2型糖尿病并发冠心病患者血清同型半胱氨酸、氧化低密度脂蛋白和血小板参数的变化及意义研究

目的探讨2型糖尿病(T2DM)并发冠心病(CHD)患者血清同型半胱氨酸(Hcy)、氧化低密度脂蛋白(Ox-LDL)和血小板参数的变化及意义。方法回顾性分析了2011年11月至2014年11月收治的18例T2DM不伴CHD患者、21例CHD不伴T2DM患者及19例T2DM合并CHD患者的临床资料,另外选择同期行体检的26例健康者作为对照组。采用化学发光法、酶联免疫吸附(ELISA)法及血常规分析法分别对上述各组血清Hcy、Ox-LDL及血小板参数进行检测,并进行对比。结果 1CHD不伴T2DM组血清Hcy、Ox-LDL水平均显著高于对照组与T2DM不伴CHD组,T2DM合并CHD组血清Hcy、Ox-LDL水平均显著高于其他3组(P0.05)。2T2DM合并CHD组血清Hcy水平与Ox-LDL水平具有显著的正相关性(r=0.861,P0.01)。3CHD不伴T2DM组MPV、PDW水平均显著高于对照组与T2DM不伴CHD组(P0.05),T2DM合并CHD组MPV、PDW水平均显著高于其他3组(P0.05)。结论 T2DM患者血清高水平MPV、PDW、Hcy及Ox-LDL均为造成CHD的危险因素,因此T2DM患者应注意定期对上述指标水平变化情况进行检测,以预防并发CHD。     

2型糖尿病合并冠心病与同型半胱氨酸及胱抑素C的相关性分析

目的探讨2型糖尿病(T2DM)合并冠心病(CHD)与同型半胱氨酸(HCY)及胱抑素C(CysC)的关系及二者相关性。方法选择确诊T2DM患者151例[分为T2DM组(89例)和T2DM合并CHD(T2DM+CHD)组(62例)]及健康者50例(对照组),检测血清HCY、CysC水平,进行比较分析。结果 T2DM组血清HCY、CysC水平高于对照组(P<0.05),T2DM+CHD组高于T2DM组(P<0.05);T2DM合并CHD组血清HCY与CysC呈显著正相关(r=0.649,P<0.05)。结论 T2DM患者体内存在HCY、CysC水平异常,合并CHD患者更为显著,且HCY、CysC水平具有相关性,二者联合检测可有助于了解病情、指导治疗及判断预后。     

凝血因子Ⅴ、Ⅷ和组织因子与2型糖尿病合并冠心病的关系

目的探讨凝血因子Ⅴ活性(FⅤ:C)、凝血因子Ⅷ活性(FⅧ:C)和组织因子(TF)在2型糖尿病(T2DM)合并冠心病(HD)诊断中的应用价值。方法测定85例T2DM合并CHD患者[T2DM合并CHD组,根据CHD不同类型再分为T2DM合并急性心肌梗死(AMI)组(19例)、T2DM合并陈旧性心肌梗死(OMI)组(23例)、T2DM合并不稳定型心绞痛(UAP)组(25例)、T2DM合并稳定型心绞痛(SAP)组(18例)]、29例无合并症的单纯T2DM患者(单纯T2DM组)和24名健康对照者(正常对照组)FⅤ:C、FⅧ:C、血浆TF和血管性血友病因子(VWF)活性及血小板聚集率(PAR),并分析FⅤ:C、FⅧ:C、TF与VWF、PAR的相关性。结果 T2DM合并CHD组和单纯T2DM组FⅤ:C、FⅧ:C和TF水平均明显高于正常对照组(P0.001),且T2DM合并CHD组明显高于单纯T2DM组(P0.01)。T2DM合并CHD组中,T2DM合并AMI组和T2DM合并UAP组FⅤ:C、FⅧ:C和TF水平均明显高于单纯T2DM组(P0.001),且T2DM合并AMI组明显高于T2DM合并UAP组(P0.01);T2DM合并OMI组和T2DM合并SAP组TF水平明显高于单纯T2DM组(P0.01),但FⅤ:C和FⅧ:C水平3组之间差异无统计学意义(P0.05)。FⅤ:C、FⅧ:C、TF与VWF、PAR均呈明显正相关(P0.01)。结论FⅤ:C和FⅧ:C及TF水平可作为T2DM患者并发CHD的诊断指标。TF对判断T2DM合并CHD患者病情的进展有重要价值。     

TCF7L2基因rs7903146位点基因多态性与2型糖尿病合并冠状动脉粥样硬化性心脏病的相关性研究

目的探讨转录因子7类似物2(TCF7L2)基因rs7903146位点基因多态性与2型糖尿病(T2DM)合并冠状动脉粥样硬化性心脏病(CHD)发病风险的相关性,寻找T2DM合并CHD的易感基因及影响因素。方法选取该院100例T2DM患者为T2DM组,100例CHD患者为CHD组,100例T2DM合并CHD患者为T2DM+CHD组,100例体检健康者为对照组,检测4组TCF7L2基因rs7903146位点基因多态性,分析基因型分布特点;比较4组不同基因型血脂、血糖等指标的差异;Logistic回归分析T2DM合并CHD的影响因素。结果TCF7L2基因rs7903146位点CC/CT基因型分布在各组间比较,差异均无统计学意义(P0.05)。各组CC/CT基因型间血糖、血脂水平比较,差异均无统计学意义(P0.05)。Logistic回归分析结果显示,高龄、高水平糖化血红蛋白是T2DM合并CHD的独立危险因素,低水平高密度脂蛋白胆固醇是预防T2DM合并CHD的保护因素,而rs7903146位点基因型不是发生T2DM合并CHD的影响因素。结论TCF7L2基因rs7903146位点基因多态性与T2DM合并CHD发病风险,血糖、血脂水平无关。     

巨噬细胞移动抑制因子在2型糖尿病合并冠心病中的作用研究

目的探讨巨噬细胞移动抑制因子(MIF)水平与2型糖尿病(T2DM)合并冠心病(CHD)的关系及其临床意义。方法选取T2DM合并CHD(T2DM+CHD组)患者46例、单纯T2DM(T2DM组)患者45例、单纯CHD(CHD组)患者44例、门诊体检者(对照组)45例,检测各组血清MIF水平、空腹血糖(FBG)、总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)浓度、糖化血红蛋白(HbA1c)和空腹血清胰岛素(FINS),计算胰岛素抵抗指数(HOMA-IR)、体重指数(BMI),并作相关分析。结果 T2DM+CHD组血清MIF水平均明显高于T2DM组、CHD组和对照组,差异均有统计学意义(q分别=2.58、2.33、2.87,P均<0.05)。T2DM+CHD组和T2DM组MIF水平均与TG、HbA1c呈正相关(r分别=0.35、0.26、0.29、0.31,P均<0.05);T2DM与MIF、HbA1c密切相关(OR分别=2.11、1.09,P均<0.05),T2DM合并CHD与MIF、TG密切相关(OR分别=3.95、2.29,P均<0.05)。结论血清MIF与T2DM合并CHD的发病有一定联系。     

血清成纤维细胞生长因子-21在2型糖尿病合并冠心病中的作用研究

目的探讨血清成纤维细胞生长因子-21(FGF-21)水平与2型糖尿病(T2DM)合并冠心病(CHD)的关系及其临床意义。方法选取单纯T2DM患者50例(T2DM组)、T2DM合并CHD患者48例(T2DM+CHD组)、单纯CHD患者47例(CHD组)、门诊健康体检者50例(对照组),用酶联免疫吸附法检测血清FGF-21水平,并测定空腹血糖、总胆固醇、三酰甘油、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇浓度,糖化血红蛋白和空腹血清胰岛素,计算胰岛素抵抗指数、体重指数及腰臀比,并作相关比较和分析。结果 T2DM+CHD组血清FGF-21水平均明显高于T2DM组、CHD组和对照组,差异均有统计学意义(q分别=3.55、3.74、3.96,P均<0.05);T2DM+CHD组FGF-21水平与腰臀比、三酰甘油和胰岛素抵抗指数呈正相关(r分别=0.195、0.255、0.189,P均<0.05);FGF-21和糖化血红蛋白是T2DM危险因素,FGF-21和三酰甘油是T2DM合并CHD的危险因素。结论血清FGF-21与T2DM合并CHD的发病有一定联系。     

血清ox-LDL/β2-GPI复合物在2型糖尿病合并冠心病中的作用研究

目的探讨血清氧化低密度脂蛋白(ox-LDL)/β2-糖蛋白Ⅰ(β2-GPI)复合物水平与2型糖尿病(T2DM)合并冠心病(CHD)的关系及其临床意义。方法选取T2DM合并CHD患者68例、单纯T2DM患者69例、单纯CHD患者65例、门诊健康体检者60名。用酶联免疫吸附试验(ELISA)检测血清ox-LDL/β2-GPI复合物水平,并测定空腹血糖(FBG)、总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、糖化血红蛋白(HbA1C)和空腹血清胰岛素(FINS)、计算体重指数(BMI)及腰臀比(WHR),并作相关分析。结果 T2DM合并CHD组血清ox-LDL/β2-GPI复合物水平均显著高于单纯T2DM组、单纯CHD组和对照组,差异有统计学意义(P<0.05);T2DM合并CHD组ox-LDL/β2-GPI复合物水平均与TG和HOMA-IR呈正相关(r=0.219、0.228,P均<0.01);TG和ox-LDL/β2-GPI复合物是T2DM危险因素,ox-LDL/β2-GPI复合物和HbA1C是T2DM合并CHD的危险因素。结论血清ox-LDL/β2-GPI复合物与T2DM合并CHD的发病有一定联系。     

瑞舒伐他汀对冠心病合并2型糖尿病患者血浆Omentin-1的影响

目的探讨冠心病(CHD)合并2型糖尿病(T2DM)患者血浆网膜素-1(Omentin-1)水平的变化及瑞舒伐他汀治疗对Omentin-1水平的影响。方法选择临床确诊的住院和门诊单纯T2DM患者42例和CHD合并T2DM患者47例。同期选择健康体检者37例作为正常对照组(NC组)。采用ELISA法测定所有研究对象及CHD合并T2DM组瑞舒伐他汀治疗后血浆Omentin-1水平,并分析血浆Omentin-1水平与白细胞介素6(IL-6)、空腹胰岛素(FINS)、体重指数(BMI)、内皮素(ET)、胰岛素抵抗指数(HOMA-IR)和一氧化氮(NO)等的关系。结果与NC组(24.79±6.18ng/ml)比较,CHD合并T2DM组治疗前(14.75±4.02 ng/ml)和单纯T2DM组(19.32±5.17 ng/ml)患者血浆Omentin-1水平均明显降低(P均0.01),CHD合并T2DM组治疗前血浆Omentin-1水平显著低于单纯T2DM组(14.75±4.02vs.18.30±5.17 ng/ml,P0.01)。CHD合并T2DM患者血浆Omentin-1水平与FINS、BMI、HOMA-IR、IL-6、ET呈明显负相关,与NO呈正相关(P0.01或P0.05)。HOMA-IR、IL-6和NO是影响CHD合并T2DM患者血浆Omentin-1水平的独立相关因素。CHD合并T2DM患者经瑞舒伐他汀治疗后TC、LDL-C、IL-6和ET均显著降低,而HDL-C和NO则显著增高(P0.05),同时血浆Omentin-1水平也明显升高(18.35±3.97 vs.14.75±4.02 ng/ml,P0.01)。结论瑞舒伐他汀在有效调节CHD合并T2DM患者脂代谢,减轻炎症反应,改善内皮功能的同时,升高血浆Omentin-1水平。     

2型糖尿病及合并冠心病患者内脏脂肪素表达差异及临床意义

目的:探讨2型糖尿病(T2DM)及合并冠心痛(CHD)患者内脏脂肪素(visfatin)表达与体重指数(BMI)、腰臀比(WHR)、空腹血糖(FPG)、糖化血红蛋白(HbAlc)、胰岛素抵抗指数(Homa-IR)等相关因素的关系.方法:用ELISA法检测单纯T2DM组、T2DM合并CHD组及正常对照组的血清visfatin水平和胰岛素,用日立全自动生化分析仪测定FPG、血脂,测量所有观察对象的身高、体重、腰围和臀围.结果:单纯T2DM组、T2DM合并CHD组visfatin水平均高于正常对照组(P<0.01);T2DM合并CHD组显著高于T2DM组(P<0.01);肥胖组高于同组非肥胖组.visfatin水平与Homa-IR、WHR呈独立正相关.结论:T2DM合并CHD患者血清visfatin表达与Homa-IR、WHR存在密切的相关性,在T2DM及合并CHD的发生发展中起着重要作用.     

高龄老年男性2型糖尿病合并冠状动脉粥样硬化性心脏病患者的临床特征及危险因素

目的探讨高龄老年2型糖尿病(type 2 diabetes,T2DM)合并冠状动脉粥样硬化性心脏病(coronary atherosclerotic heart disease,CHD)患者临床特征并分析T2DM患者发生CHD并发症的危险因素。方法采用回顾性队列研究方法,选取2017年1月至2020年1月上海交通大学医学院附属新华医院收治的406例高龄(≥75周岁)老年男性T2DM患者,分为T2DM未合并CHD组(165例)与T2DM合并CHD组(241例),分析高龄老年T2DM合并CHD患者临床特征及发生CHD的危险因素。结果T2DM合并CHD组患者年龄[(86.78±5.35)岁]、病程[(12.32±0.46)年]、空腹血糖(fasting plasma glucose,FPG)[(7.64±2.81)mmol/L]、糖化血红蛋白(hemoglobin a1c,HbA1c)[(7.59±1.21)%]、高血压占比[84.65%(204/241)]、D-二聚体[(0.50±0.13)mg/L]、血栓栓塞事件发生率[46.06%(111/241)]、血肌酐[(94.81±12.70)μmol/L]、尿素氮[(8.31±4.46)mmol/L]、尿酸[(376.44±116.01)μmol/L]均高于T2DM未合并CHD组[(78.51±4.81)岁、(10.66±0.67)年、(6.84±2.19)mmol/L、(7.02±2.15)%、63.03%(104/165)、(0.21±0.04)mg/L、13.33%(22/165)、(83.01±14.40)μmol/L、(6.79±2.89)mmol/L、(333.56±95.15)μmol/L],差异有统计学意义(t=15.908、t=2.042、t=3.055、t=3.088、χ^(2)=23.828、t=5.059、χ^(2)=42.098、t=2.401、t=4.188、t=4.075,P均<0.05);T2DM合并CHD组患者总胆红素[(8.80(6.60,11.60)μmol/L]、肾小球滤过率[glomerular filtration rate,GFR][(76.49±29.80)mL/(min·1.75 m^(2))]均低于T2DM未合并CHD组[11.25(8.23,15.28)μmol/L、(91.81±28.31)mL/(min·75 m^(2))],差异有统计学意义(Z=2.304、t=5.126,P均<0.001);T2DM合并CHD组患者总胆固醇[(3.84±0.85)mmol/L]、低密度脂蛋白胆固醇[low-density lipoprotein cholesterol,LDL-C][(2.12±0.68)mmol/L]低于T2DM未合并CHD组[(4.10±1.00)mmol/L、(2.45±0.85)mmol/L],差异有统计学意义(t=2.828、4.156,P均<0.05);T2DM合并CHD组患者启动降脂稳定斑块治疗率[82.57%(199/261)]高于T2DM未合并CHD组[42.42%(70/165)],差异有统计学意义(χ^(2)=70.614,P<0.001);受降脂治疗影响,T2DM合并CHD组总胆固醇和LDL-C明显降低。Logistic回归分析显示,年龄增加(OR 1.346,95%CI 1.263~1.434,P<0.001)、糖化血红蛋白浓度升高(OR 1.427,95%CI 1.140~1.785,P=0.002)、合并高血压(OR 3.534,95%CI 1.684~7.418,P=0.001)、D-二聚体升高(OR 3.969,95%CI 1.227~12.841,P=0.021)以及尿酸升高(OR 1.005,95%CI 1.001~1.008,P=0.006)是高龄老年男性T2DM患者CHD发病的独立危险因素。结论T2DM合并CHD高龄老年患者更易处于高凝状态,更容易发生血栓栓塞事件,肾功能损伤更为明显;空腹血糖控制不佳、总胆红素浓度降低是高龄老年男性T2DM患者发生CHD的影响因素,年龄增加、糖化血红蛋白浓度升高、合并高血压、D-二聚体升高及尿酸浓度升高是高龄老年男性T2DM患者CHD发病的独立危险因素。     

Migraine and genetic and acquired vasculopathies

It is remarkable that migraine is a prominent part of the phenotype of several genetic vasculopathies, including cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL), retinal vasculopathy with cerebral leukodystrophy (RVCL) and hereditary infantile hemiparessis, retinal arteriolar tortuosity and leukoencephalopahty (HIHRATL). The mechanisms by which these genetic vasculopathies give rise to migraine are still unclear. Common genetic susceptibility, increased susceptibility to cortical spreading depression (CSD) and vascular endothelial dysfunction are among the possible explanations. The relation between migraine and acquired vasculopathies such as ischaemic stroke and coronary heart disease has long been established, further supporting a role of the (cerebral) blood vessels in migraine. This review focuses on genetic and acquired vasculopathies associated with migraine. We speculate how genetic and acquired vascular mechanisms might be involved in migraine.     

Fibrinogen and fibrin structure and functions

Fibrinogen molecules are comprised of two sets of disulfide-bridged Aalpha-, Bbeta-, and gamma-chains. Each molecule contains two outer D domains connected to a central E domain by a coiled-coil segment. Fibrin is formed after thrombin cleavage of fibrinopeptide A (FPA) from fibrinogen Aalpha-chains, thus initiating fibrin polymerization. Double-stranded fibrils form through end-to-middle domain (D:E) associations, and concomitant lateral fibril associations and branching create a clot network. Fibrin assembly facilitates intermolecular antiparallel C-terminal alignment of gamma-chain pairs, which are then covalently 'cross-linked' by factor XIII ('plasma protransglutaminase') or XIIIa to form 'gamma-dimers'. In addition to its primary role of providing scaffolding for the intravascular thrombus and also accounting for important clot viscoelastic properties, fibrin(ogen) participates in other biologic functions involving unique binding sites, some of which become exposed as a consequence of fibrin formation. This review provides details about fibrinogen and fibrin structure, and correlates this information with biological functions that include: (i) suppression of plasma factor XIII-mediated cross-linking activity in blood by binding the factor XIII A2B2 complex. (ii) Non-substrate thrombin binding to fibrin, termed antithrombin I (AT-I), which down-regulates thrombin generation in clotting blood. (iii) Tissue-type plasminogen activator (tPA)-stimulated plasminogen activation by fibrin that results from formation of a ternary tPA-plasminogen-fibrin complex. Binding of inhibitors such as alpha2-antiplasmin, plasminogen activator inhibitor-2, lipoprotein(a), or histidine-rich glycoprotein, impairs plasminogen activation. (iv) Enhanced interactions with the extracellular matrix by binding of fibronectin to fibrin(ogen). (v) Molecular and cellular interactions of fibrin beta15-42. This sequence binds to heparin and mediates platelet and endothelial cell spreading, fibroblast proliferation, and capillary tube formation. Interactions between beta15-42 and vascular endothelial (VE)-cadherin, an endothelial cell receptor, also promote capillary tube formation and angiogenesis. These activities are enhanced by binding of growth factors like fibroblast growth factor-2 (FGF-2) and vascular endothelial growth factor (VEGF), and cytokines like interleukin (IL)-1. (vi) Fibrinogen binding to the platelet alpha(IIb)beta3 receptor, which is important for incorporating platelets into a developing thrombus. (vii) Leukocyte binding to fibrin(ogen) via integrin alpha(M)beta2 (Mac-1), which is a high affinity receptor on stimulated monocytes and neutrophils.     

Telemedicine and teleradiology technologies and applications

Summary. Telemedicine and teleradiology hold the key for improving future health care delivery. In this paper we first review current communication and computer technologies used in telemedicine and teleradiology. Five examples in teleradiology applications are given including hospital-integrated picture archiving and communication systems, tele-neuro-imaging, telemammography, university consortium teleradiology service, and teleradiology for second opinion. Parameters important to teleradiology applications like costs, image quality, system reliability, and turn around time are considered. Data security is discussed, including patient confidentiality and image authenticity-which will be a major issue in future teleradiology applications.     

创伤高血糖与感染和MODS早期诊断和干预

本文详细介绍了创伤后血糖应激适度理论,以及高血糖与感染和多器官功能不全综合征的关系;提出涉及胰岛B细胞功能不全的MODS实验诊断新方案和极化液个体化干预新措施,可早期发现创伤MODS、降低感染率及MODS发生率和病死率。     

腹膜后纤维化与肾积水发生关系的临床研究

目的：探讨腹膜后纤维化（RPF）导致肾积水的原因及诊治经验。方法：回顾分析2004年1月—2010年12月24例腹膜后纤维化致肾积水患者的诊治资料。结果：（1）RPF患者常见首发症状为腰背痛或腹痛（69.2%）;（2）红细胞沉降率（ESR）增快和血清IgG4升高最常见。超声检查仅提示上尿路积水。RPF的静脉肾盂造影（IVP）和CT尿路成像（CTU）表现具有特征性。IVP肾盂输尿管显影不良时,CTU能较清晰的显示上尿路影像。CT扫描发现腹膜后软组织肿块9例（37.5%）,优于超声检查;（3）输尿管松解和腹腔化手术治疗22例;行肾切除术1例;行输尿管置双J管术1例。最终确诊为继发性RPF8例,其中4例为术前诊断,3例为术中腹膜后软组织肿块冷冻活检证实,1例为术后病理证实;（4）特发性RPF手术后肾积水均获长期缓解,而继发性RPF的预后取决于原发疾病及其治疗方案。结论：影像学检查是诊断RPF的重要手段,CTU优于超声检查和IVP。输尿管松解和腹腔化手术可以使特发性RPF输尿管梗阻得到长期的缓解,术中对肿块进行冷冻活检有助于鉴别特发性和继发性RPF,及时调整治疗方案。     

探讨儿童慢性顽固性咳嗽与支原体感染的关系及临床治疗观察

目的探讨儿童慢性顽固性咳嗽与肺炎支原体（MP）感染的关系及临床疗效观察。方法采用回顾性研究方法对于现将2005年3月至2008年3月在我院的55例确诊慢性顽固性咳嗽患儿,主要表现为肺炎支原体感染为临床特点进行分析,并进一步临床治疗研究。结果①临床特点：在55例确诊慢性咳嗽的患儿中,以慢性顽固性咳嗽为主要症状。58％（32／55）的病例无肺部体征;②外周血：85％（47／55）的病例外周血变化不大,WBC（4—10）×10 9／L之间,嗜酸性粒细胞增多;③特别检查：47．27％（26／55）肺炎支原体IgM（MP—IgM）抗体阳性,83．64％（46／55）PeR技术检测肺炎支原体特异性DNA;④X光报告为多种形式。结论肺炎支原体（MP）感染是引起儿童慢性顽固性咳嗽的病因之一,对儿童慢性咳嗽,特别是顽固性咳嗽的诊治中应更加重视。     

Acetaminophen and acetylcysteine dose and duration: Past,present and future

Abstract

Acetylcysteine has been utilized successfully in the treatment of acetaminophen overdose since the 1970s. Although prospective trials as to efficacy and safety of acetylcysteine were conducted, there were no randomized controlled trials. This commentary addresses the reasons for this, and the background to choice of dose of acetylcysteine utilized in the oral and IV dosing regimens. Nomograms to predict possible hepatotoxicity based upon time of ingestion of acetaminophen were developed from a relatively arbitrary definition of toxicity as an aspartate aminotransferase/alanine aminotransferase (ALT/AST) greater than 1000 IU/L. While these have proved generally useful, patients still continue to develop hepatic damage after acetaminophen overdose, particularly if they present late after ingestion. The optimum management of these patients remains unclear, and one area of uncertainty is the dose and duration of acetylcysteine in various circumstances. This article discusses the issues that need to be elucidated to better target changes in acetylcysteine dose. The potential for measurements of other markers to improve treatment selection is the subject of further research.     

VEGF和NSE在良恶性嗜铬细胞瘤中的表达及意义

目的探讨肿瘤标志物血管内皮生长因子（VEGF）和神经元特异性烯醇化酶（NSE）在良、恶性嗜铬细胞瘤组织中的表达,分析其可能的临床价值及病理学意义,为临床鉴别良、恶性嗜铬细胞瘤提供辅助依据。方法应用免疫组化（SP法）检测16例恶性嗜铬细胞瘤、18例良性嗜铬细胞瘤及17例正常肾上腺髓质组织中细胞因子VEGF和NSE表达情况,显微镜下判断组织切片的染色结果。结果①恶性嗜铬细胞瘤VEGF表达明显强于正常肾上腺髓质和良性嗜铬细胞瘤（P〈0.01）。良性肿瘤和正常肾上腺髓质的VEGF表达差异无统计学意义（P〉0.05）。恶性嗜铬细胞瘤强阳性率明显高于良性嗜铬细胞瘤（P〈0.01）。②良、恶性嗜铬细胞瘤NSE表达差异有统计学意义（P〈0.05）,良性嗜铬细胞瘤NSE的表达高于正常肾上腺髓质的NSE表达（P〈0.05）。恶性嗜铬细胞瘤强阳性率高于良性嗜铬细胞瘤（P〈0.05）。③VEGF和NSE共同阳性表达在良、恶性嗜铬细胞瘤之间差异有统计学意义（P=〈0.01）。结论临床上检测VEGF和NSE可能为鉴别良、恶性嗜铬细胞瘤提供辅助依据,共同检测VEGF和NSE可能提高良、恶性嗜铬细胞瘤鉴别的敏感性。