G-CSF-induced decrease of the anti-granulocyte autoantibody levels in a patient with autoimmune granulocytopenia

Abstract

Disclaimer/Complaints regulationsIf you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: http://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. Abstract We present a case of an 81-year-old man with secondary autoimmune granulocytopenia in association with autoimmune thrombocytopenia. Treatment with granulocyte colony-stimulating factor (G-CSF) (5 mg/ kg/day s.c.) resulted in a rapid increase in the number of circulating granulocytes with a pronounced left shift. These changes were accompanied by up-regulation of the surface expression of FcgRI (CD64) and FcgRII (CD32) on the granulocytes. In addition, we noted a strong up-regulation of the FcgRIII (CD16) and the activation markers CD11b and CD66b on the granulocytes. The increase in the number of circulating granulocytes was followed by a dramatic decrease in the level of cell-bound as well as circulating anti-granulocyte antibodies. It is hypothezised that the decrease in the level of cell-bound as well as circulating anti-granulocyte antibodies may be the result of an increased adsorption of the antibodies by the granulocytes.

Treatment of stiff person syndrome with rituximab

“…Antineutrophil antibodies have been described in association with both systemic lupus erythematosus (SLE) 10 and idiopathic thrombocytopenic purpura. 11 Rituximab has been used with success both in the treatment of other autoimmune conditions (for review see Silverman and Weisman 12 ), including rheumatoid arthritis and SLE, and combined with cytotoxic chemotherapeutic agents in the treatment of non-Hodgkin's lymphoma. 13 Rituximab specifically targets cells expressing the surface antigen CD20 and therefore depletes mature B lymphocytes, but spares plasma cells and early pre-B cells, which do not express CD20.…”

Idiopathic, immune, infectious, and idiosyncratic neutropenias

“…An important effect of G-CSF is that by stimulating neutrophil production, in vivo absorption and consumption of autoantibodies also occurs, leading to their disappearance from the circulation. 42,72,60 A number of patients with severe AIN have demonstrated only transient responses with corticosteroids, antilymphocyte globulin, and G-CSF, and are resistant to treatment with azathioprine, cyclosporin, and IVIG. A course of intravenous Campath-1H monoclonal antibody in these patients resulted in prolonged hematologic responses.…”

Inverse relation between plasma G-CSF levels and neutrophil counts in a patient with autoimmune neutropenia treated with G-CSF

“…Recently, we treated a patient with an antibody‐mediated autoimmune neutropenia with repeated injections of G‐CSF. Before treatment the endogenous G‐CSF levels were only mildly elevated and upon G‐CSF administration we observed a rapid decrease in the trough levels of G–CSF in association with a rapid increase in the circulating neutrophil count ( Vlasveld et al 1997 ).…”