Systemic Lupus Erythematosus

The only current US FDA-approved therapy for SLE is prednisone (see Figure 1 and Table 2); however, many biologics and drugs, some new, are being tested in clinical trials.1,44 Corticosteroids (described above) have long been used to treat SLE. Prednisone given for a short period seems to prevent severe flares and exposure to high-dose steroids.

Cyclophosphamide has long been the standard treatment for severe SLE, particularly LN. A low-dose intravenous cyclophosphamide regimen followed by maintenance azathioprine (see Figure 1 and Table 2) may be as, or more, effective, and less toxic than the standard high-dose cyclophosphamide regimen; nonetheless, a significant proportion of patients fail to achieve remission, or experience a relapse of active LN during maintenance therapy. Socioeconomic and ethnic factors have been shown to influence cyclophosphamide efficacy in patients with proliferative LN.

It is generally agreed that B cell dysfunction, specifically loss of tolerance, plays a central role in SLE pathogenesis. Thus, many of the pharmacotherapies currently being tested in clinical trials for SLE (mycophenolate mofetil, rituximab, belimumab, epratuzumab, and abetimus sodium - described above) exert their effects on some aspect of B cell proliferation or function. Mycophenolate mofetil appears to have an equal or superior efficacy to intravenous cyclophosphamide, with fewer side effects. This along with its oral administration argue for its consideration as an alternative to intravenous cyclophosphamide - at least for LN. Rituximab shows promise as a therapy for various SLE manifestations. Abetimus sodium holds promise as a new therapeutic option developed specifically to reduce the number and severity of renal flares in SLE.

IL-6 levels are elevated in both human and murine SLE. Blocking the action of IL-6 ameliorates disease activity in murine models of SLE; this approach is being tested in an early stage clinical trial using a monoclonal antibody to the IL-6 receptor.

Some patients on IFN-a develop autoimmune conditions, such as SLE. In addition, serum levels of IFN-a are elevated in SLE patients. This and animal studies suggest the potential therapeutic value of IFN-a inhibition for the treatment of SLE.

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