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Longterm Clinical and Immunological Effects of Anti-CD20 Treatment in Patients with Refractory Systemic Lupus Erythematosus CATHARINA LINDHOLM, KATHARINA BÖRJESSON-ASP, KIANDOKHT ZENDJANCHI, ANNA-CARIN SUNDQVIST, ANDREJ TARKOWSKI, and MARIA BOKAREWA
ABSTRACT. Methods. Anti-CD20 treatment (rituximab) was added to the ongoing immunosuppressive treatment in 31 SLE patients with active nephritis (n = 17), thrombocytopenia (n = 10), and hemolytic anemia (n = 4) refractory to conventional therapy. Disease activity was evaluated by the SLE Disease Activity Index. The median followup time after anti-CD20 treatment was 22 months (range 1–61 mo). Results. Complete B cell depletion was obtained in all patients. In 11 of the 17 lupus nephritis patients complete or partial responses were achieved after 6–12 months. Eight of these patients increased their glomerular filtration rate (GFR) by > 25%. The responders were characterized by having shorter nephritis duration, a baseline GFR > 30 ml/min, and detectable circulating CD19+ B lymphocytes before B cell depletion. Anti-CD20 treatment was highly effective in patients with autoimmune thrombocytopenia, inducing a significant increase of platelet counts after 1 month (p < 0.01). Five of 10 patients achieved complete normalization of their platelet counts within 6 months. The anti-CD20 treatment was followed by a significant reduction of autoantibodies against dsDNA and platelets, in nephritic and in thrombocytopenic patients, respectively. Conclusion. Addition of anti-CD20 treatment to conventional immunosuppressive therapy may be a beneficial strategy in refractory lupus nephritis and autoimmune cytopenias, possibly by reducing the levels of pathogenic autoantibodies. (First Release April 1 2008; J Rheumatol 2008;35:826-33) Key Indexing Terms:
SYSTEMIC LUPUS ERYTHEMATOSUS
From the Department of Rheumatology and Inflammation Research, Göteborg University, and the Rheumatology Clinic, Sahlgrenska University Hospital, Gothenburg, Sweden. Supported by grants from the Göteborg Medical Society, Swedish Association Against Rheumatism, Swedish Medical Research Council, and Roche AB, Sweden. C. Lindholm, MD, PhD, Department of Rheumatology and Inflammation Research, Göteborg University, and Sahlgrenska University Hospital; K. Börjesson-Asp, MD; K. Zendjanchi, RN; A.C. Sundqvist, RN, Sahlgrenska University Hospital; A. Tarkowski, MD, Professor; M. Bokarewa, MD, Associate Professor, Department of Rheumatology and Inflammation Research, Göteborg University, and Sahlgrenska University Hospital. Address reprint requests to Dr. C. Lindholm, Department of Rheumatology and Inflammation Research, Göteborg University, Guldhedsgatan 10A, S-413 46 Gothenburg, Sweden. E-mail: catharina.lindholm@rheuma.gu.se Accepted for publication December 9, 2007. |
