Hepatitis C virus(HCV)and hepatitis B virus(HBV)infections are increasingly recognized as significant etiological factors in the pathogenesis of B-cell non-Hodgkin’s lymphomas(B-NHLs).Epidemiological and molecular st...Hepatitis C virus(HCV)and hepatitis B virus(HBV)infections are increasingly recognized as significant etiological factors in the pathogenesis of B-cell non-Hodgkin’s lymphomas(B-NHLs).Epidemiological and molecular studies have demonstrated a consistent association between chronic viral infection and B-NHLs.Multiple pathogenic mechanisms have been implicated in lymphomagenesis,both direct and indirect,including chronic antigenic stimulation,direct infection of B cells,and viral protein-mediated oncogenic signaling,It is likely that a combination of several pathogenic conditions is required to eventually lead to the development of lymphoma.The prevalence of B-cell lymphomas among individuals with chronic HCV or HBV infection presents a complex pathogenetic scenario,given the tumor heterogeneity and variable clinical behavior,and poses therapeutic challenges,due to the partial efficacy of current treatment options.The advent of direct-acting antivirals(DAAs)for HCV and high-genetic barrier nucleos(t)ide analogues(NAs)for HBV has improved patient outcomes.In indolent HCV-associated B-NHLs,antiviral therapy with DAAs alone often achieves sustained virologic response and may lead to lymphoma regression.Conversely,aggressive subtypes like diffuse large B-cell lymphomas require combination treatment with immunochemotherapy.In the setting of HBV-associated lymphomas,antiviral prophylaxis with potent NAs(e.g.,entecavir or tenofovir)is essential to prevent HBV reactivation during rituximab-containing chemotherapy regimen.The integration of antiviral and anticancer therapies has been shown to enhance survival outcomes while mitigating hepatic toxicity.A comprehensive understanding of the biological interplay between chronic viral infection and B-cell transformation is critical for optimizing diagnostic and therapeutic strategies.Aim of this viewpoint is to provide evidence that early viral detection and prompt management remain the most effective strategies to improve survival rates and to reduce treatment-related morbidity in these patients.展开更多
目的:探讨丙型肝炎(H C V)IgG阳性患者的血清抗-H C V IgM、丙氨酸转移酶(A LT)水平与H C V R N A之间的关系。方法:通过第三代E IA试剂盒检测抗-H C V IgG、抗-H C V IgM,全自动生化分析仪检测丙型肝炎患者A LT水平,荧光定量逆转录聚...目的:探讨丙型肝炎(H C V)IgG阳性患者的血清抗-H C V IgM、丙氨酸转移酶(A LT)水平与H C V R N A之间的关系。方法:通过第三代E IA试剂盒检测抗-H C V IgG、抗-H C V IgM,全自动生化分析仪检测丙型肝炎患者A LT水平,荧光定量逆转录聚合酶链反应(R T-PC R)方法检测H C V R N A,并进行比较。结果:在丙型肝炎IgG阳性患者中,抗-H C V IgM阳性率为8.3%,H C V R N A阳性率为41.7%。H C V R N A的检出在A LT异常情况下较正常明显高(P<0.05),但A LT水平与H C V R N A含量无线性相关性(r=0.346,P>0.05)。结论:抗-H C V IgM不能反映病毒复制,A LT异常情况下H C V R N A检出率高,但A LT水平与H C V R N A含量无线性相关性,H C V R N A仍是反映H C V复制的可靠指标。展开更多
目的发现HIV/HCV合并感染者中HCV自发清除特点,找出HCV自发清除的影响因素及HCV自发清除者与HCV-RNA阳性患者之间的差异,为HIV/HCV合并感染者HCV-RNA筛查及治疗提供临床指导。方法以2022年1月—2024年5月云南省传染病医院符合纳入标准的...目的发现HIV/HCV合并感染者中HCV自发清除特点,找出HCV自发清除的影响因素及HCV自发清除者与HCV-RNA阳性患者之间的差异,为HIV/HCV合并感染者HCV-RNA筛查及治疗提供临床指导。方法以2022年1月—2024年5月云南省传染病医院符合纳入标准的HIV/HCV合并感染者作为研究对象,其中未治疗的HCV-RNA阴性者作为实验组(清除组)、未治疗的HCV-RNA阳性者作为对照组(阳性组),收集2组患者的人口统计学、临床特征、治疗和实验室检测指标,计算HCV自发清除的能力,采用logistic回归分析探讨HIV与HCV合并感染后HCV自发清除的影响因素,并比较清除组和阳性组实验室指标及其肝功能损伤情况。结果共收集到148例HIV/HCV合并感染者,其中清除组70例、阳性组78例(剔除资料不全者3例),HCV自发清除率为9.1%(70/773)。单因素分析结果表明年龄、抗反转录病毒治疗(antiretroviral therapy,ART)方案、抗病毒治疗时间≥16年均有统计学意义(P<0.05)。多因素回归分析表明使用含蛋白酶抑制剂方案(OR=0.228,95%CI:0.064~0.810)是阻碍HCV自发清除的影响因素,抗病毒治疗时间≥16年(OR=8.587,95%CI:1.854~39.775)是促进HCV自发清除的影响因素。比较阳性组和清除组实验室指标发现阳性组ALT、AST、天冬氨酸氨基转移酶与血小板比率指数(aspartate aminotransferase to platelet ratio index,APRI)评分、纤维化指数(fibrosis 4 score,FIB-4指数)平均值及异常率均高于HCV自发清除组(P<0.001)。结论HCV合并感染HIV患者的HCV自发清除率降低,使用含蛋白酶抑制剂的ART方案、抗病毒治疗时间≥16年是HCV自发清除的独立影响因素,HCV自发清除者较HCV阳性者的肝功能损伤程度更轻。展开更多
基金supported by the National Italian Research Council(CNR)“Progetto DSB.AD007.305.001”to Monica Rinaldi。
文摘Hepatitis C virus(HCV)and hepatitis B virus(HBV)infections are increasingly recognized as significant etiological factors in the pathogenesis of B-cell non-Hodgkin’s lymphomas(B-NHLs).Epidemiological and molecular studies have demonstrated a consistent association between chronic viral infection and B-NHLs.Multiple pathogenic mechanisms have been implicated in lymphomagenesis,both direct and indirect,including chronic antigenic stimulation,direct infection of B cells,and viral protein-mediated oncogenic signaling,It is likely that a combination of several pathogenic conditions is required to eventually lead to the development of lymphoma.The prevalence of B-cell lymphomas among individuals with chronic HCV or HBV infection presents a complex pathogenetic scenario,given the tumor heterogeneity and variable clinical behavior,and poses therapeutic challenges,due to the partial efficacy of current treatment options.The advent of direct-acting antivirals(DAAs)for HCV and high-genetic barrier nucleos(t)ide analogues(NAs)for HBV has improved patient outcomes.In indolent HCV-associated B-NHLs,antiviral therapy with DAAs alone often achieves sustained virologic response and may lead to lymphoma regression.Conversely,aggressive subtypes like diffuse large B-cell lymphomas require combination treatment with immunochemotherapy.In the setting of HBV-associated lymphomas,antiviral prophylaxis with potent NAs(e.g.,entecavir or tenofovir)is essential to prevent HBV reactivation during rituximab-containing chemotherapy regimen.The integration of antiviral and anticancer therapies has been shown to enhance survival outcomes while mitigating hepatic toxicity.A comprehensive understanding of the biological interplay between chronic viral infection and B-cell transformation is critical for optimizing diagnostic and therapeutic strategies.Aim of this viewpoint is to provide evidence that early viral detection and prompt management remain the most effective strategies to improve survival rates and to reduce treatment-related morbidity in these patients.
文摘目的:探讨丙型肝炎(H C V)IgG阳性患者的血清抗-H C V IgM、丙氨酸转移酶(A LT)水平与H C V R N A之间的关系。方法:通过第三代E IA试剂盒检测抗-H C V IgG、抗-H C V IgM,全自动生化分析仪检测丙型肝炎患者A LT水平,荧光定量逆转录聚合酶链反应(R T-PC R)方法检测H C V R N A,并进行比较。结果:在丙型肝炎IgG阳性患者中,抗-H C V IgM阳性率为8.3%,H C V R N A阳性率为41.7%。H C V R N A的检出在A LT异常情况下较正常明显高(P<0.05),但A LT水平与H C V R N A含量无线性相关性(r=0.346,P>0.05)。结论:抗-H C V IgM不能反映病毒复制,A LT异常情况下H C V R N A检出率高,但A LT水平与H C V R N A含量无线性相关性,H C V R N A仍是反映H C V复制的可靠指标。
文摘目的发现HIV/HCV合并感染者中HCV自发清除特点,找出HCV自发清除的影响因素及HCV自发清除者与HCV-RNA阳性患者之间的差异,为HIV/HCV合并感染者HCV-RNA筛查及治疗提供临床指导。方法以2022年1月—2024年5月云南省传染病医院符合纳入标准的HIV/HCV合并感染者作为研究对象,其中未治疗的HCV-RNA阴性者作为实验组(清除组)、未治疗的HCV-RNA阳性者作为对照组(阳性组),收集2组患者的人口统计学、临床特征、治疗和实验室检测指标,计算HCV自发清除的能力,采用logistic回归分析探讨HIV与HCV合并感染后HCV自发清除的影响因素,并比较清除组和阳性组实验室指标及其肝功能损伤情况。结果共收集到148例HIV/HCV合并感染者,其中清除组70例、阳性组78例(剔除资料不全者3例),HCV自发清除率为9.1%(70/773)。单因素分析结果表明年龄、抗反转录病毒治疗(antiretroviral therapy,ART)方案、抗病毒治疗时间≥16年均有统计学意义(P<0.05)。多因素回归分析表明使用含蛋白酶抑制剂方案(OR=0.228,95%CI:0.064~0.810)是阻碍HCV自发清除的影响因素,抗病毒治疗时间≥16年(OR=8.587,95%CI:1.854~39.775)是促进HCV自发清除的影响因素。比较阳性组和清除组实验室指标发现阳性组ALT、AST、天冬氨酸氨基转移酶与血小板比率指数(aspartate aminotransferase to platelet ratio index,APRI)评分、纤维化指数(fibrosis 4 score,FIB-4指数)平均值及异常率均高于HCV自发清除组(P<0.001)。结论HCV合并感染HIV患者的HCV自发清除率降低,使用含蛋白酶抑制剂的ART方案、抗病毒治疗时间≥16年是HCV自发清除的独立影响因素,HCV自发清除者较HCV阳性者的肝功能损伤程度更轻。
