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
目的探析脑梗死患者髓鞘碱性蛋白(myelin basic protein,MBP)、S100钙结合蛋白B(S100 calcium-binding protein B,S100-B)水平与介入治疗后早期神经功能恶化的关联性。方法纳入2021年7月–2024年7月期间本院收治的258例脑梗死患者,采用...目的探析脑梗死患者髓鞘碱性蛋白(myelin basic protein,MBP)、S100钙结合蛋白B(S100 calcium-binding protein B,S100-B)水平与介入治疗后早期神经功能恶化的关联性。方法纳入2021年7月–2024年7月期间本院收治的258例脑梗死患者,采用美国国立卫生研究院卒中量表(National Institutes of Health Stroke Scale,NIHSS)评分评估患者的神经功能状况,将死亡患者或介入治疗24 h后NIHSS评分增加4分及以上患者纳入早期神经功能恶化组,其余患者纳入未恶化组。测定所有患者MBP、S100-B水平,并分析其水平变化与介入治疗后神经功能恶化风险的关系。结果脑梗死患者早期神经功能恶化组血清MBP、S100-B水平高于未恶化组〔t=9.062(95%CI:2.348~3.663)、7.708(95%CI:0.221~0.375),P<0.001〕;Spearman相关性显示:恶化组血清MBP、S100-B水平与NIHSS评分增加情况呈正相关〔r=0.323(95%CI:0.095~0.542)、0.292(95%CI:0.066~0.488),P<0.05〕;分层回归分析显示:血清MBP〔比值比(odds ratio,OR)=1.996,95%CI:1.607~2.478〕、S100-B(OR=1.005,95%CI:1.003~1.007)水平是影响脑梗死患者早期神经功能恶化的危险因素(P<0.05),即使校正混杂因素后依然是其危险因素,此外入院NIHSS评分(OR=1.224,95%CI:1.142~1.310)及合并高血压(OR=2.542,95%CI:1.139~5.669)、高脂血症(OR=2.618,95%CI:1.101~6.228),其中入院NIHSS评分与MBP存在交互作用(OR=1.081,95%CI:1.034~1.130);受试者工作特征曲线显示:血清MBP、S100-B水平评估脑梗死患者早期神经功能恶化的曲线下面积分别为0.822(95%CI:0.764~0.879)、0.788(95%CI:0.724~0.853)。结论脑梗死患者介入治疗后血清MBP、S100-B水平较高与早期神经功能恶化风险相关,且对神经功能恶化风险有一定的评估价值。展开更多
目的:探讨血清高迁移率族蛋白B1(HMGB1)、S100β联合脑电双频指数(BIS)在脓毒症相关性脑病(SAE)早期诊断中的应用价值。方法:回顾性分析脓毒症病人87例临床资料,根据是否合并SAE,分为SAE组35例和非SAE组52例。比较2组病人相关临床资料...目的:探讨血清高迁移率族蛋白B1(HMGB1)、S100β联合脑电双频指数(BIS)在脓毒症相关性脑病(SAE)早期诊断中的应用价值。方法:回顾性分析脓毒症病人87例临床资料,根据是否合并SAE,分为SAE组35例和非SAE组52例。比较2组病人相关临床资料和血清HMGB1、S100β水平及24 h BIS,分析脓毒症病人发生SAE的影响因素和HMGB1、S100β、BIS联合检测早期诊断SAE的临床价值。结果:SAE组病人APACHEⅡ评分、SOFA评分均明显高于非SAE组(P<0.01);SAE组血清HMGB1、S100β水平均明显高于非SAE组(P<0.01),而BIS明显低于非SAE组(P<0.01)。APACHEⅡ评分、SOFA评分和HMGB1、S100β、BIS均为脓毒症病人发生SAE的独立影响因素(P<0.01)。ROC曲线分析显示,血清HMGB1、S100β联合BIS早期诊断脓毒症病人发生SAE的AUC为0.891,敏感度为91.43%,特异度为84.62%,优于各指标独立诊断。结论:血清HMGB1、S100β联合BIS在SAE早期诊断中具有较好的临床应用价值。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.
文摘目的探析脑梗死患者髓鞘碱性蛋白(myelin basic protein,MBP)、S100钙结合蛋白B(S100 calcium-binding protein B,S100-B)水平与介入治疗后早期神经功能恶化的关联性。方法纳入2021年7月–2024年7月期间本院收治的258例脑梗死患者,采用美国国立卫生研究院卒中量表(National Institutes of Health Stroke Scale,NIHSS)评分评估患者的神经功能状况,将死亡患者或介入治疗24 h后NIHSS评分增加4分及以上患者纳入早期神经功能恶化组,其余患者纳入未恶化组。测定所有患者MBP、S100-B水平,并分析其水平变化与介入治疗后神经功能恶化风险的关系。结果脑梗死患者早期神经功能恶化组血清MBP、S100-B水平高于未恶化组〔t=9.062(95%CI:2.348~3.663)、7.708(95%CI:0.221~0.375),P<0.001〕;Spearman相关性显示:恶化组血清MBP、S100-B水平与NIHSS评分增加情况呈正相关〔r=0.323(95%CI:0.095~0.542)、0.292(95%CI:0.066~0.488),P<0.05〕;分层回归分析显示:血清MBP〔比值比(odds ratio,OR)=1.996,95%CI:1.607~2.478〕、S100-B(OR=1.005,95%CI:1.003~1.007)水平是影响脑梗死患者早期神经功能恶化的危险因素(P<0.05),即使校正混杂因素后依然是其危险因素,此外入院NIHSS评分(OR=1.224,95%CI:1.142~1.310)及合并高血压(OR=2.542,95%CI:1.139~5.669)、高脂血症(OR=2.618,95%CI:1.101~6.228),其中入院NIHSS评分与MBP存在交互作用(OR=1.081,95%CI:1.034~1.130);受试者工作特征曲线显示:血清MBP、S100-B水平评估脑梗死患者早期神经功能恶化的曲线下面积分别为0.822(95%CI:0.764~0.879)、0.788(95%CI:0.724~0.853)。结论脑梗死患者介入治疗后血清MBP、S100-B水平较高与早期神经功能恶化风险相关,且对神经功能恶化风险有一定的评估价值。
文摘目的:探讨血清高迁移率族蛋白B1(HMGB1)、S100β联合脑电双频指数(BIS)在脓毒症相关性脑病(SAE)早期诊断中的应用价值。方法:回顾性分析脓毒症病人87例临床资料,根据是否合并SAE,分为SAE组35例和非SAE组52例。比较2组病人相关临床资料和血清HMGB1、S100β水平及24 h BIS,分析脓毒症病人发生SAE的影响因素和HMGB1、S100β、BIS联合检测早期诊断SAE的临床价值。结果:SAE组病人APACHEⅡ评分、SOFA评分均明显高于非SAE组(P<0.01);SAE组血清HMGB1、S100β水平均明显高于非SAE组(P<0.01),而BIS明显低于非SAE组(P<0.01)。APACHEⅡ评分、SOFA评分和HMGB1、S100β、BIS均为脓毒症病人发生SAE的独立影响因素(P<0.01)。ROC曲线分析显示,血清HMGB1、S100β联合BIS早期诊断脓毒症病人发生SAE的AUC为0.891,敏感度为91.43%,特异度为84.62%,优于各指标独立诊断。结论:血清HMGB1、S100β联合BIS在SAE早期诊断中具有较好的临床应用价值。
