Journal of the Pediatric Infectious Diseases Society · 2014
Hepatotoxicity in Children Receiving Isoniazid Therapy for Latent Tuberculosis Infection.
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Chang Shiow-Huey, Nahid Payam, Eitzman Sarah R
Аннотация
BACKGROUND: The frequency of isoniazid hepatotoxicity is low in children receiving isoniazid therapy for latent tuberculosis infection. However, isoniazid hepatotoxicity may cause liver failure and death. We evaluated children who developed isoniazid hepatotoxicity to determine demographic and clinical characteristics.
METHODS: A retrospective review was performed of medical records of 1582 patients aged <18 years who were evaluated for isoniazid therapy at a public health department and clinic in California.
RESULTS: There were 13 patients who had latent tuberculosis infection and who developed isoniazid hepatotoxicity (0.8% of all 1582 patients who started isoniazid; 1.1% of 1235 patients who completed the 9-month isoniazid therapy). There were 8 girls (62%) and 9 Hispanic children (69%) who had hepatotoxicity. Sex, age, and race were not independently associated with the development of isoniazid hepatotoxicity. Symptoms and signs of hepatotoxicity were present in 11 of the 13 patients, and 2 other patients had alanine aminotransferase >5 times the upper limit of normal and no signs of hepatotoxicity. The most common symptoms included abdominal pain, anorexia, vomiting, and nausea. Most patients developed hepatotoxicity within 6 months of starting isoniazid, but 3 patients developed hepatotoxicity ≥6 months after starting isoniazid. After stopping isoniazid, the alanine aminotransferase levels decreased to normal in all patients.
CONCLUSIONS: In children who have latent tuberculosis infection, isoniazid hepatotoxicity has low frequency and typically is reversible when isoniazid is stopped. Evidence of late drug-induced liver injury indicates the importance of monitoring symptoms and serum transaminases throughout isoniazid therapy.
METHODS: A retrospective review was performed of medical records of 1582 patients aged <18 years who were evaluated for isoniazid therapy at a public health department and clinic in California.
RESULTS: There were 13 patients who had latent tuberculosis infection and who developed isoniazid hepatotoxicity (0.8% of all 1582 patients who started isoniazid; 1.1% of 1235 patients who completed the 9-month isoniazid therapy). There were 8 girls (62%) and 9 Hispanic children (69%) who had hepatotoxicity. Sex, age, and race were not independently associated with the development of isoniazid hepatotoxicity. Symptoms and signs of hepatotoxicity were present in 11 of the 13 patients, and 2 other patients had alanine aminotransferase >5 times the upper limit of normal and no signs of hepatotoxicity. The most common symptoms included abdominal pain, anorexia, vomiting, and nausea. Most patients developed hepatotoxicity within 6 months of starting isoniazid, but 3 patients developed hepatotoxicity ≥6 months after starting isoniazid. After stopping isoniazid, the alanine aminotransferase levels decreased to normal in all patients.
CONCLUSIONS: In children who have latent tuberculosis infection, isoniazid hepatotoxicity has low frequency and typically is reversible when isoniazid is stopped. Evidence of late drug-induced liver injury indicates the importance of monitoring symptoms and serum transaminases throughout isoniazid therapy.