[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address Please contact the publisher to request reinstatement.
[Skip to Content Landing]
October 1972

Lupus Erythematosus

Author Affiliations

San Francisco

From the Department of Dermatology, University of California School of Medicine, San Francisco.

Arch Dermatol. 1972;106(4):553-566. doi:10.1001/archderm.1972.01620130077019

A genetically predetermined host immune response apparently disposes certain individuals to develop lupus erythematosus. Drugs, ultraviolet light, and viral infection are among the sources of antigenic stimulation. Patients with milder forms of the disease, such as discoid lupus, may have a protective immune response.

Knowledge of the clinical manifestations of lupus erythematosus provides the basic tool for patient management. However, rapid advances in technology have been of real value in diagnosis and estimation of disease activity. Serological studies of antibodies to DNA and RNA, estimation of serum and spinal fluid complement components, direct and indirect immunofluorescence, and electron microscopy are all of use to the clinician.

Corticosteroids remain the main therapeutic agent in serious forms of the disease. Antimalarials are of proven value. The role of the immunosuppressive agents is still problematical.