title: FCGR3A-158V/F polymorphism may correlate with the levels of immunoglobulin in patients with non-Hodgkin's lymphoma after rituximab treatment as an adjuvant to autologous stem cell transplantation.
abstract: OBJECTIVE
  Recent studies have indicated that patients who receive stem cell transplantation (SCT) and rituximab demonstrate an increased risk of developing hypogammaglobulinemia. Such hypogammaglobulinemia has been found to be due to delayed recovery of memory B cells with an abnormal cell marker expression and impaired immunoglobulin production in vitro. However, no predictive factors for the levels of immunoglobulin after autologous SCT and rituximab therapy have been reported. The aim of this study is to clarify the relationships between the FCGR3A-158V/F genotype and the levels of serum immunoglobulin after SCT.
  
  
  METHODS
  A total of 24 non-Hodgkin's lymphoma (NHL) patients received autologous SCT with an adjuvant rituximab. The FCGR3A-158V/F genotype was determined in these patients. We also included ten NHL patients who received an identical conditioning regimen and autologous SCT but no rituximab as control patients.
  
  
  RESULTS
  The levels of IgG were significantly lower in FCGR3A-158F homozygous patients (n = 9) in comparison to those in FCGR3A-158V carriers (n = 15). Moreover, the levels of IgG and IgA of FCGR3A-158F homozygous patients, but not those of FCGR3A-158V carriers, were significantly lower than those of control patients.
  
  
  CONCLUSIONS
  The genotype of FCGR3A determines not only the response to rituximab, but also the levels of immunoglobulin after SCT and an adjuvant rituximab.
authors.affiliation: Department of Medicine II, Hokkaido University Graduate School of Medicine, Sapporo, Japan. m-nishio@med.hokudai.ac.jp
authors.forename: Mitsufumi
authors.initials: M
authors.lastname: Nishio
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Endo
authors.forename: Katsuya
authors.initials: K
authors.lastname: Fujimoto
authors.forename: Satoshi
authors.initials: S
authors.lastname: Yamamoto
authors.forename: Masato
authors.initials: M
authors.lastname: Obara
authors.forename: Keisuke
authors.initials: K
authors.lastname: Yamaguchi
authors.forename: Yukari
authors.initials: Y
authors.lastname: Takeda
authors.forename: Hideki
authors.initials: H
authors.lastname: Goto
authors.forename: Ikumi
authors.initials: I
authors.lastname: Kasahara
authors.forename: Norihiro
authors.initials: N
authors.lastname: Sato
authors.forename: Takao
authors.initials: T
authors.lastname: Koike
mesh_terms: D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D058846:Antibodies, Monoclonal, Murine-Derived; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000008:administration & dosage / Q000627:therapeutic use*; D003520:Cyclophosphamide / Q000008:administration & dosage; D004317:Doxorubicin / Q000008:administration & dosage; D005260:Female; D018380:Hematopoietic Stem Cell Transplantation; D006801:Humans; D007136:Immunoglobulins / Q000097:blood*; D008228:Lymphoma, Non-Hodgkin / Q000097:blood / Q000188:drug therapy / Q000235:genetics / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D011241:Prednisone / Q000008:administration & dosage; D017452:Receptors, IgG / Q000235:genetics*; D000069283:Rituximab; D014750:Vincristine / Q000008:administration & dosage
chemical_list: D000911:Antibodies, Monoclonal; D058846:Antibodies, Monoclonal, Murine-Derived; C496124:FCGR3A protein, human; D007136:Immunoglobulins; D017452:Receptors, IgG; D000069283:Rituximab; D014750:Vincristine; D004317:Doxorubicin; D003520:Cyclophosphamide; D011241:Prednisone