An adolescent cirl with severe longstanding hyperthyro aism, poor response to propylthiouracil and two previous episoces of au^dice, had clinical,y oclive hyperhyroidisn during propylthiouracil treatment, *ogethe r with jaundice and liver enargemert. The etiologic study of her hepa'ic disease was oriented to several posibilities of hepatic dysfunction including d r ug ^oxicity, cardiac failure, hyperthyrcidism by its own and autoimmune hepcritis. Conrrol of hyperthircidism was eventually achieved by stoping propylthiouracil administration and a management schedule that included high calory diet, propanolol and two doses of I 13] . Labo'atory workup showed high serum total and direct oillirrubin, SGOT, SPT and plasma garnmaglobulin levels. Liver biopsy specimens showed mononuclear and polinuclear inflamatory infi'trates, with moderate fibrosis, mic'ovccualated hepotocytes and hepatocelluiar necrosis, which were considered to be consisrent with ch'onically active hepatitis, that has been managed with oral prednisone. Liver functional tests became normal two months after supression of t^e antithyroid drug and one month after begining stero^cal treatment. Two months later reduction or 'he inflarratory reaction but persistent hepatic cell necrosis was shown oy the second liver biopsy.