Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease caused by autoantibodies and the deposition of immune complexes. The disease affects primarily women and has a higher prevalence among African Americans. A series of clinical findings is associated with SLE. These include a characteristic malar rash, photosensitivity, arthritis, serositis, and a discoid rash. In addition, involvement of the renal, neurologic, and hematologic systems present with system-specific symptoms. The presence of autoantibodies (e.g., anti-Sm, anti–double-stranded DNA) can also assist in making the diagnosis. When a patient exhibits four or more of these criteria the diagnosis can be made with a sensitivity and specificity of 75% and 95%, respectively.

SLE can present with an acute or subacute onset. Most patients undergo some elements of acute exacerbation and remission during the natural course of the disease. This is important because the goals of SLE treatment include mainly the control of symptoms and prevention of the worsening of organ failure. Treatment usually involves a number of systemically administered medications. For minor disease, arthritis and pain can be treated with nonsteroidal antiinflammatory medications or COX-2 inhibitors. Antimalarial agents (chloroquine, quinacrine) can also benefit patients with generalized symptoms. For severe systemic disease, the use of steroids is the mainstay of treatment. These drugs can be administered in high doses, with attempts to reduce the dose at frequent intervals once symptoms are under control. Cytotoxic agents are used for aggressive disease including renal manifestations.