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Genetic and immunologic studies of patients on procainamide

L E Adams1, K Balakrishnan, S Malik

  • 1Department of Medicine, University of Cincinnati Medical Center, Ohio 45267-0563, USA.

Human Immunology
|April 21, 1998
PubMed

Insights

Procainamide (PA) therapy for cardiac arrhythmias is linked to increased class III C4 complement allotypes and DQw3 phenotypes. Genetic factors may influence patient response to PA treatment.

Area of Science:

  • Immunogenetics
  • Pharmacogenetics
  • Cardiology

Background:

  • Cardiac arrhythmias necessitate drug therapies like procainamide (PA).
  • Genetic factors can influence drug efficacy and adverse reactions.
  • Human Leukocyte Antigen (HLA) and complement system variations are implicated in immune responses.

Purpose of the Study:

  • To investigate associations between HLA class II, DQB1*03 subtypes, and complement C4 allotypes in patients receiving PA.
  • To evaluate the role of acetylation phenotype and cytokine production (IL-1 beta, TNF alpha) in PA-treated patients.
  • To identify potential genetic markers influencing host responsiveness to PA therapy.

Main Methods:

  • Analysis of HLA class II phenotypes (DRB1*04, DQB1*03) in 40 PA patients and 24 controls.
  • Assessment of complement C4 null alleles and acetylation phenotype in PA patients.
  • Measurement of Interleukin-1 beta and Tumor Necrosis Factor alpha secretion by stimulated cells and peripheral blood leukocytes.

Main Results:

  • No association found between acetylation phenotype and HLA class II or C4 allotypes.
  • Significant increase in class III C4 complement allotypes in PA patients compared to controls.
  • Significant increase in autoantibodies and DQw3 phenotypes observed in the PA patient group.
  • Spontaneous IL-1 and TNF production suggested a possible link between certain HLA class II phenotypes and PA response.

Conclusions:

  • Class III C4 complement allotypes and DQw3 phenotypes are more prevalent in patients on procainamide therapy.
  • Genetic variations, particularly in HLA class II, may play a role in individual responses to PA.
  • Further research is warranted to elucidate the immunogenetic mechanisms underlying PA treatment outcomes.

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