Inhibition of the complement activation by an adrenal androgen, dehydroepiandrosterone.
The effect of dehydroepiandrosterone (DEA), an adrenal androgen successfully used for preventing attacks in hereditary angioneurotic edema (HANE) patients was studied on the activation of classical and alternative complement pathway. The steroid inhibited both the spontaneous and immune activation of the classical complement pathway (CP), the former effect, however, was found to be more marked than the latter one. DEA exerted its inhibiting effect most probably by interfering with the internal activation of C1. Because DEA rendered HANE patients symptom free but induced only a slight increase in their serum C1-INH level, our present findings suggest that inhibition of CP activation may have a significance in the therapeutic effect of DEA and possibly of other androgens as well.
D000799:Angioedema / Q000188:drug therapy*; D003167:Complement Activation / Q000187:drug effects*; D003172:Complement C1 / Q000378:metabolism; D003174:Complement C1 Inactivator Proteins / Q000378:metabolism; D003181:Complement C4 / Q000378:metabolism; D003687:Dehydroepiandrosterone / Q000494:pharmacology* / Q000627:therapeutic use; D006461:Hemolysis; D006801:Humans
D003172:Complement C1; D003174:Complement C1 Inactivator Proteins; D003181:Complement C4; D003687:Dehydroepiandrosterone