A 40-year-old woman with postablative hypothyroidism from Graves Disease presented with 3 weeks of fatigue and myalgias. She reported severe constipation and worsening bilateral anterior thigh pain exacerbated by movement. Physical examination revealed a depressed, flat affect, bilateral exophthalmos, dry skin with pretibial edema, and hypoactive bowel sounds. Strength and reflexes were intact and symmetric, but there was tenderness to palpation of the proximal muscles of both upper and lower extremities. No visible bruising or injuries noted to suggest undisclosed recent trauma. Initial labs were significant for creatine kinase (CK) 4163 U/L (normal 35-200), creatinine 1.8 mg/dl (0.7-1.2), moderate blood with 2 RBC on urinalysis, serum myoglobin 175 ng/mL (25-58), thyroid stimulating hormone (TSH) 57.3 microU/ml (0.4-4.7), and free T4 0.1 ng/dL (0.7-1.8). She was subsequently admitted for suspected rhabdomyolysis with acute kidney injury from uncontrolled hypothyroidism. Rhabdomyolysis and kidney injury resolved with aggressive hydration. Within 6 months of adequate levothyroxine treatment, TSH normalized and constipation and weakness resolved.
Rhabdomyolysis is commonly seen on the inpatient medicine wards. Though treatment with hydration and supportive care generally results in resolution of metabolic abnormalities and muscle pain, the condition may recur if an underlying cause is not identified and treated. Hypothyroid induced muscle disorders often cause mild CK elevation. However, in most cases described in the literature, the development of significant rhabdomyolysis in hypothyroidism was precipitated by another pathogenetic factor such as hypoxia, hypotension, medications, trauma, or exercise. Our patient had no such identifiable risk factors, suggesting that uncontrolled hypothyroidism alone can result in clinically significant rhabdomyolysis. The pathophysiology behind thyroid induced muscle injury is unclear but thyroid hormones are known to play an important role in regulating glycogenolysis, lipid metabolism, protein synthesis, and mitochondrial oxidative metabolism. Thyroxine deficiency may lead to changes in muscle fibers, deposition of glycosaminoglycans, poor contractility of actin-myosin units, low myosin ATPase activity, and low ATP turnover in skeletal muscle. These injuries would result in increased sarcoplasmic calcium and persistent muscle contraction, ultimately causing muscle fiber necrosis and leakage of muscle-cell contents including potassium, phosphates, myoglobin, CK, and uric acid into the extracellular space and bloodstream.
Hypothyroidism should be considered in patients presenting with rhabdomyolysis for whom an alternate etiology is not immediately clear. Identifying and treating this underlying disease could prevent recurrence of muscle breakdown in patients with hypothyroidism.
To cite this abstract:Pham A, Chang S. Rhabdomyolysis with Kidney Injury in a Patient with Uncontrolled Hypothyroidism. Abstract published at Hospital Medicine 2015, March 29-April 1, National Harbor, Md. Abstract 653. Journal of Hospital Medicine. 2015; 10 (suppl 2). https://www.shmabstracts.com/abstract/rhabdomyolysis-with-kidney-injury-in-a-patient-with-uncontrolled-hypothyroidism/. Accessed January 24, 2020.