CD20 monoclonal antibody(The First Affiliated Hospital of Soochow University)

Objective: This study aimed to summarize the clinical characteristics and prognosis of patients with bone marrow invasive follicular lymphoma (FL) and discuss the treatment modalities. Methods: This study included 183 consecutive patients with FL accompanied by bone marrow invasion and receiving regular treatment at the Hospital of Hematology, Chinese Academy of Medical Sciences, from January 2013 to December 2022. Clinical data were retrospectively collected and analyzed, and single and multifactorial analyses of survival prognosis were conducted with the Kaplan-Meier method and Cox regression model. Results: The median age was 48 (range: 19 - 78) years, and the male-to-female ratio was 0.9∶1. All of the patients had bone marrow invasion, 27.8% had increased lactate dehydrogenase levels, 42.1% had lymphocyte counts of >5×10(9)/L, 18.4% had abnormal chromosomal karyotypes, and 48.6% had Ki-67 index of ≥30% in lymphoid tissue. Comparison of different subgroups: lymphocyte counts of >5×10(9)/L, number of lymph nodes of ≥5 involved, and proportion of bone marrow chromosomal abnormalities occurring were higher in the anthracycline-intensive treatment group than in the rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) protocol and the nucleoside analog (including CD20 monoclonal antibody in combination with fludarabine and bendamustine) groups (all P<0.05). The complete remission rate was 39.1% in the conventional R-CHOP group, which was lower and statistically significant than that in the intensive treatment group (55.1%) and the nucleoside analog group (62.5%) (P=0.042). The multivariate analysis for survival analysis revealed high risk of FLIPI (HR= 1.910, 95% CI 1.036 - 3.522, P=0.036), chromosomal abnormalities karyotype (HR=2.666, 95% CI 1.333-5.331, P=0.006), and conventional R-CHOP treatment (HR=2.287, 95% CI 1.140-4.591, P=0.020) were the independent adverse prognostic factors affecting progression-free survival (PFS), whereas POD24 was the only independent adverse prognostic factor affecting overall survival (OS) adverse prognostic factor (HR=9.581, 95% CI 3.000 - 30.593, P<0.001) . Conclusions: The clinical presentations of patients with bone marrow invasive FL were easy to combine the clinical features, including increased lymphocyte count, chromosomal abnormalities, and Ki-67 index in lymphoid tissues. The FLIPI score, chromosomal abnormal karyotype, and high-lymphoid-tissue Ki-67 index were the poor prognostic factors influencing PFS. R-CHOP therapy demonstrated a poor prognosis in this group of patients.

Considering its proven clinical usefulness and supportive evidence, intravenous immunoglobulin (IVIg) is used as first-line therapy for chronic inflammatory demyelinating polyneuropathy (CIDP) during the acute and chronic stages. However, the pathomechanism underlying IVIg administration for CIDP remains unclear. Autoantibodies, complement, inflammatory cytokines, chemokines, T cells, B cells, macrophages, and the blood-nerve barrier contribute to the onset and progress of CIDP. The mechanisms underlying the actions of IVIg in CIDP include the following: (1)neutralization of pathological autoantibodies by anti-idiotype antibodies, (2)inhibition of the neonatal Fc receptor (FcRn) with a consequent decrease in pathological autoantibodies, (3)neutralization of cytokines, chemokines, and complement, (4)activity modulation of T cells, B cells, and macrophages, and (5) recovery of blood-nerve barrier function. Compared with the management of typical CIDP, IVIg therapy is less effective for management of autoimmune nodopathy associated with anti-neurofascin-155 or contactin-1 IgG4 antibodies because (1)anti-idiotype antibodies associated with IVIg cannot effectively neutralize IgG4 owing to the strong antigen specificity of IgG4 autoantibodies, and (2)complement, T cells, and macrophages play an insignificant role in the pathomechanism of autoimmune nodopathy. Further understanding of the mechanisms underlying IVIg action and effectiveness of molecular targeted therapy, such as use of FcRn or complement inhibitors and the CD20 monoclonal antibody, is warranted to develop novel therapeutic strategies against CIDP.