ETHIONAMIDE-INDUCED HEPATITIS - REVIEW WITH REPORT OF ADDITIONAL CASE

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Abstract
A small percentage of patients treated with ethionamide developed hepatitis which was attributed to the toxicity of this drug. Although overt instances of jaundice are unusual, anicteric cases were found with variable frequency. Ethionamide-induced hepatitis seems to be a disease similar to infectious hepatitis that occurs occasionally in patients receiving ethionamide for the treatment of tuberculosis. The typical syndrome, which appears after 1 to 8 months of treatment, is characterized clinically by anorexia, nausea, vomiting, malaise, dark urine, and jaundice. Occasionally the latent period is as short as 10 or 11 days. Although its course is usually benign, several fatal cases were reported. An increase in serum transaminase activity is the most consistent laboratory abnormality. Serum bilirubin, brom-sulfophthalein retention, thymol turbidity, and alkaline phosphatase levels may range from normal to moderately elevated. Although the alkaline phosphatase is sometimes increased, the clinical picture does not suggest obstructive jaundice or cholangiolitic hepatitis. Liver biopsies, which were performed in several patients, have shown changes similar to those of infectious hepatitis. The disease probably represents a hypersensitivity reaction to ethionamide. This conclusion is based on the relative infrequency of liver toxicity, the great variation in length of the latent period, the subsidence of symptoms on cessation of the drug, and prompt recurrence on readministration of ethionamide. Fever has sometimes preceded or accompanied the hepatitis. One patient developed arthralgia and several, an erythematous rash, which persisted until ethionamide was stopped. Eosinophilia was present in some patients. The development of anorexia and nausea should alert the physician to the possibility of ethionamide-induced hepatitis. Severe liver damage may be averted by monitoring serum transaminase levels in patients receiving ethionamide. Prompt discontinuation of the medication will usually result in rapid clinical and laboratory improvement. Several intriguing aspects of this disorder merit further investigation. The first is the apparent increased susceptibility of diabetic patients to the development of ethionamide-induced hepatitis. The second is the virtual absence of ethionamide-induced liver disease in France, compared with its occasional occurrence in other Western countries, and its very high incidence in Japan.

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