last updated 15-07-2024

Systemic lupus erythematosus

Systemic lupus erythematosus

Systemic lupus erythematosus is an autoimmune disease characterized by the production of auto-antibodies against cell content, especially DNA (antinuclear antibodies, ANA). This results in a type III hypersensitivity reaction which is immune complex-mediated. Deposition of immune complexes (antigen-antibody) activates complement components resulting in leukocyte chemotaxis, tissue injury, and vasculitis. The immune disturbance promotes B cell hyperactivity to both self and foreign antigens. Subsequent activation (flare-ups) can occur from triggering the antibody response to foreign antigens such as viruses or even sunlight. The resulting inflammation is commonly seen in skin and joints, and in more advanced stages in kidneys, nervous system, lungs, and heart.

The progression of the disease is difficult to predict. Flare-ups and more severe stages require high doses of corticosteroids and other more potent immunosuppressants such as cyclophosphamide and azathioprine. Otherwise patients are treated with NSAIDs, methotrexate or antimalarials for their mild symptoms. (Click the underlined drugs to see their action in other disease states). In late stages of the disease when renal damage progresses, kidney failure requires dialysis or kidney transplantation.

Abetimus sodium (Riquent®) is currently being developed as a novel treatment for SLE. B-cell antibodies against double-stranded DNA are believed to cause lupus kidney disease that can lead to kidney failure, dialysis, kidney transplantation, and death. Abetimus sodium is designed to arrest the production of antibodies to double-stranded DNA (dsDNA) in lupus patients and to arrest or delay lupus renal disease without suppressing the healthy functions of the immune system.

Unfortunately, drugs can also cause SLE. To date about 75 drugs have been described which either cause or exacerbate SLE. Common agents include hydralazine, procainamide (class I antiarrhythmic), isoniazide, sulfasalazine, β-blockers and many more. Fortunately, the drug-induced syndrome improves after stopping therapy.


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