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Systemic lupus erythematosus (SLE) is an inflammatory autoimmune disorder that may affect multiple organ systems. Many of its clinical manifestations are secondary to the trapping of antigen-antibody complexes in capillaries of visceral structures or to autoantibody-mediated destruction of host cells (eg, thrombocytopenia).
Before making a diagnosis of spontaneous SLE, it is imperative to ascertain that the condition has not been induced by a drug. A host of pharmacologic agents have been implicated as causing a lupus-like syndrome, but only a few cause the Procainamide, hydralazine, and isoniazid are the best-studied drugs. While antinuclear antibody tests and other serologic findings become positive in many persons receiving these agents.
Drugs associated with lupus erythematosus
Definite association
Chlorpromazine Methyldopa
Hydralazine Procainamide
Isoniazid Quinidine
Possible association
Acebutolol Nitrofurantoin
Atenolol Oxprenolol
Captopril Penicillamine silicone
Carbamazepine
The prevalence of SLE is influenced by many factors, including gender, race, and genetic inheritance. About 85% of patients are women. Sex hormones appear to play some role, since most cases develop after menarche and before menopause. Among the patients who develop SLE during childhood or after the age of 50, the preponderance of women is less. Race is also a factor, as SLE occurs in 1:1000 white women but in 1:250 black women. Familial occurrence of SLE has been repeatedly documented, and, silicone, breast implants.
Four features of drug-induced lupus separate it from spontaneously occurring disease: (1) the sex ratio is nearly equal; (2) nephritis and central nervous system features are not ordinarily present; (3) depressed serum complement and, silicone, breast implants.
Treatment
Some patients with SLE have a benign form of the disease requiring only supportive care and need little or no medication. Emotional support, as described for rheumatoid arthritis, is especially important for patients with lupus.