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We read with interest the article “Variability in the biological response to anti-CD20 B cell depletion in systemic lupus erythematosus” by Albert D. et al. (1) regarding the potential efficacy of rituximab administration in patients with lupus nephritis. Systemic lupus erythematosus (SLE) is a challenging disease associated to important and diverse immuno-regulatory alterations, including those of B and T c...
We read with interest the article “Variability in the biological response to anti-CD20 B cell depletion in systemic lupus erythematosus” by Albert D. et al. (1) regarding the potential efficacy of rituximab administration in patients with lupus nephritis. Systemic lupus erythematosus (SLE) is a challenging disease associated to important and diverse immuno-regulatory alterations, including those of B and T cells and their networks, responsible for the clinical manifestations and
production of great diversity of autoantibodies, which are associated to tissue damage (2). Rituximab, a monoclonal chimeric antibody, depletes CD20+ B cells through antibody-dependent cell and complement-mediated cytotoxicity and induction of apoptosis (3). In addition, we have reported
that this therapy is associated with a significant enhancement in the levels and function of regulatory T cells (4). All these mechanisms of action seem to account for the efficacy of B cell depletion therapy in this autoimmune disease with renal, neurologic, hematologic and pulmonary,among other, manifestations (5).
Although it has been proposed that the standard total dose of Rituximab for the therapy of refractory SLE is a course of 2.0 g (5), Albert D. et al. reported that some patients that received 50% or less of this dosage showed a complete depletion of B cells, with apparent good clinical response (1). These interesting data are in agreement with a previous report of our group (4), which shows that a total dose 0.5 g of rituximab is sufficient to induce B cell depletion and a favorable clinical response. It is also of interest that in our hands, these low doses of rituximab exert their therapeutic effect despite no simultaneous administration of glucocorticoids or cyclophosphamide (4). As expected, we have observed few adverse events in these patients that received low doses
of rituximab without simultaneous administration of other
immunosuppressive drugs. Therefore, it seems very important to confirm, through controlled clinical trials, whether or not low doses of rituximab are as effective, in selected SLE patients, as the conventional therapeutic schedule of this biological agent. This issue is very relevant in third world countries, where very limited resources for health care are available, and it is evident that biological agents are very expensive, with a restricted access.
1. Albert D, Dunham J, Khan S, Stansberry J, Kolasinski S, Tsai D, et al. Variability in the biological response to anti-CD20 B cell depletion in systemic lupus erythaematosus. Ann Rheum Dis 2008;67:1724-31.
2. Rahman A, Isenberg DA. Systemic lupus erythematosus. N Engl J Med 2008;358:929-39.
3. Liossis SN, Sfikakis PP. Rituximab-induced B cell depletion in autoimmune diseases: potential effects on T cells. Clin Immunol 2008;127:280-5.
4. Vigna-Perez M, Hernández-Castro B, Paredes-Saharopulos O, Portales -Pérez D, Baranda L, Abud-Mendoza C, et al. Clinical and immunological effects of Rituximab in patients with lupus nephritis refractory to conventional therapy: a pilot study. Arthritis Res Ther 2006;8(3):R83.
5. García-Carrasco M, Jiménez-Hernández M, Escárcega RO, Mendoza-Pinto C, Galarza-Maldonado C, Sandoval-Cruz M, et al. Use of rituximab in patients with systemic lupus erythematosus: An update. Autoimmun Rev 2008 Nov 23 (in press).