Plasmapheresis and Immunoadsorption

Impaired clearance of immune complexes and the production of autoantibodies are characteristic features of LE. Therefore, it was conceivable that the extracorporal removal of these proteins may help improve LE lesions or support current treatments. Plasmapheresis is a procedure that separates plasma/proteins from whole blood by cell centrifugation techniques or membrane technology. Subsequently, the plasma is replaced by albumin and saline. Usually plasmapheresis is combined with an immunosuppressive therapy to prevent antibody rebound or rapid resynthesis of immunoglobulins. This modality was first considered for therapy of lupus patients with hyperviscosity, cryoglobulinemia, pulmonary hemorrhage, or thrombotic thrombocytopenic purpura (Wallace 2001a). It also has been used successfully in the management of acute central nervous system involvement of lupus when other therapies have failed (Neuwelt et al. 1995). However, in a large international prospective controlled trial in patients with SLE, plasmapheresis did not reveal any additional benefit compared with conventional treatment (Leweis et al. 1992). Therefore, plasmapheresis currently is not recommended for the treatment of SLE, unless the disease is complicated by hyperviscosity, cryoglobulinemia, pulmonary hemorrhage, or thrombotic thrombocytopenic purpura.

A promising alternative to plasmapheresis is immunoadsorption (Terman et al. 1979), which via the use of different technologies, such as sepharose columns coupled with polyclonal sheep antibodies binding human IgG heavy and light chains (Ig-Therasorb), allows for a more specific approach to eliminate antibodies as well as immune complexes. Accordingly, selective immunoadsorption of immunoglobulin, anti-ds-DNA antibodies, immune complexes, antiphospholipid antibodies, and anti-C1q antibodies was applied successfully in single cases or uncontrolled trials of SLE. In addition, patients with SLE suffering from nephritis, pneumonitis, hemolytic anemia, central nervous system involvement, and skin lesions refractory to immunosup-pression were treated with immunoadsorption and subsequently substituted with normal human immunoglobulins to avoid the rebound of autoantibody production (Gaubitz et al. 1998, Graninger et al. 2002, Viertel et al. 2000). All patients showed an improvement in clinical and laboratory signs of disease activity. The therapy was well tolerated without significant side effects. During follow-up (up to 1 year), organ function remained stable, requiring only low-dose prednisolone (5-7.5 mg daily per os).

C1q is believed to contribute to the defective clearance of apoptotic cells (Walport et al. 1998), and high titers of C1q autoantibodies correlate with the relapse of lupus nephritis (Haseley et al. 1997,Walport et al. 1998). Therefore, clearance of C1q by a specific immunoadsorption seemed to be a promising approach for the treatment of SLE. Eight patients with non-life-threatening disease flares were treated with C1q immunoadsorption (Pfuller et al. 1998). Five patients experienced improvement of organ involvement, and no severe side effects have been reported (Hiepe et al. 1999). In a recent case report, a 25-year-old women with SLE, relapsing malar, and discoid rash, which extended to almost the whole integument, was treated by C1q immunoadsorption (MIRO adsorbers) (Berner et al. 2001).The cutaneous lesions have been refractory to previous treatment with chloroquine or MTX in combination with prednisone (up to >60 mg daily). During C1q immunoadsorption, a rapid and complete resolution of skin involvement was observed, as was a decrease of ds-DNA and C1q autoantibodies. However, the persisting proteinuria indicated that lupus nephritis did not improve. During follow-up of 12 months after stopping C1q immunoadsorption and therapy with MTX (15mg/wk) as well as low-dose prednisone (5mg/d), no relapse of CLE lesions or increase in clinical disease activity has been reported. Finally, the therapy was well tolerated,without any evidence of severe side effects after 12 therapy courses.

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