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

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. 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. 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. The genotype of FCGR3A determines not only the response to rituximab, but also the levels of immunoglobulin after SCT and an adjuvant rituximab.