Improvement of our understanding of the pathogenesis of SLE has led to reasonable therapeutic strategies that have improved dramatically the well-being and life expectancy of patients with SLE, whose survival rate at 10 years is now 80%. The therapeutic approach to each patient is determined by the extent of the disease and, most importantly, by the nature and extent of organ involvement. Careful avoidance of factors implicated in the in-duction of relapses—high-risk medications, exposure to sunlight, infections, etc.—is al-ways indicated, but in most cases administration of anti-inflammatory and immunosuppressive drugs is essential.
Corticosteroids combine anti-inflammatory effects with a weak immunosuppressive capacity. The anti-inflammatory effect is probably beneficial in disease manifestations sec-ondary to immune complex deposition, while the immunosuppressive effect may help to curtail the activity of the B-cell system.
Nonsteroidal anti-inflammatory drugs are frequently used to control arthritis and serositis.
In patients with vital organ involvement (i.e., glomerulonephritis, CNS involve-ment), immunosuppressive drugs may be indicated. Cyclophosphamide, given intra-venously, has been successfully used to prolong adequate renal function with few side ef-fects. Maximal benefit is achieved when long-term treatment is started early, with relatively good renal function. In some patients, clinical effects require the administration of high (nonablative) doses of cyclophosphamide.
A number of experimental therapeutic approaches have been used, or are under study, in patients with SLE. These new approaches capitalize on information that has been generated from the study of the pathogenesis of the disease.
As discussed earlier, much of the produced autoantibody is the result of cognate in-teraction between helper T cells and B lymphocytes. Therefore, the interruption of this in-teraction by either humanized antibodies or recombinant downregulating ligands (recombinant molecules constituted by the binding site of a molecule that delivers downregulating signals and the Fc portion of IgG to prolong serum half-life) is expected to have therapeutic value. Such reagents include anti-CD40 ligand antibody and the CTLA4-Ig.
Since levels of IL-10 have been found to be increased in the sera of patients with lu-pus and because IL-10 promotes B-cell function, ongoing trials will determine the value of anti–IL-10 antibody in the treatment of human lupus.
Complement activation mediates significant pathology in human lupus. An anti-C5 antibody that disrupts complement activation is currently in clinical trials to determine its role in the treatment of lupus.
Additional trials will determine the possibility of curing, lupus or setting back the lu-pus clock, by ablating (by means of administration of large doses of cytotoxic drugs or to-tal body irradiation) the patient’s own immune system and reinfusing autologous hematopoietic stem cells.
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