Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

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.

Type

Journal article

Journal

Lancet

Publication Date

29/04/1989

Volume

1

Pages

922 - 924

Keywords

Alleles, Complement C3, Complement C3a, Complement C4, Complement C4a, Disease Susceptibility, Genetic Linkage, HLA Antigens, HLA-DR Antigens, HLA-DR4 Antigen, Haplotypes, Humans, Hydralazine, Lupus Erythematosus, Systemic, Polymorphism, Genetic