Severe Rhabdomyolysis With Minimal Muscular Symptoms After Long-Term Rosuvastatin Use: A Case Report and Brief Literature Review
- 1Internal Medicine, Jackson Memorial Hospital, Miami, USA
- 2Surgery, University of Vermont Larner College of Medicine, Burlington, USA
Abstract
Severe rhabdomyolysis may present with limited muscular symptoms despite substantial biochemical injury. We describe a case of suspected statin-associated rhabdomyolysis during prolonged rosuvastatin exposure. A 65-year-old man with advanced chronic kidney disease, poorly controlled type 2 diabetes mellitus, peripheral arterial disease requiring bilateral below-knee amputations, and previous rhabdomyolysis presented with generalized weakness, abdominal discomfort, and left flank pain. He had taken rosuvastatin for more than 10 years. Admission investigations demonstrated creatine kinase of 23,107 U/L, creatinine of 7.80 mg/dL, markedly elevated aminotransferases, and brown urine. Creatine kinase subsequently peaked at 38,747 U/L despite limited muscular complaints. Progressive azotemia and encephalopathy prompted hemodialysis. Rosuvastatin was discontinued, and supportive treatment was provided without immunosuppression. The reported myositis panel was negative, while magnetic resonance imaging (MRI) demonstrated mild, nonspecific muscle edema. By discharge, weakness and encephalopathy had resolved, strength was preserved on focused examination, and creatine kinase had decreased to 1,003 U/L. The patient was advised to avoid all statins. Outpatient hemodialysis, rheumatology follow-up, and serial creatine kinase measurements were arranged, with anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase (anti-HMGCR) antibody testing and muscle biopsy planned if creatine kinase remained persistently elevated after discharge. This case highlights the discrepancy between biochemical severity and muscular symptoms during long-standing statin exposure. Improvement after statin withdrawal and supportive care supported a suspected statin-associated process but did not establish causality or exclude an autoimmune mechanism. Continued clinical and biochemical follow-up was essential to document recovery and determine the need for further investigation.
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BibTeX
@article{bidgoli2026severe,
title = {{Severe Rhabdomyolysis With Minimal Muscular Symptoms After Long-Term Rosuvastatin Use: A Case Report and Brief Literature Review}},
author = {Alireza Izadian Bidgoli and Alberto Gomez Usatorres and Hellen Ailette Gomez Usatorres and Alberto Gomez Veliz and Tariq Qayum},
journal = {Cureus},
year = {2026},
month = oct,
doi = {10.7759/cureus.117283},
url = {https://europepmc.org/article/PMC/PMC13723042},
note = {CC BY},
}
RIS
TY - JOUR
TI - Severe Rhabdomyolysis With Minimal Muscular Symptoms After Long-Term Rosuvastatin Use: A Case Report and Brief Literature Review
AU - Alireza Izadian Bidgoli
AU - Alberto Gomez Usatorres
AU - Hellen Ailette Gomez Usatorres
AU - Alberto Gomez Veliz
AU - Tariq Qayum
PY - 2026
DA - 2026/10/01
JO - Cureus
DO - 10.7759/cureus.117283
UR - https://europepmc.org/article/PMC/PMC13723042
AB - Severe rhabdomyolysis may present with limited muscular symptoms despite substantial biochemical injury. We describe a case of suspected statin-associated rhabdomyolysis during prolonged rosuvastatin exposure. A 65-year-old man with advanced chronic kidney disease, poorly controlled type 2 diabetes mellitus, peripheral arterial disease requiring bilateral below-knee amputations, and previous rhabdomyolysis presented with generalized weakness, abdominal discomfort, and left flank pain. He had taken rosuvastatin for more than 10 years. Admission investigations demonstrated creatine kinase of 23,107 U/L, creatinine of 7.80 mg/dL, markedly elevated aminotransferases, and brown urine. Creatine kinase subsequently peaked at 38,747 U/L despite limited muscular complaints. Progressive azotemia and encephalopathy prompted hemodialysis. Rosuvastatin was discontinued, and supportive treatment was provided without immunosuppression. The reported myositis panel was negative, while magnetic resonance imaging (MRI) demonstrated mild, nonspecific muscle edema. By discharge, weakness and encephalopathy had resolved, strength was preserved on focused examination, and creatine kinase had decreased to 1,003 U/L. The patient was advised to avoid all statins. Outpatient hemodialysis, rheumatology follow-up, and serial creatine kinase measurements were arranged, with anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase (anti-HMGCR) antibody testing and muscle biopsy planned if creatine kinase remained persistently elevated after discharge. This case highlights the discrepancy between biochemical severity and muscular symptoms during long-standing statin exposure. Improvement after statin withdrawal and supportive care supported a suspected statin-associated process but did not establish causality or exclude an autoimmune mechanism. Continued clinical and biochemical follow-up was essential to document recovery and determine the need for further investigation.
SN - 2168-8184
ER -