Case Presentation: A 55 year-old-male with ischemic cardiomyopathy and hypertension presented with 1 week of abdominal bloating, jaundice, and lower extremity edema. He denied any alcohol, drug, or supplement use. He reported only taking Tylenol 1000mg twice per week. On initial presentation, his vital signs were stable except for mild tachycardia. On exam, he was thin with jaundice, bilateral scleral icterus, and 2+ lower extremity edema. His labs were notable for total bilirubin 18.4, direct bilirubin 13, alkaline phosphatase 132, AST 84, ALT 106, and INR 1.4. A liver ultrasound and MRCP did not reveal any liver or biliary etiology to explain his acute liver injury. Further workup of acute liver injury, including hepatitis, CMV, EBV, autoimmune hepatitis, and primary biliary cirrhosis, were negative. His thyroid function tests were abnormal with a TSH less than 0.01 and free T4 of 5.29. Thyroid peroxidase antibody, thyrotropin receptor antibody, and thyroid-stimulating immunoglobulin were significantly elevated consistent with Graves disease. He was initiated on Methimazole, and his liver function tests subsequently improved.
Discussion: Hyperthyroidism is caused by the excess release of thyroid hormone and manifests in a wide variety of clinical presentations, including anxiety, palpitations, and weight loss. Abnormal liver function tests is frequently seen in patients who have hyperthyroidism with its prevalence ranging from 15-79%. More rarely, patients with hyperthyroidism present with a cholestatic pattern of liver injury and severe hyperbilirubinemia with one such study noting a 9% incidence rate. The etiology of acute liver injury with or without severe hyperbilirubinemia is not well-established. It is thought that excess thyroid hormone can increase mitochondrial oxygen consumption. This produces more free oxygen radicals leading to increased oxidative stress of hepatocytes and subsequent apoptosis. Treatment of hyperthyroidism with medications such as Methimazole can minimize this process. Although one of Methimazole’s well-known adverse reactions is hepatotoxicity, the benefit of starting this medication likely outweighs this risk, especially in the case of severe cholestasis and/or impending thyroid storm.
Conclusions: A patient with abnormal liver function tests is commonly diagnosed with a hepatic or biliary pathology. Once that is ruled out, it is essential to look for alternative causes outside of the hepatobiliary system with one such cause being hyperthyroidism or Graves disease. Abnormal liver function tests in hyperthyroidism is routinely associated with a hepatocellular pattern of liver injury. Less frequently, patients can also present with severe hyperbilirubinemia and a cholestatic pattern of liver injury. A timely diagnosis and expedited treatment of hyperthyroidism can improve a patient’s liver function tests and overall symptoms.