Abstract
Introduction: Propylthiouracil rarely triggers liver toxicity, generally, subclinical and transient. Fatal forms can occur. The pathogenesis point to an allergic response of the host, however, the drug can trigger chronic autoimmune hepatitis.
Objective: To report a Graves disease patient who developed fulminant hepatitis under propylthiouracil, with favorable outcome after medication withdrawal.
Case Report: A women with 36 years of age with Graves? hyperthyroidism referred cutaneous rash under methimazole therapy. At the diagnosis, TSH<0.01 mIU/mL (Reference values, RV:0.35-4.2), FT4>7.77 ng/dL (RV 0.9-1.8), TPOAb=138 IU/mL (RV<35 IU/mL), TgAb=166 IU/mL (RV><115). The drug had changed to PTU 300mg/day and after 4 weeks, she developed acute hepatitis, needing intensive care. Laboratorially: ALT=310 U/L (RV:0-55), AST=268 U/L (RV:0-34), alkaline phosphatase=390 U/L (RV><104), GGT 218 U/L (RV><42), total bilirubin=30.3 mg/dL (RV:0.2-1.2), direct bilirubin=22.02 mg/dL (RV:0.1-0.5), indirect bilirubin=8.3 mg/dL, INR=9.5 (RV=1-1.3), R=3.3 (RV><1.26), albumin=2.1 g/dL (RV:3.5-5.2), anti-nuclear factor=1:80 stippled fine (RV=negative). We excluded the diagnosis of A, B and C hepatitis. Liver biopsy: sub-acute hepatitis with massive necrosis and hepatocellular regeneration in pseudo-rosettes, not allowed differentiate the etiology, autoimmune or drug. Ultrassonography: chronic hepatitis. After propyltiouracil withdrawal and corticosteroid administration the transaminases normalized in 8 weeks. The patient was submitted to radioiodinetherapy. Currently, maintains TSH=0.02 mIU/mL and FT4=2.1 ng/dL.
Conclusions: Hepatotoxicity by propyltiouracil can promote serious damages to the patient and should be promptly recognized. Facing the diagnosis, the early withdrawal of tionamide is a key to the satisfactory outcome. There is great difficulty in the differential diagnosis between autoimmune hepatitis and hepatotoxicity by propyltiouracil.