Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Drugs that induce systemic lupus erythematosus inhibit complement component C4.

E Sim, E W Gill, R B Sim

    Lancet (London, England)
    |August 25, 1984
    PubMed
    Summary

    Long-term use of hydralazine and isoniazid can cause a lupus-like syndrome by inhibiting complement C4. Drug metabolites do not appear to cause this immune complex deposition, suggesting the parent drugs are responsible.

    Related Concept Videos

    You might also read

    Related Articles

    Articles linked to this work by shared authors, journal, and citation graph.

    Sort by
    Same author

    'Who Listens to the Listener, Who Cares for the Carer?' A Cross-Sectional Study of Social Connectedness and Sleep Experiences of Young Siblings of Neurodivergent People.

    Child: care, health and development·2024
    Same author

    C2 by-pass: Cross-talk between the complement classical and alternative pathways.

    Immunobiology·2022
    Same author

    Human VEGF165-myoblasts produce concomitant angiogenesis/myogenesis in the regenerative heart.

    Molecular and cellular biochemistry·2016
    Same author

    Complement research in the 18th-21st centuries: Progress comes with new technology.

    Immunobiology·2016
    Same author

    Multivariate assessment of site of lingual nerve.

    The British journal of oral & maxillofacial surgery·2015
    Same author

    Complement system proteins which interact with C3b or C4b A superfamily of structurally related proteins.

    Immunology today·2014

    Area of Science:

    • Immunology
    • Pharmacology
    • Rheumatology

    Background:

    • Long-term use of hydralazine and isoniazid is associated with a syndrome resembling systemic lupus erythematosus (SLE).
    • The exact mechanism underlying this drug-induced SLE remains unclear, but immune complex deposition is implicated.
    • The complement system, particularly C4, plays a crucial role in immune complex clearance.

    Purpose of the Study:

    • To investigate whether hydralazine and isoniazid, or their metabolites, are responsible for inhibiting complement C4.
    • To determine if this inhibition contributes to immune complex deposition in drug-induced SLE.
    • To compare the inhibitory effects of the parent drugs and their metabolites on C4 binding.

    Main Methods:

    • In vitro experiments were conducted to assess the effect of hydralazine and isoniazid on C4 binding.

    Related Experiment Videos

  • Concentrations of drugs and metabolites tested were relevant to therapeutic ranges.
  • The inhibitory concentrations of parent drugs and metabolites were compared to iproniazid, a non-SLE-inducing drug.

    • Main Results:

    • Hydralazine and isoniazid directly inhibited C4 binding in a dose-dependent manner.
    • Inhibitory concentrations of hydralazine and isoniazid were within therapeutic ranges.
    • Acetylated metabolites of these drugs showed no significant inhibition of C4 binding.
    • Iproniazid demonstrated minimal C4 inhibition at concentrations far exceeding therapeutic use.

    Conclusions:

    • Hydralazine and isoniazid, the parent drugs, are likely responsible for inhibiting complement C4.
    • This inhibition may lead to increased immune complex deposition, contributing to the SLE-like syndrome.
    • The findings highlight a potential mechanism for drug-induced autoimmunity and suggest caution in long-term use of these medications.