Complement system protein C4 and susceptibility to hydralazine-induced systemic lupus erythematosus

Lancet. 1989 Apr 29;1(8644):922-4. doi: 10.1016/s0140-6736(89)92506-3.

Abstract

21 patients with systemic lupus erythematosus induced by long-term treatment with hydralazine were investigated to see whether susceptibility to this syndrome was associated with deficiency of the classical pathway complement protein, C4. 16 of 21 (76%) patients had one or more C4 null (ie, non-productive) alleles compared with 35 of 82 normal subjects (43%). This difference was significant. The HLA-DR4 antigen, known to be in linkage disequilibrium with the C4B null allele, was also significantly more frequent in the patients (14 of 21 patients compared with 31 of 81 normal subjects). Susceptibility to hydralazine-induced lupus, as in idiopathic systemic lupus erythematosus, may depend partly upon genetically determined C4 levels.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alleles
  • Complement C3 / analysis
  • Complement C3 / genetics
  • Complement C3a
  • Complement C4 / analysis
  • Complement C4 / deficiency*
  • Complement C4 / genetics
  • Complement C4a
  • Disease Susceptibility
  • Genetic Linkage
  • HLA Antigens / analysis*
  • HLA Antigens / genetics
  • HLA-DR Antigens / analysis
  • HLA-DR Antigens / genetics
  • HLA-DR4 Antigen
  • Haplotypes
  • Humans
  • Hydralazine / adverse effects*
  • Lupus Erythematosus, Systemic / blood
  • Lupus Erythematosus, Systemic / chemically induced*
  • Lupus Erythematosus, Systemic / genetics
  • Polymorphism, Genetic*

Substances

  • Complement C3
  • Complement C4
  • HLA Antigens
  • HLA-DR Antigens
  • HLA-DR4 Antigen
  • Hydralazine
  • Complement C3a
  • Complement C4a