糖尿病肾病患者透析前期心脏结构功能特征及相关因素分析

目的 分析糖尿病肾病患者心脏结构及功能的改变及其与相关因素的关系.方法 对48例血清肌酐<445μmol/L、未行血液净化的糖尿病肾病患者的血压、血红蛋白、血生化指标、尿微量白蛋白排泄率、血浆甲状旁腺素和胰岛素等进行检测,描记超声心动图,计算左心室心肌重量指数(LVMI),对心脏的结构和功能特征进行分析,并对LVMI与上述指标进行相关分析.结果 48例中有左心室肥厚(LVH)者占58.3%,其中向心性肥厚占37.5%;无LVH而有向心性重构者占16.7%;20.8%左心室收缩功能障碍;有LVH组和无LVH组的血红蛋白、收缩压、血清白蛋白、血脂、血浆甲状旁腺激素以及内生肌酐清除率等,均存在明显差异;LVMI与血红蛋白、内生肌酐清除率呈负相关(r值分别为-0.34、-0.45,P值分别为P<0.05、P<0.01),与血浆全段PTH(iPTH)、尿微量白蛋白排泄率以及甘油三酯呈正相关(r值分别为0.514,0.35、0.48,P值分别为0.01、<0.05、<0.01).结论 处于透析前期糖尿病肾病患者,左心室肥厚尤其向心性肥厚发生率比较高,收缩压、贫血、高脂血症、营养不良、肾损害程度、代谢性酸中毒、继发性甲旁亢等都是重要的影响因素,早期检查心脏结构和功能,及早对这些影响因素进行干预具有重要意义.     

维持性血液透析患者肾素-血管紧张素-醛固酮系统与心脏结构及功能的相关性

目的检测维持性血液透析患者血浆中肾素-血管紧张素-醛固酮系统（RAAS）活性,探讨其与患者左心室的结构及功能的关系,为改善患者的心功能及提高生存质量提供临床依据。方法用放射免疫法测定天津市人民医院肾内科40例血液透析患者和20例健康对照组的RAAS活性并进行比较,同时将两组的RAAS水平与心脏超声指标进行相关分析。结果①血液透析组患者的RAAS活性较健康对照组明显增高,左心室肥厚发生率也远高于对照组;②血液透析组血浆血管紧张素（AngⅡ）、醛固酮（ALD）水平与左心室心肌重量指数（LVMI）存在显著正相关性,患者的血浆AngⅡ水平与收缩压有明显正相关。对照组血浆RAAS活性与LVMI无相关性;③血液透析组左心室肥厚（LVH）与收缩压呈正相关,与血红蛋白、红细胞压积呈负相关;但与患者的年龄、性别、透析龄及血肌酐水平无关;④根据LVMI值将血液透析组患者分为有LVH组和无LVH组,两组间血红蛋白、收缩压差异有显著性;而两组之间患者的年龄、透析龄、舒张压、透析前血肌酐差异无显著性。结论透析患者LVH的发生率显著高于正常人,LVH发生与体内RAAS活性升高呈正相关,与血红蛋白水平呈负相关。     

110例慢性肾功能衰竭患者的心脏结构及心功能状况分析

目的研究分析慢性肾功能衰竭(CRF)患者左心室肥厚(LVH)、心功能异常的情况.方法CRF患者110例,男57例,女53例.年龄20～90岁,平均年龄(53.5±10.9)岁.其中维持性血液透析(HD)患者56例,接受肾替代治疗前(ND)患者54例.维持性血液透析患者透析前检查心脏超声左心室舒张末内径(LVEDd),室间隔舒张末厚度(IVS),左心室后壁舒张末厚度(PWTH),左心室射血分数(EF),公式计算左心室心肌重量指数(LVMI).分析上述检查异常的发生情况.结果110例CRF患者70.9%有LVH[LVMI:(182.56±52.90)g/m2],32.97%存在LVEDd增大(50.03±5.39)mm,61.8%存在IVS增厚(12.14±1.55)mm,60.9%存在PWTH增厚(11.83±1.52)mm,19.1%有EF下降(60.49±10.54)%.接受肾替代治疗前的患者43%存在LVEDD增大(48.78±4.16)mm,72%存在IVS增(1.55±1.72)mm,68.5%存在PWTH增厚(11.29±1.65)mm,17.6%有左心室EF下降(60.2±13.65)%.接受肾替代治疗前患者(54例)与维持性血液透析患者(56例)比较存在较重的贫血、高血压,且LVH在接受肾替代治疗前患者中更明显.结论本研究证实CRF患者普遍存在左心室肥厚及心功能异常,并且在接受肾替代治疗前就存在严重的左心室结构异常;提示对CRF患者早期常规心脏结构及心功能状况检查,防治LVH及心功能异常,作为降低CRF患者死亡危险的重要措施.     

40岁以下青年狼疮性肾炎患者左心室肥厚发生率及危险因素

目的:探讨青年狼疮性肾炎(lupus nephritis,LN)患者左心室肥厚的发生率及其相关危险因素。方法:回顾性分析2000年1月至2014年7月我院310例小于40岁确诊LN的患者,按照左室质量指数(left ventricular mass index,LVMI)分为左室肥厚(LVH)组及非左室肥厚(Non-LVH)组,比较两组患者一般情况、生化指标之间的差异,同时了解LVH的相关危险因素。结果:310例青年LN患者中LVH发生率为40.6%(n=126)。与Non-LVH组患者相比,LVH组患者男性比例少,血压(收缩压、舒张压)、血脂(总胆固醇、甘油三酯)、血肌酐、血尿酸、血磷、高敏C反应蛋白、补体C4、24h尿蛋白高,同时血钙、eGFR、血红蛋白低(P0.05)。多因素Logistic分析示收缩压、高敏C反应蛋白与LVH发生率呈正相关,血红蛋白、e GFR与LVH发生率负相关(P0.05)。结论:青年LN患者LVH发生率较高,其中高血压、贫血、炎症状态及肾功能减退是其LVH的独立危险因素。     

慢性肾功能衰竭患者心脏结构及心功能改变的影响因素

目的　研究慢性肾功能衰竭 (CRF)患者心脏左室肥大 (LVH)和相关危险因素。方法　CRF患者 83例 ,男 4 2例 ,女 4 1例。年龄 2 0～ 90岁 ,平均年龄 (5 3 7± 12 7)岁。彩色多普勒心脏超声检查左室舒张末内径增大 (LVEDD) ,室间隔舒张末厚度 (IVS) ,左室后壁舒张末厚度 (PWTH) ,射血分数 (EF) ,检测血Hb和HCT ,空腹血清甲状旁腺素 (PTH)及肌酐 (Cr) ,测量血压。透析患者于透析前采血和超声检查。公式计算左室心肌重量指数 (LVMI)。结果　 83例CRF患者 71 8%有LVH[LVMI(179 2 8± 6 6 92 )g m2 ]。 37 35 %存在LVEDd增大 (49 6 4± 6 5 5 )mm ,5 7 83%存在IVS增厚 (12 0 6± 1 94 )mm ,5 7 83%存在PWTH增厚 (11 6 7± 1 95 )mm ,14 4 6 %有EF下降 (6 1 17± 11 16 ) %。CRF患者其PWHT、IVST、LVEDD、LVMI与PTH、Cr及血压呈正相关 ;EF与Cr、PTH、HCT、Hb及血压无相关性。结论　LVH是CRF患者预测死亡危险度的重要指标 ,而LVH与Cr水平、PTH增高、血压明显相关 ,心功能EF也与Cr、PTH增高有关 ,控制Cr水平 ,治疗甲状旁腺功能更亢进和合理的降压治疗应有助于减少左室肥厚的发生 ,提高肾功能不全患者的生存质量。     

高血压左室肥厚患者T波峰-末间期的改变

目的:探讨高血压左室肥厚(LVH)患者T波峰-末间期(TpTe间期)的改变及其临床意义.方法:随机抽取原发性高血压(EH)患者313例,依据超声心动图(UCG)测定的左室重量指数(LVMI)分为LVH组和非LVH (NLVH)组.比较LVH组和NLVH组TpTe间期、TpTec、QT间期、QTc、QRS时限、LVMI、LVD、IVS、LVPW的改变及EH左室不同构型TpTe间期改变的特点.结果:(1) LVH组较NLVH组TpTe间期、TpTec、QTc、QRS时限延长(P＜ 0.05 ～ 0.01),LVMI、LVD、IVS、LVPW增大(P＜0.01),QT间期延长,但差别不显著(P＞ 0.05);(2) TpTe间期值在不同左室构型间的改变为:离心型肥厚＞向心性肥厚＞向心性重构＞正常组,后两组差别不显著(P＞0.05).结论:TpTe间期可作为检测EH患者左心室肥厚靶器官损害及预测心脏事件的新指标.     

高血压患者血压变异性和左室肥厚关系的研究

目的观察原发性高血压患者血压变异性与左心室肥厚的关系。方法原发性高血压患者60例,分别进行超声心动图检查和24 h动态血压监测,根据超声心动图测量指标计算所得的左心室重量指数(LVMI)分为左心室肥厚(LVH)组和无LVH组,分析比较两组间的血压均值和血压变异性。结果 LVH组24 h、白昼、夜间的收缩压和舒张压水平以及各阶段的收缩压和舒张压标准差均比无LVH组明显增大,差异有显著性;且LVH组LVMI高于无LVH组,差异有显著性。结论原发性高血压患者LVH的发生和血压变异性密切相关,血压变异性增高对左心室肥厚风险有一定预测价值。     

尿毒症患者血液透析后心脏结构功能的改变及相关因素分析

目的探讨尿毒症患者血液透析后心脏结构功能的改变及其相关因素。方法回顾性分析64例维持性血液透析患者透析前、透析1年后的超声心动图资料,研究血红蛋白、血清白蛋白、血肌酐等对心脏结构功能的影响。结果透析前与透析1年后相比,左心室舒张末内径、室间隔厚度、左心室壁厚度、左室射血分数的变化无显著性差异。结论维持性血液透析对尿毒症患者的舒张功能无明显改善。控制干体重、血压及改善贫血、营养状况、微炎症状态有利于心脏结构功能的改变。     

尿毒症患者血液透析后心脏结构功能的改变及相关因素分析

目的探讨尿毒症患者血液透析后心脏结构功能的改变及其相关因素。方法回顾性分析64例维持性血液透析患者透析前、透析1年后的超声心动图资料,研究血红蛋白、血清白蛋白、血肌酐等对心脏结构功能的影响。结果透析前与透析1年后相比,左心室舒张末内径、室间隔厚度、左心室壁厚度、左室射血分数的变化无显著性差异。结论维持性血液透析对尿毒症患者的舒张功能无明显改善。控制干体重、血压及改善贫血、营养状况、微炎症状态有利于心脏结构功能的改变。     

慢性肾脏病3期糖尿病肾病患者左心结构与功能改变的多因素分析

目的:分析慢性肾脏病3期(CKD3)2型糖尿病肾病患者超声心动图变化,探讨其变化特点与年龄、血脂、血压、血红蛋白、尿蛋白等因素之间的关系.方法:121例确诊为CKD3期的患者,按照原发痛不同分为糖尿病肾病组和非糖尿病肾病组,对其年龄、血脂、血压、血红蛋白、尿蛋白等相关临床资料及超声心动图检查结果进行对比分析和多因素分析.结果:CKD3期糖尿病肾病患者贫血发生率84%,与非糖尿病肾病患者相比.贫血发生率高、程度重,尿蛋白排泄率高.心脏结构改变以左室舒末内径增大,左室肥厚为主.功能改变以舒张功能减退为特点.血红蛋白(Hb)与左室舒张末期内径(LVEDd)、左室心肌质量指数(LVMI)相关;尿蛋白(Pr)与二尖瓣血流心房收缩期最大流速(AV)及其比值E/A相关.结论:CKD3期糖尿病肾病患者心脏病变受多因素影响,贫血、尿蛋白等因素作用不容忽视.提示早期积极纠正贫血,控制血压,减少尿蛋白排泄可能是糖尿病肾病患者减少或延缓心血管并发症的重要措施.     

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。