慢性阻塞性肺病急性加重期CRP检测的临床意义

慢性阻塞性肺病 (COPD)急性加重期的治疗中 ,在病原学资料取得前的有效控制肺部感染至关重要。临床上普遍采用早期经验性用药 ,有一定盲目性 ,而常规评价疗效的指标因受诸多因素的影响 ,敏感性不高 ,常延误抗生素的及时调整。为探讨血 CRP(C反应蛋白 )检测在慢性肺加重期治疗中的临床意义 ,总结我院 2 0 0 0年 3月至 2 0 0 2年 9月 5 1例患者血 CRP动态检则 ,现报道如下 :资料和方法1.临床资料5 1例 COPD患者均于入院前一周内因呼吸道感染而致病情加重 ,男 38例 ,女 13例 ,平均年龄 6 5 .7岁 ,所有患者均符合我国 1997年《COPD诊治…     

慢性阻塞性肺病急性加重期的临床代谢分析

慢性阻塞性肺病(COPD)多合并有营养不良，其发生率往往与疾病的严重程度及预后有关。为了进一步了解慢性阻塞性肺病的发生、发展．以及提高临床治疗水平和病人生活质量。自2002年8月至2003年12月．收集我科住院慢性阻塞性肺病病人共222例，进行临床代谢等方面的全面分析，具体报道如下。     

盐酸氨溴索辅助治疗慢性阻塞性肺病急性加重期患者43例

慢性阻塞性肺病(COPD)以气流受限、不完全可逆为主要特征,在临床上表现为稳定期与急性加重期(AECOPD)交替出现.AECOPD表现为咳嗽、咳痰、气短和(或)喘息加重、痰量增多,痰呈脓性或黏液脓性,导致气道阻塞和感染加重,发生低氧血症及呼吸衰竭,严重威胁患者的生命.本研究在合理抗感染、止咳、平喘等治疗基础上,采用盐酸氨溴索辅助治疗AECOPD,观察其疗效.     

慢性阻塞性肺病急性加重期患者血糖浓度变化

目的分析慢性阻塞性肺病(COPD)急性加重期(AECOPD)患者血糖浓度对住院时间、病死率及肺功能的影响。方法收集187例AECOPD患者的临床资料,记录性别、平均年龄、肺功能、住院时间、病死率等指标。根据空腹血糖浓度分为4组[组1:5.6 mmol/L(n=41);组2:5.6～6.9 mmol/L(n=41);组3:7.0～8.9 mmol/L(n=50);组4:≥9.0 mmol/L(n=55)。结果组3,组4住院时间显著延长(P0.05);组4病死率、合并糖尿病病例数显著高于其他3组(P均0.05);合并糖尿病患者肺功能以弥散损害为主。结论 AECOPD患者高血糖与住院时间和病死率密切相关,血糖异常对肺弥散功能损害明显。     

不同年龄组慢性阻塞性肺病患者急性加重期痰培养结果比较

目的探讨不同年龄组慢性阻塞性肺病患者急性加重期痰培养结果的差异。方法收集2008年8月至2010年8月间安庆市立医院呼吸科收治的慢性阻塞性肺病患者急性加重期患者,依据三个年龄段分为三组：A组：小于65岁,B组：65~75岁,C组：75~85岁。入院后未使用抗生素之前对患者行痰培养,比较三组患者之间痰培养的差异。结果 A组患者痰培养阳性率19.0%,多重耐药菌阳性率3.4%;B组患者痰培养阳性率39.0%,多重耐药菌阳性率14.1%;C组患者痰培养阳性率62.1%,多重耐药菌阳性率27.3%。三组患者之间痰培养阳性率（P〈0.05）多重耐药阳性率（P〈0.05）差异有统计学意义。结论慢性阻塞性肺病患者急性加重期痰培养阳性率及多重耐药菌阳性率随年龄增长而升高。     

雾化吸入布地奈德和静脉用泼尼松龙治疗慢性阻塞性肺病急性加重期疗效比较

目的 比较雾化吸入布地奈德和静脉用泼尼松龙治疗慢性阻塞性肺病（COPD）急性加重期的疗效。方法 将40例COPD急性加重期患者随机分成两组：布地奈德组18例，接受布地奈德混悬液1d2mg，分两次雾化吸入治疗；泼尼松龙组22例，接受泼尼松龙40mg静脉注射，1次／d。其他标准治疗相同。比较两组患者治疗后第2，5天的动脉血气中PaO2、PaCO2、pH、SaO2指标以及两组患者最终预后。结果 两组患者基础值无明显差异。第2天泼尼松龙组SO2、PO2较基础值有显著改善；布地奈德组血气指标较基础值无显著改善。第5天两组患者血气指标均较基础值有明显改善。第2、5天两组之间比较无显著差异。两组患者住院时间、需要辅助通气的比例均无显著差别。结论 雾化吸入布地奈德可能可以替代全身使用激素治疗COPD急性加重期的患者。     

慢性阻塞性肺病急性加重期合并低钠血症90例临床分析

目的 探讨慢性阻塞性肺病患者低钠血症对治疗及预后的影响.方法 选取我院慢性阻塞性肺病急性加重期（AECOPD）住院患者90例进行回顾性分析,探讨其预后.结果 AECOPD常导致低钠血症,且年龄越大,低钠发生率越高,肺、脑、肾等重要器官系统的功能失调越重,病死率明显增加.结论 COPD患者合并低钠血症病因复杂,控制原发病,预防并及早治疗低钠血症有重要的临床意义.     

苏子降气汤治疗慢性阻塞性肺病急性加重疗效观察

目的观察使用中药苏子降气汤联合西医治疗慢性阻塞性肺病急性发作的临床疗效。方法122例慢性阻塞性肺病急性发作的住院患者,在患者自愿的情况下,被分为两组:对照组(63例)和观察组(59例)。对照组:给予单纯的常规西药治疗;观察组在西医治疗基础上,给予中药苏子降气汤煎剂,每日一剂,并依据辩证随证加减。每个患者经过一到两周的治疗后,评估和分析治疗效果。结果观察组:一周观察:显效43例,有效12例,无效8例,有效率87.30%;二周后观察:显效51例,有效9,无效3例,总有效率95.2%;对照组:第一周有效率79.66;二周后观察,:显效41例,有效12例,无效6例,总有效率89.8%。观察组总有效率高于对照组,并且第1周疗效已等同对照组对照组二周的疗效;差异具有统计学意义(P0.05)。结论以苏子降气汤结合西医治疗慢阻肺急性加重能够有效的提高治疗效果,值得推广与应用。     

布地奈德雾化吸人治疗慢性阻塞性肺病急性加重期的疗效分析（附35例报告）

目的观察布地奈德雾化吸入治疗慢性阻塞性肺病急性加重期（AECOPD）的疗效。方法将67例患者随机分为治疗组35例和对照组32例,2组患者均接受吸氧、抗感染、化痰、雾化吸入沙丁胺醇等常规治疗,治疗组于常规治疗基础上加用布地奈德雾化吸入,比较两组间的疗效。结果治疗组和对照组治疗后FEV1、PaO2、PaCO2较治疗前改善,两者差异有统计学意义（P〈0．05）;而治疗组治疗后FEV1、PaO2、PaCO2较对照组改善更明显,两者差异有统计学意义（P〈0．05）。结论布地奈德雾化吸入治疗AECO—PD,能改善肺功能和血气,疗效较好。     

慢性阻塞性肺病急性加重期C反应蛋白与前白蛋白变化的临床意义

目的探讨慢性阻塞性肺病(COPD)急性加重期治疗前后C反应蛋白(CRP),前白蛋白(PA)的变化及临床意义。方法选择2004年7月—2008年7月我院住院COPD急性加重期患者138例,记录入院时的临床情况,分别测定入院时及病情缓解后患者的CRP,PA,血沉(ESR)及血常规等情况,并进行比较。结果COPD患者急性发作期CRP较缓解期明显升高,PA下降,差异有统计学意义;白细胞,ESR治疗前后变化不明显。结论血清CRP,PA可作为评估COPD患者急性加重期炎症控制的敏感性指标。     

血清白蛋白、前白蛋白水平在AECOPD的临床意义

目的探讨血清白蛋白(ALB)、血清前白蛋白(PA)水平在COPD患者急性加重期的临床意义。方法入选COPD急性加重期老年男性患者52例,比较其血清ALB、PA浓度与患者住院时间及心衰纠正时间的相关性,并分析ALB、PA与患者动脉血PH值、PaO2、PaCO2之间的关系。结果低ALB、低PA组患者的平均住院时间及心衰纠正时间明显延长,差异有统计学意义(P<0.05)。ALB正常组与ALB降低组血气PaCO2存在显著性差异(P<0.05),PA正常组与PA降低组血气PaO2存在显著性差异(P<0.05)。结论血清ALB、PA水平可作为评估COPD急性加重期患者预后的一项指标,PA明显降低更加提示预后不良。     

C反应蛋白和前白蛋白在AECOPD中的临床意义

目的观察AECOPD患者血清C-反应蛋白(C-reactive protein,CRP)、及前白蛋白(preal-bumin,PA)的变化,探讨其与病情严重程度及预后的关系。方法监测152例AECOPD患者入院后第1、3、5、7天CRP和PA水平,根据患者的预后将患者分成死亡与非死亡组,根据住院日数以14日为界分为两组,结果死亡组及非死亡组第1、2天CRP水平差异无统计学意义(P>0.05),第3、5、7天死亡组患者CRP明显高于非死亡组,差异有统计学意义(P<0.05),死亡组PA在第5、7天明显低于非死亡组,差异有统计学意义(P<0.05),结论 AECOPD患者病情越重,CRP水平升高越明显,PA水平呈持续下降趋势。     

The role of immunoglobulin G and fibrinogen in platelet aggregation by Streptococcus sanguis

Previous work has shown that the type strain of Streptococcus sanguis , NCTC 7863, induces aggregation of normal platelets by a complement-dependent mechanism. We investigated the roles of IgG and fibrinogen in the aggregation process. Plasma depleted of IgG by passage through protein A–sepharose failed to support platelet aggregation, as did plasma absorbed at 0°C with whole bacteria. However, absorption of plasma with a non-aggregating strain of S. sanguis , SK96, did not remove aggregating activity for NCTC 7863. Supplementing 0°C-absorbed plasma with purified IgG restored the aggregation supporting activity. A monoclonal antibody to the FcγRII receptor inhibited platelet aggregation by the bacteria, indicating a requirement for bacteria–IgG complexes interacting with the Fc receptor in platelet aggregation. There was a lag time to the onset of platelet aggregation of 7–19 min depending upon the platelet donor, but the length of this lag did not correlate with either total IgG concentration recognizing NCTC 7863 in subjects' plasma, or the concentration any of the four IgG subclasses or with IgG avidity levels.
Fibrinogen was shown to bind rapidly to the bacterial cell surface. Monclonal antibody to GPIIb/IIIa, RGDS peptide, and a specific antagonist for the platelet fibrinogen receptor, GPIIb/IIIa, FK633, inhibited platelet aggregation by NCTC 7863, indicating that platelet aggregation is fibrinogen dependent. These data suggest that platelet aggregation by some strains of S. sanguis requires multiple stimuli/agonists, including IgG–Fc receptor interaction, complement and fibrinogen.     

血清降钙素原对AECOPD抗生素使用的指导价值

目的研究血清降钙素原(PCT)检测在慢性阻塞性肺疾病急性加重期(AECOPD)对使用抗生素的指导价值。方法选取收治的AECOPD患者63例,随机分配成两组:PCT指导治疗组32例(简称PCT组)和常规治疗组31例(简称对照组),检测血清PCT水平。在常规治疗的基础上,对照组按照临床抗生素使用指南决定抗生素疗程,PCT组按照血清PCT水平决定抗生素的使用,当血清PCT≥0.25ng/mL时,进行抗生素治疗,当PCT0.25 ng/mL时,则停止使用抗生素。并观察两组患者抗生素的使用疗程,抗生素所用费用及住院时间。结果 PCT组抗生素疗程[7(5~11)d]短于对照组[13(7~16)d](P=0.03);PCT组抗生素费用低于对照组(P=0.001),两组的住院时间及预后无明显差异。结论 AECOPD患者根据PCT水平使用抗生素,能够明显缩短抗生素的所用疗程,减少医疗费用。     

Effect of epinephrine on fibrinogen receptor exposure by aspirin-treated platelets and platelets from concentrates in response to ADP and thrombin

Synergistic effects between agonists on platelet aggregation have long been appreciated. Recently epinephrine was reported to induce maximal aggregation of aspirin-treated platelets when combined with ADP or thrombin, and to increase fibrinogen binding of non-aspirin treated platelets stimulated with low doses of ADP. The present study extends these observations to correlate fibrinogen binding in response to various combinations of ADP, epinephrine, and thrombin with platelet aggregation and 14C-serotonin release using aspirin-treated platelets as well as platelets from stored concentrates. When fresh platelets were stimulated with epinephrine (5 microM) together with either ADP (10 microM) or thrombin (150 mU/ml), fibrinogen binding increased by 180% compared to binding observed in response to ADP or thrombin alone. This was accompanied by enhanced platelet aggregation, but no increase in 14C-serotonin release. While both ADP and epinephrine potentiated the aggregation and fibrinogen binding of stored platelets in response to high doses of thrombin (150 mU/ml), maximal aggregation was achieved only with thrombin (150 mU/ml) and epinephrine (5 microM) in combination. The data thus suggest that 1) epinephrine induces maximal aggregation of aspirin-treated platelets stimulated with thrombin or ADP by significantly enhancing fibrinogen receptor exposure independently of the cyclooxygenase-mediated release reaction; 2) epinephrine stimulates platelets by a mechanism different from that of thrombin or ADP; and 3) as demonstrated by others, the ability of platelets from stored concentrates to aggregate and to bind fibrinogen in response to ADP can be enhanced by epinephrine, and, in addition, these platelets can aggregate and bind fibrinogen maximally when stimulated with combinations of epinephrine and thrombin.     

The effect of thrombin on the dynamic exchange between intraplatelet and extraplatelet fibrinogen

We examined the distribution of platelet fibrinogen and the exchange between intra- and extra-platelet fibrinogen in unstimulated and thrombin-stimulated platelets. In unstimulated platelets 60% of platelet fibrinogen was found in the soluble platelet fraction and 40% in the insoluble one. In platelets activated with thrombin, changes took place in the distribution of intraplatelet fibrinogen but not in the total fibrinogen content. At 0.5 U/ml of thrombin the fibrin(ogen) content of the insoluble and soluble fractions was approximately 80% and 20%, respectively. When we evaluated how extraplatelet fibrinogen affects the content and distribution of intraplatelet fibrinogen, we found that when unlabelled fibrinogen was added to unstimulated and thrombin-stimulated platelets the content and distribution of intraplatelet fibrinogen remained unaltered. However, when ¹²⁵I-fibrinogen was added, it was incorporated into unstimulated and thrombin-stimulated platelets. In unstimulated platelets, 70% of the incorporated ¹²⁵I-fibrinogen was in the soluble fraction and 30% in the insoluble. In thrombin-stimulated platelets the distribution of the incorporated ¹²⁵I-fibrinogen was 62% and 38% in soluble and insoluble fractions respectively. MoAb to GPIIb–IIIa produced 80% and 60% inhibition of ¹²⁵I-fibrinogen incorporation by unstimulated and thrombin-stimulated platelets. Our data showed dynamic exchange between intraplatelet and extraplatelet fibrinogen both in unstimulated and thrombin-stimulated platelets mediated mainly by GPIIb–IIIa.     

The effect of thrombin on the dynamic exchange between intraplatelet and extraplatelet fibrinogen

We examined the distribution of platelet fibrinogen and the exchange between intra- and extra-platelet fibrinogen in unstimulated and thrombin-stimulated platelets. In unstimulated platelets 60% of platelet fibrinogen was found in the soluble platelet fraction and 40% in the insoluble one. In platelets activated with thrombin, changes took place in the distribution of intraplatelet fibrinogen but not in the total fibrinogen content. At 0.5 U/ml of thrombin the fibrin(ogen) content of the insoluble and soluble fractions was approximately 80% and 20%, respectively. When we evaluated how extraplatelet fibrinogen affects the content and distribution of intraplatelet fibrinogen, we found that when unlabelled fibrinogen was added to unstimulated and thrombin-stimulated platelets the content and distribution of intraplatelet fibrinogen remained unaltered. However, when ¹²⁵I-fibrinogen was added, it was incorporated into unstimulated and thrombin-stimulated platelets. In unstimulated platelets, 70% of the incorporated ¹²⁵I-fibrinogen was in the soluble fraction and 30% in the insoluble. In thrombin-stimulated platelets the distribution of the incorporated ¹²⁵I-fibrinogen was 62% and 38% in soluble and insoluble fractions respectively. MoAb to GPIIb–IIIa produced 80% and 60% inhibition of ¹²⁵I-fibrinogen incorporation by unstimulated and thrombin-stimulated platelets. Our data showed dynamic exchange between intraplatelet and extraplatelet fibrinogen both in unstimulated and thrombin-stimulated platelets mediated mainly by GPIIb–IIIa.     

高血压病患者血浆纤维蛋白原与血小板聚集功能的变化及降压治疗的影响

为了探讨高血压病患者血浆纤维蛋白原和血小板聚集功能的改变及降压治疗对其影响，本文采用免疫比浊法，比浊法测定15例正常人及53例高血压病患者血浆纤维蛋白原、血小板聚集率，并对高血压病患者分别以氯压定（赖诺普利）或圣通平（缓释硝苯吡啶）降压治疗12周。结果表明，高血压病患者血浆纤维蛋白原水平升高，血小板聚集增强，且纤维蛋白原与血小板聚集率呈正相关。氯压定及圣通平降压治疗均使血小板聚集下降、氯压定还降低纤维蛋白原，而圣通平无此作用，提示血管紧张素转换酶抑制剂在防治高血压病缺血性心、脑并发症方面更有益。     

福多司坦对慢性阻塞性肺病急性加重期患者预后的影响

目的观察福多司坦联合标准治疗对慢性阻塞性肺病急性加重期患者炎症反应和再发风险的影响。方法将60例慢性阻塞性肺病急性加重期患者随机分为两组,对照组给予抗生素、支气管舒张剂等标准治疗,实验组给予福多司坦联合标准治疗,分别测定治疗前和治疗后10天、30天的C反应蛋白和肺功能,随访治疗后60天内是否再次出现急性发作和出现时间。结果实验组可在短时间内更快降低慢性阻塞性肺病急性加重期患者的血清CRP水平,同时改善肺功能;实验组患者60天内的再次发作风险降低27.6%,再次急性加重时间延长(P=0.072)。结论福多司坦与标准治疗联用后可降低炎症反应,对慢性阻塞性肺病急性加重期患者的肺功能和预后存在改善作用。     

VerifyNow对比血小板聚集仪分析氯吡格雷药效

目的比较检测氯吡格雷抗血小板功能的2种实验方法的异同。方法随机收集207例门诊和住院急性冠状动脉综合征患者,其服用氯吡格雷后,抽取静脉血,同时进行光比浊法二磷酸腺苷诱导的血小板聚集实验与Ver-ifyNow抗血小板治疗监测系统实验,并进行分析。结果血小板聚集仪测得的血小板聚集率(PAgP)156例在40%～80%,占75.4%,25例<40%,占12.1%,26例>80%,占12.6%。VerifyNow分析P2Y_(12)受体的化学反应数值(PRU)126例在240～350,占60.9%,50例PRU<240,占24.2%,31例PRU>350,占15.0%。PAgP与PRU呈正相关,PAgP与抑制血小板聚集率(INHI)呈负相关,PAgP+INHI趋近于一个定值。结论 VerifyNow抗血小板治疗监测系统可作为氯吡格雷药效监测的良好实验方法 。