major market across the globe. Although the case was successfully treated by withholding rosuvastatin, it added to significant morbidity and health-care costs. Therefore, this case report not only calls for increased pharmacovigilance when prescribing rosuvastatin but also adds to the already existing safety controversies surrounding this drug.

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