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Risk factors for isoniazid (NIH)-induced liver dysfunction

D S Dickinson, W C Bailey, B I Hirschowitz

    Journal of Clinical Gastroenterology
    |September 1, 1981
    PubMed
    Summary
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    Isoniazid (INH) preventive therapy can cause liver damage. Slow acetylators and older age increase the risk of INH-induced liver injury, with fast acetylation potentially being protective.

    Area of Science:

    • Hepatology
    • Pharmacology
    • Infectious Diseases

    Background:

    • Isoniazid (INH) is a cornerstone of tuberculosis (TB) treatment and prophylaxis.
    • Hepatotoxicity is a significant concern associated with INH therapy.
    • Identifying risk factors for INH-induced liver injury is crucial for patient safety.

    Purpose of the Study:

    • To prospectively identify risk factors for isoniazid-induced liver damage.
    • To evaluate the role of acetylator phenotype, age, and alcohol consumption in INH hepatotoxicity.

    Main Methods:

    • Prospective examination of 113 patients receiving INH preventive therapy for at least 8 weeks.
    • Monitoring of liver function tests and assessment of patient demographics, including age and alcohol use.
    • Analysis of acetylator phenotype (fast vs. slow) in relation to liver enzyme elevations.

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    Main Results:

    • 19 out of 101 patients with normal baseline liver tests developed significant liver dysfunction.
    • Slow acetylator phenotype and older age (>35 years) were identified as significant risk factors for INH-induced liver injury.
    • The risk of liver enzyme elevation increased with age and slow acetylation, with the highest risk observed in older slow acetylators (37%).
    • Fast acetylation appeared to be associated with a lower risk of liver dysfunction.

    Conclusions:

    • Slow acetylator phenotype and advanced age are significant risk factors for INH-induced liver damage.
    • Fast acetylation may be a protective factor against INH hepatotoxicity.
    • Risk stratification based on age and acetylator status can help predict and potentially mitigate INH-induced liver injury.