[Systemic lupus erythematosus induced by drugs]

The clinical and morphological characteristics of drug-induced lupus (DIL) are not unlike those of systemic lupus erythematosus (SLE). However, DIL is characterised by several distinct features: the two sexes are equally affected; onset occurs in advanced middle-age; the black population is seldom affected. Genetic predisposition seems to influence the onset of disease: subjects affected by DIL are prevalently HLA-DR4 haplotypes with a slow acetylator condition. Modifications in humoral immunity include the presence of anti-nuclear antibodies, denatured anti-DNA antibodies, and antihistone antibodies. Likewise, anti-lymphocytotoxic antibodies, increased ESR and hypocomplementemia are often observed. Little is known about alterations in cellular immunity but the dysregulation of lymphocyte T-helper and T-suppressor activity may be an important feature. Drugs most often leading to DIL include hydralazine, beta-blockers, procainamide and hydantoin. Current pathogenetic theories include a possible immune drug-DNA cross-reaction, the induction of new antigenic structures, an interaction between drugs and immunomodulating cells.