Case Presentation: A 49-year-old male presented with altered mental status and diffuse body pain. He denied any alcohol or drug intoxication, chest pain, shortness of breath, or infectious symptoms. His past history included chronic hypothyroidism and alcoholism. He had a temperature of 36.8 degrees Celsius with a heart rate of 96 bpm and was alert and oriented to person only. He had hepatomegaly with diffuse abdominal tenderness without rebound or guarding. There was no scleral icterus, spider angiomas, or asterixis. Extremities were warm and non-edematous. Venous blood gas showed pH 7.44 and pCO2 38 mmHg. A complete blood count revealed hemoglobin 10.5 g/dL, mean corpuscular volume 106.5 fL, and platelets 51 K/cumm without leukocytosis. Other labs included sodium 125 mmol/L, chloride 83 mmol/L, bicarbonate 21 mmol/L, BUN 17 mg/dL, creatinine 1.47 mg/dL, alkaline phosphatase 836 U/L, AST 1,501 U/L, ALT 441 U/L, total bilirubin 11.6 mg/dL, and direct bilirubin 9.5 mg/dL. Hepatitis panel and urine toxicology were negative and acetaminophen and ethanol levels were normal. Creatine kinase was elevated to 16,006 U/L. Thyroid stimulating hormone was elevated to 57.86 uIU/ml with free T4 less than 0.11 ng/dL. Random cortisol was normal at 10.5 mcg/dL. Lipid panel showed cholesterol 612 mg/dL, HDL 24 mg/dL, direct LDL 30 mg/dL, and triglyceride 2,424 mg/dL. CT scan of his head was normal and a right upper quadrant ultrasound showed hepatic steatosis without stones or common bile duct dilation. Following a discussion with Endocrinology and Hepatology, he was treated for myxedema coma with Levothyroxine 500 mg IV and maintained on 100 mg IV daily. He became alert and oriented to person, place, and time within 12 hours. The patient was discharged in stable condition on hospital day 5 and upon discharge, his AST and ALT had downtrended to 117 and 209 U/L, respectively, with total bilirubin 3.3 mg/dL, direct bilirubin 1.9 mg/dL, and triglycerides 546 mg/dL.
Discussion: This case represents an unusual presentation of myxedema coma. The patient was not edematous, hypothermic, or hypercapnic. He had hyponatremia, which is common in myxedema coma due to decreased free water excretion. Although transaminitis is also common and was likely also elevated given concurrent rhabdomyolysis, cholestatic patterns are not routinely observed and may be correlated with the pro-relaxing effects of thyroxine on the Sphincter of Oddi. Hyperlipidemia has also been described in chronic hypothyroidism and myxedema coma. However per our literature review, this may be one of the most severe documented cases of hypertriglyceridemia in myxedema coma.
Conclusions: Clinicians should be vigilant of these potential systemic abnormalities when treating patients with myxedema coma.