【摘要】：背景經(jīng)頸靜脈肝內(nèi)門體分流術(shù)(TIPS)是門脈高壓相關(guān)并發(fā)癥的主要治療方法之一。隨著嚴(yán)重門脈高壓并發(fā)癥得到控制,肝衰竭成為終末期肝硬化患者死亡的主要原因。研究顯示血小板計數(shù)是TIPS術(shù)后肝衰、總生存期的獨立影響因素。肝硬化患者血小板計數(shù)減少同時伴有血小板生成減少及血小板清除增加。肝細(xì)胞、巨噬細(xì)胞吞噬去唾液酸化的血小板、血小板活化聚集是血小板的主要清除機(jī)制。目前關(guān)于TIPS術(shù)后血小板變化的研究局限于血小板計數(shù),且結(jié)論尚不統(tǒng)。目的分析TIPS對血小板活化、血小板去脫唾液酸化的影響,探討TIPS對肝硬化門脈高壓患者血小板清除、血小板計數(shù)的影響。材料與方法2015年01月至2016年06月共31例患者納入本研究。于TIPS術(shù)前(t1)、術(shù)后1周(t2)、術(shù)后3～6月(t3),空腹采外周靜脈血。采用流式細(xì)胞儀檢測脫唾液酸率(RCA-1、sWAG表達(dá)率),檢測血小板PAC-1表達(dá)率及血漿血小板微粒(PMPs)水平評估血小板活化程度。使用ELISA法檢測TIPS前后血漿內(nèi)毒素(LPS)水平。同時收集各時間點血小板計數(shù)(PLT)、平均血小板體積(MPV)、血小板壓積(PCT)、血小板分布寬度(PDW)及大型血小板比率(PLCR)等數(shù)據(jù)進(jìn)行分析。結(jié)果1.血漿LPS TIPS 術(shù)后血漿 LPS 水平顯著下降(43.0±17.9pg/ml VS 29.3±13.9pg/ml,P0.01)。LPS水平與門脈壓力梯度(PPG)正相關(guān)(r=0.63,p0.01)。2.血小板計數(shù)、MPV、PCT、PDW、PLCRt1、t2、t3血小板計數(shù)分別為97.0±86.3×109/L、87.2±50.6×109/L、95.9±52.3×109/L,差異無統(tǒng)計學(xué)意義(P=0.38)。t1、t2、t3PCT 分別為 1.1±1.0ml/L、0.9±0.6 ml/L、1.0±0.6 ml/L,差異無統(tǒng)計學(xué)意義(P=0.20)。t1、t2、t3PDW 分別為 14.6±2.2f1、13.4±2.1f1、13.5±2.7f1,t1 顯著高于 t2 及 t3(P=0.01)。t1、t2、t3MPV 分別為 11.7±0.9fL、11.1±0.9fL、11.0±0.9fL,t1 顯著高于 t2 及 t3(P0.01)。t1、t2、t3 PLCR 分別為 38.6±6.8%、33.2±7.0%、33.0±7.5%,t1 顯著高于 t2 及 t3(P0.01)。3.血小板活化t1、t2、t3 PAC-1 表達(dá)率分別為 37.1±25.3%、19.4±17.5%、14.8±14.8%,對應(yīng)的血漿PMPs水平分別為14.6±10.4×105/ml、8.0±6.3×105/ml、5.6±3.2X 105/ml,差異均有統(tǒng)計學(xué)意義(P0.01)。PAC-1表達(dá)率與LPS正相關(guān)(r=0.51,p0.01),與血小板計數(shù)負(fù)相關(guān)(r=-0.27,P=0.01),與MPV正相關(guān)(r=0.41,P0.01)。4.血小板去唾液酸化t1、t2、t3 RCA-1 表達(dá)率分別為 8.5±8.2%、13.9±14.6%、9.6±9.9%,t2 顯著高于 t1 及 t3(P=0.01)。t1、t2、t3 sWAG 表達(dá)率分別為 11.5±12.7%、14.6±14.5%、11.6±8.0%,差異無統(tǒng)計學(xué)意義(P=0.40)。結(jié)論TIPS降低肝硬化門脈高壓患者血漿內(nèi)毒素濃度,減輕血小板活化,對血小板去唾液酸化則無顯著影響。雖然TIPS對血小板計數(shù)無顯著影響,但可一定程度降低硬化患者血小板清除率,延長循環(huán)血小板壽命。
[Abstract]:Background Transjugular intrahepatic portosystemic shunt (TIPS) is one of the main treatments for portal hypertension related complications. With severe portal hypertension complications under control, liver failure is the leading cause of death in patients with end-stage cirrhosis. Studies have shown that platelet count is an independent factor in the overall survival of liver failure after TIPS. Thrombocytopenia is associated with thrombocytopenia and increased platelet clearance in cirrhotic patients. Hepatocytes, macrophages, phagocytosis of salivary acidified platelets, platelet activation and aggregation is the main clearance mechanism of platelets. At present, the study of platelet changes after TIPS is limited to platelet count, and the conclusion is not uniform. Objective to investigate the effects of TIPS on platelet activation and platelet desalivation in patients with portal hypertension. Materials and methods from January 2015 to June 2016, 31 patients were included in this study. Peripheral venous blood was collected before TIPS (T1), 1 week postoperatively (T2), and 3 ~ 6 months postoperatively (T3). The desialic acid rate (RCA-1,sWAG expression rate), platelet PAC-1 expression rate and plasma platelet particulate (PMPs) level were measured by flow cytometry to evaluate platelet activation. Plasma endotoxin (LPS) levels were measured by ELISA before and after TIPS. At the same time, the data of (PLT), mean platelet volume (MPV), (PCT), platelet distribution width (PDW) and large platelet ratio (PLCR) were collected and analyzed. Result 1. The plasma LPS level decreased significantly after LPS TIPS (43.0 鹵17.9pg/ml VS 29.3 鹵13.9 PG / ml P0.01). There was a positive correlation between LPS level and portal pressure gradient (PPG) (r 0.63% P 0.01) .2. 琛，

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