Antithyroid drugs (ATDs) have been widely and effectively used for the treatment of pediatric and adult
thyrotoxicosis for more than a half century. Since the very beginning of ATD use, reports of hepatic dysfunction related to
propylthiouracil (PTU)
therapy have been published. We describe a case of a 12-year-old girl, who, after 4 weeks of
therapy for
Graves disease (GD) with PTU (300 mg/day at 100 mg given three times a day), developed
fatigue,
fever,
diarrhea,
nausea, and
vomiting. The initial diagnosis was "viral gastrointestinal
infection". Few days after the initiation of her symptoms, the patient developed
jaundice, hepatic tenderness, and dark urine. She was admitted to the hospital where, after an extensive investigation, it was found that
serum glutamic oxaloacetic transaminase (
SGOT) and serum
glutamic pyruvic transaminase (
SGPT) were elevated (2312 and 1435 IU/L, respectively),
alkaline phosphatase (ALP) was 171 IU/L and total
bilirubin was 12.7 mg/dL, whereas direct
bilirubin was 7.6 mg/dL and prothrombin time was 23.2 s (normal ratio, < 14.5 s). Serology for
hepatitis A and B was negative. The diagnosis of PTU-induced
hepatitis was established. PTU was discontinued, and a treatment with
prednisone (50 mg/day) and
vitamin K was initiated. Four weeks after admission, her hepatic tests returned to normal. We searched the English literature and we present details of all cases with PTU-related hepatic toxicity in children and adolescents published so far. Also, we provide information regarding the mechanisms and treatment of this appalling clinical entity. Finally, after recent recommendations from American Thyroid Association (ATA) and European Thyroid Association (ETA), PTU should be administered only in the first trimester of pregnancy and in cases of
drug allergy to
methimazole.