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
目的探究黑龙江地区人类免疫缺陷病毒(human immunodeficiency virus,HIV)合并丙型肝炎病毒(hepatitis C virus,HCV)感染人群流行病学特征及死亡影响因素。方法回顾性分析2019年1月至2023年12月于北大荒集团总医院就诊的712例HIV感染患...目的探究黑龙江地区人类免疫缺陷病毒(human immunodeficiency virus,HIV)合并丙型肝炎病毒(hepatitis C virus,HCV)感染人群流行病学特征及死亡影响因素。方法回顾性分析2019年1月至2023年12月于北大荒集团总医院就诊的712例HIV感染患者的临床资料,采用ELISA检测其HCV感染情况,分析HIV合并HCV感染人群流行特征;根据随访的结果将116例双重感染的患者分为存活组(n=90)和死亡组(n=26),分析HIV合并HCV双重感染患者死亡的危险因素。结果HIV合并HCV感染率为16.29%,30~50岁年龄段人群合并感染率(25.47%)最高,职业为农民的合并感染率(26.85%)最高,以静脉吸毒途径感染的合并感染率最高(61.90%)。多因素logistic回归结果显示,HIV感染确诊年龄(OR=1.827,95%CI:1.263~2.722)、感染途径(OR=1.796,95%CI:1.248~2.503)、抗病毒治疗(OR=1.724,95%CI:1.202~2.367)、首次CD4~+T淋巴细胞(OR=2.536,95%CI:1.776~3.739)、确诊至启动治疗时间间隔(OR=1.953,95%CI:1.431~2.952)是合并感染患者死亡的危险因素(P<0.05)。结论HIV合并HCV感染率为16.29%,合并感染率较高。为降低双重感染死亡率应重点关注≥40岁、静脉吸毒、未抗病毒治疗、首次CD4~+T淋巴细胞水平较低、确诊至启动治疗时间间隔较长的患者,临床积极治疗改善免疫功能,延长患者生命。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。
文摘目的探究黑龙江地区人类免疫缺陷病毒(human immunodeficiency virus,HIV)合并丙型肝炎病毒(hepatitis C virus,HCV)感染人群流行病学特征及死亡影响因素。方法回顾性分析2019年1月至2023年12月于北大荒集团总医院就诊的712例HIV感染患者的临床资料,采用ELISA检测其HCV感染情况,分析HIV合并HCV感染人群流行特征;根据随访的结果将116例双重感染的患者分为存活组(n=90)和死亡组(n=26),分析HIV合并HCV双重感染患者死亡的危险因素。结果HIV合并HCV感染率为16.29%,30~50岁年龄段人群合并感染率(25.47%)最高,职业为农民的合并感染率(26.85%)最高,以静脉吸毒途径感染的合并感染率最高(61.90%)。多因素logistic回归结果显示,HIV感染确诊年龄(OR=1.827,95%CI:1.263~2.722)、感染途径(OR=1.796,95%CI:1.248~2.503)、抗病毒治疗(OR=1.724,95%CI:1.202~2.367)、首次CD4~+T淋巴细胞(OR=2.536,95%CI:1.776~3.739)、确诊至启动治疗时间间隔(OR=1.953,95%CI:1.431~2.952)是合并感染患者死亡的危险因素(P<0.05)。结论HIV合并HCV感染率为16.29%,合并感染率较高。为降低双重感染死亡率应重点关注≥40岁、静脉吸毒、未抗病毒治疗、首次CD4~+T淋巴细胞水平较低、确诊至启动治疗时间间隔较长的患者,临床积极治疗改善免疫功能,延长患者生命。
