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【20240330期】血栓新四項在重癥患者凝血功能障礙標準化評估中的應用
2024-04-01
凝(ning)血(xue)(xue)(xue)功能(neng)(neng)(neng)是(shi)機體維(wei)持(chi)血(xue)(xue)(xue)管壁完整(zheng)性并防(fang)止(zhi)出(chu)血(xue)(xue)(xue)的(de)(de)重(zhong)(zhong)要生(sheng)理功能(neng)(neng)(neng)。據(ju)統計，重(zhong)(zhong)癥(zheng)患者入住(zhu)重(zhong)(zhong)癥(zheng)監護病(bing)房(intensive care unit，ICU)時，血(xue)(xue)(xue)小(xiao)板減(jian)少的(de)(de)發生(sheng)率(lv)(lv)可(ke)(ke)達(da)40.0%～67.6%，國際標準化(hua)比(bi)值(international normalized ratio，INR)≥1.5的(de)(de)發生(sheng)率(lv)(lv)可(ke)(ke)超過66%。發生(sheng)凝(ning)血(xue)(xue)(xue)功能(neng)(neng)(neng)障(zhang)(zhang)礙的(de)(de)重(zhong)(zhong)癥(zheng)患者不(bu)僅(jin)出(chu)血(xue)(xue)(xue)事件及(ji)輸血(xue)(xue)(xue)量(liang)顯著增加，而且更(geng)容易發展為(wei)多器(qi)官功能(neng)(neng)(neng)衰(shuai)竭，其病(bing)死(si)率(lv)(lv)也(ye)比(bi)凝(ning)血(xue)(xue)(xue)功能(neng)(neng)(neng)正(zheng)常(chang)的(de)(de)患者升高4倍(bei)以上。早期識(shi)別凝(ning)血(xue)(xue)(xue)功能(neng)(neng)(neng)障(zhang)(zhang)礙并準確評估凝(ning)血(xue)(xue)(xue)功能(neng)(neng)(neng)[7]，是(shi)盡快糾正(zheng)凝(ning)血(xue)(xue)(xue)功能(neng)(neng)(neng)障(zhang)(zhang)礙的(de)(de)前提(ti)及(ji)保障(zhang)(zhang)。
2022年發布在《中華(hua)醫學檢驗雜志》的(de)重(zhong)(zhong)癥患者凝(ning)(ning)血(xue)功(gong)能(neng)障礙(ai)標準化評估專家共(gong)識(shi)，在“重(zhong)(zhong)癥患者凝(ning)(ning)血(xue)功(gong)能(neng)障礙(ai)的(de)評估要(yao)素”中提出，新型凝(ning)(ning)血(xue)分子標志物在判斷重(zhong)(zhong)癥患者凝(ning)(ning)血(xue)功(gong)能(neng)障礙(ai)的(de)類型及預后具有重(zhong)(zhong)要(yao)意(yi)義(yi)。
文中指出：近年研究(jiu)進展快、臨床指導意(yi)義強的(de)(de)(de)(de)(de)新型(xing)凝(ning)血(xue)(xue)分子(zi)標(biao)志物(wu)(wu)(wu)(wu)包(bao)括血(xue)(xue)栓(shuan)調節蛋白(thrombomodulin，TM)、凝(ning)血(xue)(xue)酶(mei)(mei)-抗(kang)凝(ning)血(xue)(xue)酶(mei)(mei)復(fu)合(he)物(wu)(wu)(wu)(wu)(thrombin-antithrombin complex，TAT)、纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)酶(mei)(mei)-抗(kang)纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)酶(mei)(mei)復(fu)合(he)物(wu)(wu)(wu)(wu)(plasmin antiplasmin complex，PIC)及(ji)(ji)組織(zhi)型(xing)纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)酶(mei)(mei)原(yuan)激(ji)活(huo)(huo)(huo)(huo)物(wu)(wu)(wu)(wu)-纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)酶(mei)(mei)原(yuan)激(ji)活(huo)(huo)(huo)(huo)抑(yi)制(zhi)(zhi)物(wu)(wu)(wu)(wu)-1復(fu)合(he)物(wu)(wu)(wu)(wu)(tissue plasminogen activatorplasminogen activator inhibitor-1 complex，t-PAIC)。TM是(shi)(shi)血(xue)(xue)管(guan)內皮(pi)細(xi)胞表面的(de)(de)(de)(de)(de)凝(ning)血(xue)(xue)酶(mei)(mei)受體(ti)，可結(jie)合(he)凝(ning)血(xue)(xue)酶(mei)(mei)并(bing)抑(yi)制(zhi)(zhi)凝(ning)血(xue)(xue)酶(mei)(mei)的(de)(de)(de)(de)(de)活(huo)(huo)(huo)(huo)性，同(tong)時促進蛋白C活(huo)(huo)(huo)(huo)化，抑(yi)制(zhi)(zhi)凝(ning)血(xue)(xue)因子(zi)Ⅴ、Ⅷ活(huo)(huo)(huo)(huo)性及(ji)(ji)纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)酶(mei)(mei)原(yuan)激(ji)活(huo)(huo)(huo)(huo)物(wu)(wu)(wu)(wu)抑(yi)制(zhi)(zhi)劑-1(plasminogen activator inhibitor-1，PAI-1)。血(xue)(xue)漿(jiang)TM正(zheng)(zheng)常(chang)值(zhi)范圍為3.8～13.3 TU/ml。血(xue)(xue)管(guan)內皮(pi)損傷(shang)時，TM釋(shi)放入血(xue)(xue)導致血(xue)(xue)漿(jiang)TM水平(ping)明顯升(sheng)高(gao)，是(shi)(shi)血(xue)(xue)管(guan)內皮(pi)損傷(shang)的(de)(de)(de)(de)(de)敏感指標(biao)。已(yi)有較多文獻證實，腎(shen)功能(neng)損害患(huan)(huan)者TM水平(ping)可明顯升(sheng)高(gao)。凝(ning)血(xue)(xue)酶(mei)(mei)活(huo)(huo)(huo)(huo)化后可與(yu)抗(kang)凝(ning)血(xue)(xue)酶(mei)(mei)結(jie)合(he)形(xing)成TAT。TAT的(de)(de)(de)(de)(de)血(xue)(xue)漿(jiang)正(zheng)(zheng)常(chang)值(zhi)<4 ng/ml，TAT升(sheng)高(gao)表明凝(ning)血(xue)(xue)酶(mei)(mei)生(sheng)成增多，靈敏度(du)較高(gao)。PIC是(shi)(shi)纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)酶(mei)(mei)活(huo)(huo)(huo)(huo)化后與(yu)α2-抗(kang)纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)酶(mei)(mei)結(jie)合(he)形(xing)成的(de)(de)(de)(de)(de)復(fu)合(he)物(wu)(wu)(wu)(wu)，是(shi)(shi)直接(jie)反映(ying)纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)系統激(ji)活(huo)(huo)(huo)(huo)程度(du)的(de)(de)(de)(de)(de)生(sheng)物(wu)(wu)(wu)(wu)標(biao)志物(wu)(wu)(wu)(wu)。因為D-二聚(ju)體(ti)及(ji)(ji)FDP是(shi)(shi)纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)酶(mei)(mei)活(huo)(huo)(huo)(huo)化后降(jiang)解纖(xian)(xian)(xian)維(wei)蛋白(原(yuan))形(xing)成的(de)(de)(de)(de)(de)物(wu)(wu)(wu)(wu)質，因此PIC升(sheng)高(gao)理(li)論上(shang)早于(yu)D-二聚(ju)體(ti)及(ji)(ji)FDP，是(shi)(shi)目前(qian)監測纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)酶(mei)(mei)活(huo)(huo)(huo)(huo)性最敏感的(de)(de)(de)(de)(de)指標(biao)。PIC的(de)(de)(de)(de)(de)血(xue)(xue)漿(jiang)半衰(shuai)(shuai)期約(yue)6 h，血(xue)(xue)漿(jiang)正(zheng)(zheng)常(chang)值(zhi)<0.8 μg/ml。血(xue)(xue)漿(jiang)PIC水平(ping)顯著(zhu)升(sheng)高(gao)可提示(shi)纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)亢進。t-PAIC是(shi)(shi)血(xue)(xue)管(guan)內皮(pi)細(xi)胞損傷(shang)時，釋(shi)放t-PA與(yu)PAI-1共同(tong)入血(xue)(xue)形(xing)成的(de)(de)(de)(de)(de)復(fu)合(he)物(wu)(wu)(wu)(wu)。t-PAIC的(de)(de)(de)(de)(de)正(zheng)(zheng)常(chang)值(zhi)因性別而(er)有所不同(tong)，男性血(xue)(xue)漿(jiang)正(zheng)(zheng)常(chang)值(zhi)<17.0 ng/ml，女(nv)性<10.5 ng/ml。理(li)論上(shang)t-PAIC是(shi)(shi)內皮(pi)損傷(shang)及(ji)(ji)纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)系統激(ji)活(huo)(huo)(huo)(huo)的(de)(de)(de)(de)(de)產物(wu)(wu)(wu)(wu)，臨床研究(jiu)中發(fa)現t-PAIC對休克(ke)嚴重(zhong)狀(zhuang)態特(te)別是(shi)(shi)膿毒癥(zheng)休克(ke)的(de)(de)(de)(de)(de)診斷價值(zhi)很高(gao)。已(yi)有研究(jiu)顯示(shi)，膿毒性休克(ke)患(huan)(huan)者的(de)(de)(de)(de)(de)t-PAIC水平(ping)顯著(zhu)高(gao)于(yu)膿毒癥(zheng)患(huan)(huan)者，t-PAIC水平(ping)與(yu)乳酸水平(ping)及(ji)(ji)序貫器(qi)官衰(shuai)(shuai)竭(sequential organ failure assessment，SOFA)評分均呈正(zheng)(zheng)相關。Winter等研究(jiu)發(fa)現，合(he)并(bing)器(qi)官衰(shuai)(shuai)竭特(te)別是(shi)(shi)心力衰(shuai)(shuai)竭患(huan)(huan)者的(de)(de)(de)(de)(de)t-PAIC水平(ping)明顯高(gao)于(yu)無器(qi)官功能(neng)障礙的(de)(de)(de)(de)(de)患(huan)(huan)者。
膿(nong)(nong)毒癥(zheng)時(shi)，內(nei)毒素導致(zhi)內(nei)皮細胞損(sun)傷，促進凝(ning)血(xue)酶活(huo)化(hua)，此時(shi)可(ke)表現為(wei)TM及TAT升(sheng)(sheng)高，隨(sui)著(zhu)(zhu)膿(nong)(nong)毒癥(zheng)演進為(wei)膿(nong)(nong)毒癥(zheng)休(xiu)克(ke)，出現組織(zhi)低灌(guan)注導致(zhi)器(qi)官(guan)功能損(sun)害，此時(shi)t-PAIC可(ke)顯(xian)著(zhu)(zhu)升(sheng)(sheng)高，而PIC因為(wei)纖(xian)溶抑制(zhi)作用(yong)升(sheng)(sheng)高不明顯(xian)。創(chuang)傷時(shi)，出血(xue)導致(zhi)凝(ning)血(xue)酶大量活(huo)化(hua)發(fa)揮止血(xue)效(xiao)應，可(ke)表現為(wei)TAT顯(xian)著(zhu)(zhu)升(sheng)(sheng)高；內(nei)皮細胞釋放大量活(huo)化(hua)蛋白C抑制(zhi)PAI-1活(huo)性，引起(qi)纖(xian)溶亢進，表現為(wei)PIC顯(xian)著(zhu)(zhu)升(sheng)(sheng)高。如(ru)創(chuang)傷失血(xue)發(fa)展至休(xiu)克(ke)階段，出現廣(guang)泛內(nei)皮損(sun)傷，可(ke)表現為(wei)TM升(sheng)(sheng)高；如(ru)休(xiu)克(ke)加(jia)重出現明顯(xian)器(qi)官(guan)功能障礙，可(ke)出現t-PAIC顯(xian)著(zhu)(zhu)升(sheng)(sheng)高[41]。
膿(nong)毒癥及創(chuang)傷分(fen)別(bie)作(zuo)為血(xue)栓型(xing)DIC及纖溶型(xing)DIC的(de)典型(xing)代表疾病，也說明新型(xing)凝(ning)血(xue)分(fen)子標(biao)志物在(zai)區分(fen)DIC亞型(xing)方面的(de)重要作(zuo)用，特(te)別(bie)在(zai)創(chuang)傷失血(xue)性休克向膿(nong)毒癥休克轉化時(shi)有重要診斷價值。
新型(xing)凝血分子標志(zhi)物在重癥患者(zhe)凝血功能障礙(ai)常(chang)見(jian)疾(ji)病中的表現見(jian)下表。
有(you)了新的血栓四項標(biao)志物：TAT、TM、PIC和t·PAI-c，綜合反映(ying)出機(ji)體凝血，纖溶以及血管(guan)內皮系統早(zao)期(qi)激活的有(you)效(xiao)指(zhi)標(biao)，適用于各臨床學科血栓高危人(ren)群(qun)進行血栓的早(zao)期(qi)診斷、治療評(ping)估和預后(hou)判斷。
能夠能夠綜合(he)評估血(xue)管內皮受損(sun)情況，反應(ying)凝(ning)(ning)血(xue)酶、纖溶(rong)(rong)酶激活(huo)狀態(tai)，可在各個系統的反應(ying)起始階段產生，因此(ci)可以作為DIC、血(xue)栓性疾病早期診斷和預防的提示指標，也可用于溶(rong)(rong)栓療效監測，對于早期的出凝(ning)(ning)血(xue)系統狀態(tai)評估是非常重要的。
文章來源：Med J Chin PLA, Vol. 47, No. 2, February, 2022
2022年發布在《中華(hua)醫學檢驗雜志》的(de)重(zhong)(zhong)癥患者凝(ning)(ning)血(xue)功(gong)能(neng)障礙(ai)標準化評估專家共(gong)識(shi)，在“重(zhong)(zhong)癥患者凝(ning)(ning)血(xue)功(gong)能(neng)障礙(ai)的(de)評估要(yao)素”中提出，新型凝(ning)(ning)血(xue)分子標志物在判斷重(zhong)(zhong)癥患者凝(ning)(ning)血(xue)功(gong)能(neng)障礙(ai)的(de)類型及預后具有重(zhong)(zhong)要(yao)意(yi)義(yi)。
文中指出：近年研究(jiu)進展快、臨床指導意(yi)義強的(de)(de)(de)(de)(de)新型(xing)凝(ning)血(xue)(xue)分子(zi)標(biao)志物(wu)(wu)(wu)(wu)包(bao)括血(xue)(xue)栓(shuan)調節蛋白(thrombomodulin，TM)、凝(ning)血(xue)(xue)酶(mei)(mei)-抗(kang)凝(ning)血(xue)(xue)酶(mei)(mei)復(fu)合(he)物(wu)(wu)(wu)(wu)(thrombin-antithrombin complex，TAT)、纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)酶(mei)(mei)-抗(kang)纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)酶(mei)(mei)復(fu)合(he)物(wu)(wu)(wu)(wu)(plasmin antiplasmin complex，PIC)及(ji)(ji)組織(zhi)型(xing)纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)酶(mei)(mei)原(yuan)激(ji)活(huo)(huo)(huo)(huo)物(wu)(wu)(wu)(wu)-纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)酶(mei)(mei)原(yuan)激(ji)活(huo)(huo)(huo)(huo)抑(yi)制(zhi)(zhi)物(wu)(wu)(wu)(wu)-1復(fu)合(he)物(wu)(wu)(wu)(wu)(tissue plasminogen activatorplasminogen activator inhibitor-1 complex，t-PAIC)。TM是(shi)(shi)血(xue)(xue)管(guan)內皮(pi)細(xi)胞表面的(de)(de)(de)(de)(de)凝(ning)血(xue)(xue)酶(mei)(mei)受體(ti)，可結(jie)合(he)凝(ning)血(xue)(xue)酶(mei)(mei)并(bing)抑(yi)制(zhi)(zhi)凝(ning)血(xue)(xue)酶(mei)(mei)的(de)(de)(de)(de)(de)活(huo)(huo)(huo)(huo)性，同(tong)時促進蛋白C活(huo)(huo)(huo)(huo)化，抑(yi)制(zhi)(zhi)凝(ning)血(xue)(xue)因子(zi)Ⅴ、Ⅷ活(huo)(huo)(huo)(huo)性及(ji)(ji)纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)酶(mei)(mei)原(yuan)激(ji)活(huo)(huo)(huo)(huo)物(wu)(wu)(wu)(wu)抑(yi)制(zhi)(zhi)劑-1(plasminogen activator inhibitor-1，PAI-1)。血(xue)(xue)漿(jiang)TM正(zheng)(zheng)常(chang)值(zhi)范圍為3.8～13.3 TU/ml。血(xue)(xue)管(guan)內皮(pi)損傷(shang)時，TM釋(shi)放入血(xue)(xue)導致血(xue)(xue)漿(jiang)TM水平(ping)明顯升(sheng)高(gao)，是(shi)(shi)血(xue)(xue)管(guan)內皮(pi)損傷(shang)的(de)(de)(de)(de)(de)敏感指標(biao)。已(yi)有較多文獻證實，腎(shen)功能(neng)損害患(huan)(huan)者TM水平(ping)可明顯升(sheng)高(gao)。凝(ning)血(xue)(xue)酶(mei)(mei)活(huo)(huo)(huo)(huo)化后可與(yu)抗(kang)凝(ning)血(xue)(xue)酶(mei)(mei)結(jie)合(he)形(xing)成TAT。TAT的(de)(de)(de)(de)(de)血(xue)(xue)漿(jiang)正(zheng)(zheng)常(chang)值(zhi)<4 ng/ml，TAT升(sheng)高(gao)表明凝(ning)血(xue)(xue)酶(mei)(mei)生(sheng)成增多，靈敏度(du)較高(gao)。PIC是(shi)(shi)纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)酶(mei)(mei)活(huo)(huo)(huo)(huo)化后與(yu)α2-抗(kang)纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)酶(mei)(mei)結(jie)合(he)形(xing)成的(de)(de)(de)(de)(de)復(fu)合(he)物(wu)(wu)(wu)(wu)，是(shi)(shi)直接(jie)反映(ying)纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)系統激(ji)活(huo)(huo)(huo)(huo)程度(du)的(de)(de)(de)(de)(de)生(sheng)物(wu)(wu)(wu)(wu)標(biao)志物(wu)(wu)(wu)(wu)。因為D-二聚(ju)體(ti)及(ji)(ji)FDP是(shi)(shi)纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)酶(mei)(mei)活(huo)(huo)(huo)(huo)化后降(jiang)解纖(xian)(xian)(xian)維(wei)蛋白(原(yuan))形(xing)成的(de)(de)(de)(de)(de)物(wu)(wu)(wu)(wu)質，因此PIC升(sheng)高(gao)理(li)論上(shang)早于(yu)D-二聚(ju)體(ti)及(ji)(ji)FDP，是(shi)(shi)目前(qian)監測纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)酶(mei)(mei)活(huo)(huo)(huo)(huo)性最敏感的(de)(de)(de)(de)(de)指標(biao)。PIC的(de)(de)(de)(de)(de)血(xue)(xue)漿(jiang)半衰(shuai)(shuai)期約(yue)6 h，血(xue)(xue)漿(jiang)正(zheng)(zheng)常(chang)值(zhi)<0.8 μg/ml。血(xue)(xue)漿(jiang)PIC水平(ping)顯著(zhu)升(sheng)高(gao)可提示(shi)纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)亢進。t-PAIC是(shi)(shi)血(xue)(xue)管(guan)內皮(pi)細(xi)胞損傷(shang)時，釋(shi)放t-PA與(yu)PAI-1共同(tong)入血(xue)(xue)形(xing)成的(de)(de)(de)(de)(de)復(fu)合(he)物(wu)(wu)(wu)(wu)。t-PAIC的(de)(de)(de)(de)(de)正(zheng)(zheng)常(chang)值(zhi)因性別而(er)有所不同(tong)，男性血(xue)(xue)漿(jiang)正(zheng)(zheng)常(chang)值(zhi)<17.0 ng/ml，女(nv)性<10.5 ng/ml。理(li)論上(shang)t-PAIC是(shi)(shi)內皮(pi)損傷(shang)及(ji)(ji)纖(xian)(xian)(xian)溶(rong)(rong)(rong)(rong)系統激(ji)活(huo)(huo)(huo)(huo)的(de)(de)(de)(de)(de)產物(wu)(wu)(wu)(wu)，臨床研究(jiu)中發(fa)現t-PAIC對休克(ke)嚴重(zhong)狀(zhuang)態特(te)別是(shi)(shi)膿毒癥(zheng)休克(ke)的(de)(de)(de)(de)(de)診斷價值(zhi)很高(gao)。已(yi)有研究(jiu)顯示(shi)，膿毒性休克(ke)患(huan)(huan)者的(de)(de)(de)(de)(de)t-PAIC水平(ping)顯著(zhu)高(gao)于(yu)膿毒癥(zheng)患(huan)(huan)者，t-PAIC水平(ping)與(yu)乳酸水平(ping)及(ji)(ji)序貫器(qi)官衰(shuai)(shuai)竭(sequential organ failure assessment，SOFA)評分均呈正(zheng)(zheng)相關。Winter等研究(jiu)發(fa)現，合(he)并(bing)器(qi)官衰(shuai)(shuai)竭特(te)別是(shi)(shi)心力衰(shuai)(shuai)竭患(huan)(huan)者的(de)(de)(de)(de)(de)t-PAIC水平(ping)明顯高(gao)于(yu)無器(qi)官功能(neng)障礙的(de)(de)(de)(de)(de)患(huan)(huan)者。
膿(nong)(nong)毒癥(zheng)時(shi)，內(nei)毒素導致(zhi)內(nei)皮細胞損(sun)傷，促進凝(ning)血(xue)酶活(huo)化(hua)，此時(shi)可(ke)表現為(wei)TM及TAT升(sheng)(sheng)高，隨(sui)著(zhu)(zhu)膿(nong)(nong)毒癥(zheng)演進為(wei)膿(nong)(nong)毒癥(zheng)休(xiu)克(ke)，出現組織(zhi)低灌(guan)注導致(zhi)器(qi)官(guan)功能損(sun)害，此時(shi)t-PAIC可(ke)顯(xian)著(zhu)(zhu)升(sheng)(sheng)高，而PIC因為(wei)纖(xian)溶抑制(zhi)作用(yong)升(sheng)(sheng)高不明顯(xian)。創(chuang)傷時(shi)，出血(xue)導致(zhi)凝(ning)血(xue)酶大量活(huo)化(hua)發(fa)揮止血(xue)效(xiao)應，可(ke)表現為(wei)TAT顯(xian)著(zhu)(zhu)升(sheng)(sheng)高；內(nei)皮細胞釋放大量活(huo)化(hua)蛋白C抑制(zhi)PAI-1活(huo)性，引起(qi)纖(xian)溶亢進，表現為(wei)PIC顯(xian)著(zhu)(zhu)升(sheng)(sheng)高。如(ru)創(chuang)傷失血(xue)發(fa)展至休(xiu)克(ke)階段，出現廣(guang)泛內(nei)皮損(sun)傷，可(ke)表現為(wei)TM升(sheng)(sheng)高；如(ru)休(xiu)克(ke)加(jia)重出現明顯(xian)器(qi)官(guan)功能障礙，可(ke)出現t-PAIC顯(xian)著(zhu)(zhu)升(sheng)(sheng)高[41]。
膿(nong)毒癥及創(chuang)傷分(fen)別(bie)作(zuo)為血(xue)栓型(xing)DIC及纖溶型(xing)DIC的(de)典型(xing)代表疾病，也說明新型(xing)凝(ning)血(xue)分(fen)子標(biao)志物在(zai)區分(fen)DIC亞型(xing)方面的(de)重要作(zuo)用，特(te)別(bie)在(zai)創(chuang)傷失血(xue)性休克向膿(nong)毒癥休克轉化時(shi)有重要診斷價值。
新型(xing)凝血分子標志(zhi)物在重癥患者(zhe)凝血功能障礙(ai)常(chang)見(jian)疾(ji)病中的表現見(jian)下表。
有(you)了新的血栓四項標(biao)志物：TAT、TM、PIC和t·PAI-c，綜合反映(ying)出機(ji)體凝血，纖溶以及血管(guan)內皮系統早(zao)期(qi)激活的有(you)效(xiao)指(zhi)標(biao)，適用于各臨床學科血栓高危人(ren)群(qun)進行血栓的早(zao)期(qi)診斷、治療評(ping)估和預后(hou)判斷。
能夠能夠綜合(he)評估血(xue)管內皮受損(sun)情況，反應(ying)凝(ning)(ning)血(xue)酶、纖溶(rong)(rong)酶激活(huo)狀態(tai)，可在各個系統的反應(ying)起始階段產生，因此(ci)可以作為DIC、血(xue)栓性疾病早期診斷和預防的提示指標，也可用于溶(rong)(rong)栓療效監測，對于早期的出凝(ning)(ning)血(xue)系統狀態(tai)評估是非常重要的。
文章來源：Med J Chin PLA, Vol. 47, No. 2, February, 2022