摘要：Hepatic dysfunction during hyperthyroidism frequently occurs with mild abnormalities in liver function tests that are self-limited, improving after treatment of thyroid disease. With the exception of congestive heart failure or secondary hepatic disease, significant hepatic compromise during thyrotoxicosis is rare and often of unexplained origin. This report identifies a novel case of severe hepatic compromise in the setting of thyrotoxicosis that was not initially identified due to a falsely elevated TSH. A 43-year-old African-American man presented to the intensive care unit with severe jaundice, weight loss, thyroid bruit and altered mental status. Initial diagnosis of hyperthyroidism was delayed due to a non-suppressed TSH of 0.20 μU/mL. Laboratory studies identified dramatic hepatic synthetic dysfunction and elevated transaminases with a total bilirubin of 47.4 mg/dL, AST 259 U/L, and ALT 142 U/L. No toxins, structural or viral causes of liver disease were identified and the patient was prepared for potential liver biopsy. Heterophile antibodies were identified and removed by precipitation, demonstrating an undetectable TSH and free thyroxine 9.0 ng/dL consistent with hyperthyroidism. Subsequent treatment with thionamides, corticosteroids, and potassium iodide improved both thyroid and liver function and avoided unnecessary invasive testing. Heterophile antibodies remain as important interfering factors in TSH immunoassays, and thus, this case demonstrates the importance of matching the clinical picture with available laboratory data. In the absence of a known cause of hepatic dysfunction, hyperthyroidism should be considered as a potential etiology of acute liver failure of unknown origin.
关键词：Thyrotoxicosis ; Human anti-mouse antibodies (HAMA) ; Hyperbilirubinemia ; UDP-glucuronosyltransferase
