Abstract

BackgroundThiamazole is a widely used antithyroid agent that has been approved for the treatment of hyperthyroidism. Although thiamazole-induced hepatotoxicity is a main side effect, it may progress to liver failure in a very few cases.Case PresentationWe described a 24-year-old patient with hyperthyroidism and trilogy of Fallot, who developed liver failure due to thiamazole. Liver biopsy showed intrahepatic cholestasis, mild inflammatory infiltrates, as well as significant fibrosis, indicating both acute and chronic liver injuries. Although a series of potent therapies were given, the patient deceased due to severe liver decompensation.ConclusionsThis case suggests that thiamazole-induced hepatotoxicity in the setting of advanced fibrosis increases the risk of poor outcome. Regular liver function monitoring during thiamazole therapy is therefore important.

Highlights

  • Thiamazole is a widely used antithyroid agent that has been approved for the treatment of hyperthyroidism

  • This case suggests that thiamazole-induced hepatotoxicity in the setting of advanced fibrosis increases the risk of poor outcome

  • We report the first case of a patient with hyperthyroidism and Trilogy of Fallot (TOF) that was recently referred to our hospital for acute-on-chronic liver failure (ACLF) related to MMI

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Summary

Background

Liver dysfunction is a common complication observed in hyperthyroidism, either as a result of hyperthyroidism and/or the use of antithyroid drugs (ADs). ADs including thiamazole (MMI) and propylthiouracil (PTU) are widely used for treating hyperthyroidism Despite their relatively safe profiles, both can induce hepatotoxicity presenting as hepatocellular or cholestatic injury [1,2,3,4,5,6]; liver failure has rarely been encountered. Case Presentation A 24-year-old man was admitted to our hospital due to diarrhea, progressive jaundice, light stool, fatigue and excessive sweating for 18 days He was diagnosed with TOF at age 3, and had undergone pulmonary valvotomy and closure of the foramen ovale at age 19. MMI (20 mg per day) was continuously taken by himself for 20 days prior to the onset of the symptoms, which, did not arouse his alertness, and MMI administration was continued until his admission He denied use of any other concomitant prescriptions (including non-ADs), over-the-counter drugs or herbal remedies. Mechanical ventilation and intensive therapies were applied, the progression of his medical conditions could not be suspended, and he eventually expired as a result of multiple organ failure on day 27 after admission

Conclusions
Findings
Cooper DS
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