It occurs 10 times more frequently in women than in men and approximately
three times more frequently in the African-American population than in Caucasians Pathophysiology SLE is a result of disturbed immune regulation that causes an exaggerated production of autoantibodies This immunoregulatory disturbance is brought about by some combination of genetic, hormonal (as evidenced by the usual onset during the childbearing years), and environmental factors (sunlight, thermal burns). Certain medications, such as hydralazine (Apresoline), procainamide (Pronestyl), isoniazid (INH), chlorpromazine (Thorazine), and some antiseizure medications, have been implicated in chemical or drug- induced SLE. In SLE, the increase in autoantibody production is thought to result from abnormal suppressor T-cell function, leading to immune complex deposition and tissue damage. Inflammation stimulates antigens, which in turn stimulate additional antibodies, and the cycle repeats.