Herpes zoster–induced critical rhabdomyolysis with secondary hypothyroidism: a case report

Primary varicella-zoster virus (VZV) reactivation causes herpes zoster (HZ), typically presenting with dermatomal rash and neuropathic pain. Rhabdomyolysis as a systemic complication of HZ is extremely rare, and its underlying pathogenesis and optimal management remain poorly characterized, especially in elderly patients. Here we report a 63-year-old female who presented with fever, generalized myalgia, and oliguria, with serum creatine kinase (CK) rapidly escalating from 4,383 U/L to a peak of 186,383 U/L. Further investigation revealed a preceding history of lumbar herpes zoster two weeks prior, accompanied by virus-induced secondary hypothyroidism. Muscle biopsy confirmed extensive myofiber necrosis without inflammatory infiltration, consistent with non-inflammatory rhabdomyolysis. The patient developed acute kidney injury, hepatic dysfunction, and respiratory failure, and was managed with multidisciplinary intensive care including mechanical ventilation, 9 days of continuous renal replacement therapy, glucocorticoid anti-inflammatory therapy, and levothyroxine replacement. After 12 days of treatment, CK decreased to 3,381 U/L with significant recovery of multiorgan function, and the patient was transferred out of the intensive care unit. This case highlights that HZ can trigger life-threatening rhabdomyolysis, possibly via VZV-mediated immune dysregulation and secondary hypothyroidism. Detailed history taking, early CK screening, and multidisciplinary organ support are critical to improve outcomes in this rare but severe condition.