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Abstract
Standard antituberculous therapy, including isoniazid (INH), rifampin, ethambutol, and pyrazinamide (PZA), is widely used to treat active tuberculosis. The most important side effect is hepatotoxicity. In a standard four-drug regimen, PZA was the most common cause of drug-induced hepatitis and was dose-related. The incidence of drug-induced hepatitis is high at doses of 40~70 mg/kg per day but has fallen significantly since the recommended dose was reduced. Liver toxicity induced by PZA is rare at doses of 25 mg/kg per day or less. PZA-induced fulminant hepatic failure is also rare but fatal. We report a case of fulminant hepatic failure caused by a re-challenge of PZA.
Figures and Tables
Figure 1
The radiographic study of chest showed poorly defined patch opacity in right upper lung zone. There was poorly defined nodular opacities in left middle lung zone. There was ill defined hazy opacity in right lower lung zone. The both costophrenic angle blunting was noted.
Figure 2
The Contrast enhanced CT scans of the chest showed low attenuation lesion in a bronchus lumen of right middle lobe and atelectasis. Both pleural effusion was noted. There was linear branching nodular opacity and ground glass opacity in both lung fields. No definite lymphadenopathy in mediastinum was noted.
Figure 3
The clinical course of patient since admission. All antitubercular drugs were withdrawn initially. AST decreased on the 4th day, and total bilirubin also decreased a week after. Pyrazinamide 500 mg was administered on Day 18, the patient developed nausea, vomiting, and high fever the next day. Hepatic encephalopathy was manifested three days later. The patient expired two days later.
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