作者: Martin Aringer , Josef S. Smolen
DOI: 10.1016/J.AUTREV.2011.05.001
关键词:
摘要: TNF is an important mediator of inflammation, but also involved in the control autoimmunity. The latter has been demonstrated a murine model SLE (NZB/W) and by occurrence autoantibodies to nuclear antigens as well occasional, transient lupus-like syndromes patients under blockade. In contrast, data on increased levels serum, kidney skin samples results other mouse models disease point inflammatory role organ disease. Despite all due caution, given these two sides cytokine, blockade now employed for several years single cases open label studies; more than fifty have meanwhile published, vast majority which infliximab was employed. These clinical be very cautiously interpreted, always with or trials. However, some consistent pieces information emerge may inform controlled trials: (i) While antibodies double-stranded DNA commonly showed increases, lupus flares not seen so far thus apparently are at least rule; (ii) increases anti-phospholipid associated vascular adverse events; (iii) bacterial infections, pneumonia urinary tract infections particular, observed; (iv) short term induction therapy appears relatively safe, while long-term confer significant risks SLE; (v) blocker lead remission nephritis, hemophagocytic syndrome, interstitial lung disease; (vi) arthritis often respond TNF-blockade symptoms recur after cessation therapy, necessitating longer risky treatment.