PSAT302 Hypothyroidism Induced Nontraumatic Rhabdomyolysis: a Rare Cause of a Potentially Fatal Condition

Abstract

Abstract Introduction Severe hypothyroidism can present with a vast array of clinical presentations, including musculoskeletal symptoms in up to 80% of patients. These symptoms can vary from simple muscle weakness and myalgias to rare complications such as rhabdomyolysis. Rhabdomyolysis, a syndrome characterized by degradation of muscle tissue, can occasionally lead to life-threatening complications including hyperkalemia, cardiac arrhythmias, and acute renal failure. We describe an interesting case of an otherwise healthy 19-year-old female with a past medical history of asthma who presented with nontraumatic rhabdomyolysis secondary to untreated hypothyroidism. Case description A 19-year-old female and college athlete of Asian descent with a past medical history of asthma presented to her primary care provider for acute and progressive swelling in her face, hands, and lower extremities bilaterally. In addition, she reported the onset of oligomenorrhea, decreased concentration, and myalgias for the past year. After relevant labwork was sent, the patient was found to have an extremely elevated TSH of 491.6 mIU/L with an undetectable level of free T4. She was referred for emergent hospital evaluation where notable lab findings included: creatinine 1.35 mg/dL, AST 300 IU/L, ALT 155 IU/L, LDH 888 IU/L, prolactin 41 ng/dL, and creatine kinase 8,380 IU/L. She was also found to be bradycardic (heart rate of 48 beats per minute) with low voltage QRS complexes on electrocardiography. She was admitted for treatment of newly diagnosed, severe hypothyroidism complicated by significant rhabdomyolysis. During her hospitalization, TPO antibodies were found to be negative however she was found to have a positive TSI level of 263% from baseline and positive antithyroglobulin of 6.7 units. Following treatment with weight-based intravenous levothyroxine (70 mcg daily), oral liothyronine (5 mcg twice daily), and intravenous fluid replacement with normal saline, the patient's condition and lab abnormalities improved significantly. She was eventually discharged and transitioned to oral levothyroxine (88 mcg). Seen in subsequent outpatient endocrinology follow-up, the patient has had normalization of all labs, including TSH, free T4, prolactin, creatinine kinase, and creatinine levels. She has experienced a complete resolution of myxedema symptoms and has had resumption of normal menses. Discussion Untreated or suboptimally treated hypothyroidism can be causative of various musculoskeletal manifestations including rhabdomyolysis. Hypothyroidism can induce muscle damage via various mechanisms including impaired glucose and triglyceride metabolism, glycosaminoglycan deposition in type I and II muscle fibers, decreased contractility of the actin-myosin unit and slowed ATP turnover. It is important to recognize hypothyroidism as a potential cause of non-traumatic rhabdomyolysis as prompt treatment with thyroid hormone can help prevent worsening muscle injury. As typically seen alongside myxedema with or without coma, treatment should be done in the inpatient setting with close hemodynamic and clinical monitoring and should include intravenous thyroid hormone, intravenous fluids and supportive care. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.