Methotrexate was used extensively a couple of decades ago for various inflammatory processes (Jeffes et al. 1995, Cronstein 1996). Within dermatology, the drug has gone out of fashion by the misconception of dose restriction at a cumulative dose of 1.5-2 g because of possible liver damage and fibrosis. It is not clear if rheumatologic patients show different incidences of methotrexate-related liver disease than patients with psoriasis. Blood cell counts, liver enzyme levels, and fibrotic processes (procollagen III peptide at biannual intervals) should be monitored regularly.

Methotrexate was shown to be very effective in DLE and SCLE at doses as low as 15-20 mg once per week (Abe et al. 1994, Boehm et al. 1998, Bohm et al. 1997, Bot-tomley and Goodfield 1995a,b, Goldstein and Carey 1994,Kuhn et al. 2002). It maybe used as a single agent or as adjunct therapy. In SLE, apart from synovitis, cutaneous disease may effectively be treated with distinct steroid-sparing effects (Abud-Men-doza et al. 1993, Rothenberg et al. 1988, Wilke et al. 1991). Methotrexate may be administered intravenously, thus circumventing individual variations of intestinal resorption, or orally in strictly compliant patients. Patients with LE might not tolerate oral methotrexate as well as other patients and may prefer the subcutaneous or intravenous application. To lower the incidence of side effects, tetrahydrofolate should be administered the following day. On induction of stable clinical effects, both dose and time intervals of application may be tapered. Immunologic effects at these low doses are probably induced by functional interaction with immunocompetent cells rather than by their physical eradication. Modulation of chemotaxis, migration and adhesion of polymorphonuclear leukocytes, and modulation of lymphocyte activity regarding interleukin (IL) 1fi, IL-6, and tumor necrosis factor (TNF)-a receptor expression seem to be the main effects (Boehm et al. 1998, Cronstein 1996, Jeffes et al. 1995).

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