Tumor necrosis factor (TNF) alpha inhibitors are very successfully introduced as a therapy of RA, ankylosing spondylitis, and psoriatic arthritis. From these applications, it is well known that TNF alpha inhibition may lead to the formation of antinuclear and also anti-dsDNA antibodies, a finding that prevented the early use of these substances in SLE. Recently, in a retrospective national study few cases of disease induction were also published by De Bandt et al. (2005). However, after discontinuation of treatment systemic clinical manifestations abated within a few weeks in all patients except one with longer-lasting evolution (6 months).
Murine models indicate that TNF alpha might play a role in the release of immature B cells from bone marrow, in the decrease of regulatory T cells and might also participate in the inflammation of nephritis. Antagonizing these effects could be beneficial in SLE. Up to now, there is one pilot study published investigating the safety of therapeutic TNF alpha blockade in patients with SLE by Aringer et al. (2004). 4 doses of infliximab (300 mg) were given to 6 patients in addition to standard immuno-suppression. The arthritis in three patients came to remission and the lupus nephritis in 4 patients improved by a reduced proteinuria, already after 1 week of treatment. Overall, infliximab did not lead to adverse events concerning disease activity, although autoantibody titers increased as expected. Controlled trials are needed to further evaluate the benefits and risks of TNF alpha blockade in SLE.
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