Key result
High-dose atorvastatin plus ticagrelor linked to severe rhabdomyolysis and acute kidney injury at ~2 months.
Why the study?
Delayed-onset presentations of statin-induced rhabdomyolysis after uneventful use are uncommon and can delay diagnosis.
Case Report (n=1)
No
Co-administration of high-dose atorvastatin and ticagrelor can lead to delayed-onset severe rhabdomyolysis, particularly in patients with underlying renal impairment, necessitating vigilance and consideration of alternative statins.
Answers are grounded in this paper and cite their sources.
May warrant monitoring for delayed rhabdomyolysis with high-dose atorvastatin plus ticagrelor; hypothesis-generating case report leaves causality and incidence open.
Rhabdomyolysis is a rare but potentially life-threatening complication of statin therapy, typically occurring within days to weeks (mean onset approximately nine days) after initiation or dose escalation. Delayed-onset presentations after a period of uneventful use are uncommon and may delay diagnosis. We report a 62-year-old man with ischemic heart disease and chronic kidney disease (CKD stage 3a) who developed a five-day history of bilateral lower limb pain, difficulty ambulating, and dark-colored urine. During a routine post-percutaneous coronary intervention (PCI) follow-up visit, subtle lower limb weakness was incidentally noted by his cardiologist, prompting immediate referral to the emergency department for further evaluation. He had been initiated on high-intensity atorvastatin (80 mg daily) two months following PCI. There was no history of trauma, immobilization, or recent strenuous physical activity. Laboratory investigations revealed a creatine kinase level peaking at 245,550 U/L (normal <190 U/L) and a serum creatinine of 5.22 mg/dL (normal 0.7-1.2 mg/dL, patient baseline 1.6 mg/dL), consistent with severe rhabdomyolysis complicated by acute kidney injury. Urine dipstick testing was positive for blood, while microscopic examination showed few red blood cells, consistent with myoglobinuria rather than hematuria; the autoimmune myositis workup was negative. Atorvastatin was discontinued on admission, and the patient was managed with aggressive intravenous fluid resuscitation. Renal function initially worsened but subsequently recovered without the need for renal replacement therapy. This case highlights that statin-associated muscle toxicity can occur after a period of prior tolerance. It may present in a delayed fashion, particularly when a CYP3A4 inhibitor such as ticagrelor is co-administered. Early recognition and prompt withdrawal of the offending agent are essential to prevent severe complications. In patients requiring ongoing lipid-lowering therapy, consideration should be given to alternative agents with minimal CYP3A4 metabolism and lower potential for clinically significant drug interactions.
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Ansar et al. (2026) conducted a case report in Statin-induced rhabdomyolysis (n=1). Atorvastatin and Ticagrelor was evaluated on Creatine kinase level and renal function. Co-administration of high-dose atorvastatin and ticagrelor led to delayed-onset severe rhabdomyolysis (peak CK 245,550 U/L) and acute kidney injury two months after initiation.
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