中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
CHINESE JOURNAL OF EMERGENCY MEDICINE
2013年
5期
482-486
,共5页
丁欢%曹相原%马希刚%周文杰
丁歡%曹相原%馬希剛%週文傑
정환%조상원%마희강%주문걸
脓毒症%内皮细胞损伤%可溶性颗粒膜蛋白CD62P%炎症因子%凝血功能
膿毒癥%內皮細胞損傷%可溶性顆粒膜蛋白CD62P%炎癥因子%凝血功能
농독증%내피세포손상%가용성과립막단백CD62P%염증인자%응혈공능
Sepsis%Endothelial cell injury%Plasma soluble CD62P%Inflammatory factor%Coagulation
目的 观察脓毒症患者内皮细胞功能、炎症因子以及凝血指标的表达,探讨三者的关系.方法 采用前瞻性对照研究方法.选择宁夏医科大学总医院重症监护病房(ICU)收治的70例危重病患者,依据脓毒症及全身炎症反应综合征(systemic inflammatory response syndrome,SIRS)诊断标准分为脓毒症组38例、SIRS组32例.另选取健康体检者20例作为健康对照组.Sepsis组和SIRS组患者在高血压、糖尿病及其并发症构成有可比性.各组性别、年龄构成、吸烟、饮酒状况、体质量指数(BMI)方面相匹配有可比性.患者于入住ICU 24 h内抽取晨起空腹肘静脉血6ml,分离血浆.采用双抗体夹心ABC-酶联免疫吸附(ELISA)法测定标本中s-CD62P水平、TNF-α水平.同时测定超敏C-反应蛋白(hs-CRP)水平和血小板计数(PLT)、血浆凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)、D-二聚体(D-dimer)水平、抗凝血酶Ⅲ活性(AT-Ⅲ);收集纳入研究患者的临床资料,进行SOFA评分;所有数据采用SPSS 17.0版统计软件进行分析.多组间比较采用单因素方差分析,对于非配对方差不齐资料,采用非参数法秩和检验(Keuskal Wallis),比较分析各组s-CD62P水平、炎症因子和凝血指标的差异,并采用Pearson相关分析法分析s-CD62P水平与上述炎症因子和凝血指标的相关性.以P<0.05为差异具有统计学意义.结果 ①与健康对照组和SIRS组比较:脓毒症组s-CD62P水平、hs-CRP和TNF-α水平均明显升高(P<0.05);②与健康对照组比较:脓毒症组和SIRS组D-dimer、PT、APTT均显著升高,而PLT计数、AT-Ⅲ活性显著降低(P<0.05);③脓毒症患者hs-CRP和TNF-α分别与D-dimer、PT、APTT呈正相关,而与PLT计数、AT-Ⅲ活性呈负相关(P<0.05);④s-CD62P水平与hs-CRP、TNF-α、D-dimer、PT和APTT明显正相关,而与PLT计数、AT-Ⅲ活性呈明显负相关(P<0.05).结论 脓毒症患者血浆s-CD62P的表达明显增高,是内皮细胞损伤的早期生物标志物;炎症与凝血功能障碍相互作用促进了脓毒症的发生和发展;可溶性颗粒膜蛋白CD62P是脓毒症炎症-凝血网络形成的重要始动因素.
目的 觀察膿毒癥患者內皮細胞功能、炎癥因子以及凝血指標的錶達,探討三者的關繫.方法 採用前瞻性對照研究方法.選擇寧夏醫科大學總醫院重癥鑑護病房(ICU)收治的70例危重病患者,依據膿毒癥及全身炎癥反應綜閤徵(systemic inflammatory response syndrome,SIRS)診斷標準分為膿毒癥組38例、SIRS組32例.另選取健康體檢者20例作為健康對照組.Sepsis組和SIRS組患者在高血壓、糖尿病及其併髮癥構成有可比性.各組性彆、年齡構成、吸煙、飲酒狀況、體質量指數(BMI)方麵相匹配有可比性.患者于入住ICU 24 h內抽取晨起空腹肘靜脈血6ml,分離血漿.採用雙抗體夾心ABC-酶聯免疫吸附(ELISA)法測定標本中s-CD62P水平、TNF-α水平.同時測定超敏C-反應蛋白(hs-CRP)水平和血小闆計數(PLT)、血漿凝血酶原時間(PT)、活化部分凝血活酶時間(APTT)、D-二聚體(D-dimer)水平、抗凝血酶Ⅲ活性(AT-Ⅲ);收集納入研究患者的臨床資料,進行SOFA評分;所有數據採用SPSS 17.0版統計軟件進行分析.多組間比較採用單因素方差分析,對于非配對方差不齊資料,採用非參數法秩和檢驗(Keuskal Wallis),比較分析各組s-CD62P水平、炎癥因子和凝血指標的差異,併採用Pearson相關分析法分析s-CD62P水平與上述炎癥因子和凝血指標的相關性.以P<0.05為差異具有統計學意義.結果 ①與健康對照組和SIRS組比較:膿毒癥組s-CD62P水平、hs-CRP和TNF-α水平均明顯升高(P<0.05);②與健康對照組比較:膿毒癥組和SIRS組D-dimer、PT、APTT均顯著升高,而PLT計數、AT-Ⅲ活性顯著降低(P<0.05);③膿毒癥患者hs-CRP和TNF-α分彆與D-dimer、PT、APTT呈正相關,而與PLT計數、AT-Ⅲ活性呈負相關(P<0.05);④s-CD62P水平與hs-CRP、TNF-α、D-dimer、PT和APTT明顯正相關,而與PLT計數、AT-Ⅲ活性呈明顯負相關(P<0.05).結論 膿毒癥患者血漿s-CD62P的錶達明顯增高,是內皮細胞損傷的早期生物標誌物;炎癥與凝血功能障礙相互作用促進瞭膿毒癥的髮生和髮展;可溶性顆粒膜蛋白CD62P是膿毒癥炎癥-凝血網絡形成的重要始動因素.
목적 관찰농독증환자내피세포공능、염증인자이급응혈지표적표체,탐토삼자적관계.방법 채용전첨성대조연구방법.선택저하의과대학총의원중증감호병방(ICU)수치적70례위중병환자,의거농독증급전신염증반응종합정(systemic inflammatory response syndrome,SIRS)진단표준분위농독증조38례、SIRS조32례.령선취건강체검자20례작위건강대조조.Sepsis조화SIRS조환자재고혈압、당뇨병급기병발증구성유가비성.각조성별、년령구성、흡연、음주상황、체질량지수(BMI)방면상필배유가비성.환자우입주ICU 24 h내추취신기공복주정맥혈6ml,분리혈장.채용쌍항체협심ABC-매련면역흡부(ELISA)법측정표본중s-CD62P수평、TNF-α수평.동시측정초민C-반응단백(hs-CRP)수평화혈소판계수(PLT)、혈장응혈매원시간(PT)、활화부분응혈활매시간(APTT)、D-이취체(D-dimer)수평、항응혈매Ⅲ활성(AT-Ⅲ);수집납입연구환자적림상자료,진행SOFA평분;소유수거채용SPSS 17.0판통계연건진행분석.다조간비교채용단인소방차분석,대우비배대방차불제자료,채용비삼수법질화검험(Keuskal Wallis),비교분석각조s-CD62P수평、염증인자화응혈지표적차이,병채용Pearson상관분석법분석s-CD62P수평여상술염증인자화응혈지표적상관성.이P<0.05위차이구유통계학의의.결과 ①여건강대조조화SIRS조비교:농독증조s-CD62P수평、hs-CRP화TNF-α수평균명현승고(P<0.05);②여건강대조조비교:농독증조화SIRS조D-dimer、PT、APTT균현저승고,이PLT계수、AT-Ⅲ활성현저강저(P<0.05);③농독증환자hs-CRP화TNF-α분별여D-dimer、PT、APTT정정상관,이여PLT계수、AT-Ⅲ활성정부상관(P<0.05);④s-CD62P수평여hs-CRP、TNF-α、D-dimer、PT화APTT명현정상관,이여PLT계수、AT-Ⅲ활성정명현부상관(P<0.05).결론 농독증환자혈장s-CD62P적표체명현증고,시내피세포손상적조기생물표지물;염증여응혈공능장애상호작용촉진료농독증적발생화발전;가용성과립막단백CD62P시농독증염증-응혈망락형성적중요시동인소.
Objective To observe the clinical findings about the endothelial cell injury related to the genesis of inflammatory cytokines and coagulation.Methods A total of 70 critically ill patients with SIRS (systemic inflammatory response syndrome) admitted to intensive care unit (ICU) between September 2009 and February 2010 were enrolled for a prospective and control study.According to diagnostic criteria of Sepsis/SIRS,the patients were divided into two groups:sepsis group (n =38) and SIRS group (n =32),and another 20 healthy volunteers served as control group.Patients in the sepsis group and SIRS group were matched by clinical signs of high blood pressure,diabetes and its complications.The demographics of patients including age,sex,body mass index (BMI),smoking and alcohol addict were comparable among the different groups.The 6 ml peripheral blood samples were collected within 24 h after admission to ICU for enzyme-linked immunosorbent assay (ELISA) to detect the plasma levels of s-CD62P,TNF-α,and hsCRP.And variables of coagulation function such as platelet (PLT),prothrombin time (PT),activated partial thromboplastin time (APTT),D-dimer and antithrombin-Ⅲ (AT-Ⅲ) were analyzed during 24 h after admission to ICU.Meanwhile sequential organ failure assessment (SOFA) score of critically ill patients was evaluated.Data were expressed in mean ± standard deviation and were statistically analyzed by using SPSS 17.0 statistical software.The differences in plasma levels of s-CD62P of patients in each group were analyzed by ANOVA and Kruskal Wallis test.The relationship between s-CD62P and inflammatory cytokines as well as with coagulation were determined by Pearson correlation analysis.Changes were considered as statistically significant if P value was less than 0.05.Results ① Compared with control group and SIRS group,the levels of s-CD62P,TNF-α and high sensitive C-reactive protein (hs-CRP) were significantly higher in sepsis group (P < 0.05).② The plasma levels of D-dimer,PT,APTT in sepsis group and SIRS group were significantly higher than those in control group,while the platelet count (PLT) and the activity of AT-Ⅲ were obviously lower (P < 0.05).③ In sepsis group,the plasma levels of hs-CRP and TNF-α positively correlated with PT,APTT,D-dimer,and negatively correlated with AT-Ⅲ,PLT (P < 0.05).④ Plasma levels of s-CD62P were significantly correlated with plasma levels of TNF-α,hs-CRP,D-dimer,PT,APTT,whereas correlated negatively well with PLT,AT-Ⅲ (P < 0.05).Conclusions The plasma s-CD62P concentration is elevated as a early biomarker in patients with sepsis,and it acted as one of pathogenic factors responsible for endothelial cell damage.Coagulation and mediators of inflammation promotes each other,aggravating the severity of the sepsis.The plasma s-CD62P may be the important factor associated with initiation of coagulation development and inflammatory reaction.