Cyclosporine

This component is derived from the fungus streptomyces. Based on its effectiveness to suppress T-cell activity, it was introduced into transplantation medicine in the 1980s and is established within immunosuppressive regimens of transplanted solid organs. The drug interferes with the calmodulin-mediated intracellular signal transduction and thus inhibits the nuclear factor of activated T-cells (NFAT)-mediated transcription of several cytokines, mainly IL-2. Apart from T cells, various other cells are influenced, including mast cells, which are involved in different inflammatory processes.

Doses of 2.5-5 mg/kg body weight are usually applied to induce clinical effects and can often be tapered within 3-4 weeks. In CLE, however, prolonged treatment for several months may be needed to induce clinical improvement. Classic side effects include renal dysfunction and arterial hypertension. Thus, before initiation and dur ing the first few months of therapy, these parameters should be monitored. Cyclosporine is approved for the treatment of rheumatoid arthritis and psoriasis. Beneficial effects were seen for thrombocytopenia, pancytopenia, and membranous nephritis associated with SLE, and steroid-sparing effects were suggested (Conti et al. 2000, Griffiths and Emery 2001). However, similar to arthralgia, myalgia, and fatigue, cutaneous disease is hardly improved (Conti et al. 2000, Lernia and Bisighini 1996, Obermoser et al. 2002, Saeki et al. 2000,Yell and Burge 1994). In a single patient, development of DLE was reported during treatment of psoriasis with cyclosporine (Lernia et al. 1996). Based on these results, the benign prognosis of CLE, and the possible side effects, cyclosporine should re regarded as second-line therapy in CLE.

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