MON-381 - The Masked Marauder: A Case of Hypothyroidism-Induced Rhabdomyolysis

Rhabdomyolysis is a potentially fatal condition characterized by skeletal muscle breakdown and release of intracellular contents, including myoglobin and creatinine kinase (CK), into the bloodstream. While common etiologies include trauma, exertion, and medication toxicity (e.g. statins), endocrine causes such as hypothyroidism are uncommon and can be overlooked. Hypothyroidism is a hypometabolic state due to insufficient thyroid hormone synthesis, and can lead to muscle injury, impaired gluconeogenesis, and mitochondrial dysfunction. Hypothyroidism-induced rhabdomyolysis is a rare yet life-threatening condition. The few published cases report muscular-predominant symptoms with minimal signs of thyroid dysfunction. While nonspecific features may contribute to diagnostic delay, this condition is reversible once identified and treated.

Our patient is a 75-year-old female with a history of autoimmune hypothyroidism and hyperlipidemia, who presented with progressive weakness and functional decline over several months. Her initial vitals demonstrated a blood pressure of 182/99, a heart rate of 60, and a respiratory rate of 19. Physical exam notable for an anxious mood and non-pitting lower extremity edema. Laboratory evaluation revealed acute kidney injury with an elevated serum creatinine of 9.72, from a baseline of 1.05 mg/dL, and urinalysis with 3+ blood in the absence of red blood cells, consistent with myoglobinuria. Broadened testing revealed a CK of 25,000 IU/L, thyroid-stimulating hormone level of 91 uIU/mL, and an undetectable T4. The patient was diagnosed with rhabdomyolysis secondary to severe hypothyroidism and treated with aggressive intravenous fluid resuscitation and levothyroxine therapy. Over the hospital course, CK levels progressively declined, and renal function improved without dialysis.

Hypothyroidism can cause rhabdomyolysis in the absence of typical precipitants, such as statins or strenuous activity. Recognition is critical, and delayed diagnosis can lead to significant morbidity. Nonspecific presentations, particularly in the absence of classic hypothyroid symptoms, can lead clinicians to prioritize more common etiologies of rhabdomyolysis and delay appropriate therapy. Treatment includes supportive care and thyroid hormone replacement. Early screening for thyroid dysfunction in patients with suspected rhabdomyolysis is recommended, particularly in the setting of the unique features of insidious, unprovoked myalgias, and disproportionately elevated CK levels to the severity of myalgias. Routine evaluation of thyroid function should also be considered in unexplained cases of rhabdomyolysis. This case addresses the diagnostic challenges of recognizing hypothyroidism in the differential diagnosis of rhabdomyolysis. Prompt recognition and treatment can prevent complications and lead to complete recovery.

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