DOI: https://doi.org/10.36347/sjmcr.2025.v13i05.057

Pages: 1004-1007

Thyroid hormones, including thyroxine (T4) and triiodothyronine (T3), play a crucial role in regulating the basal metabolic rate of all cells, including hepatocytes, thereby influencing liver function. While hepatic dysfunction is frequently observed in hyperthyroidism, it is often mild and asymptomatic. However, cholestatic jaundice as a primary manifestation of hyperthyroidism is exceedingly rare. We report the case of a 33-year-old patient presenting with jaundice and pruritus. Laboratory tests revealed elevated alanine aminotransferase (1.4× upper limit of normal [ULN]), aspartate aminotransferase (1.6× ULN), alkaline phosphatase (3× ULN), gamma-glutamyl transferase (1.4× ULN), and bilirubin (183.4 μmol/L). Abdominal ultrasound was unremarkable, and extensive investigations ruled out toxic, drug-induced, infectious, autoimmune, and obstructive biliary causes. Thyroid function tests demonstrated elevated free T4 (23.6 pmol/L; normal: 9.01–19.05 pmol/L) with suppressed TSH (<0.005 µIU/mL; normal: 0.35–4.94 µIU/mL), and positive TSH receptor antibodies (8.3 IU/L; normal: <1.5 IU/L). Thyroid ultrasound revealed a diffuse, hypervascular goiter, confirming the diagnosis of Graves’ disease with hepatic involvement, in the absence of cardiac dysfunction. The patient’s condition improved significantly with carbimazole treatment. This case highlights the importance of considering hyperthyroidism in the differential diagnosis of unexplained cholestatic jaundice. Early recognition and appropriate management can prevent unnecessary interventions and ensure favorable outcomes.