血脂与下肢深静脉血栓的相关性研究
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摘要
【目的】
     本文通过对108例下肢深静脉血栓患者和100例对照患者的血脂水平的研究,探讨血脂的各项指标和下肢深静脉血栓形成的关系。
     1.探讨血脂的各项指标,包括:胆固醇、甘油三酯、低密度脂蛋白、高密度脂蛋白、氧化型低密度脂蛋白和脂蛋白(a)等,与下肢深静脉血栓的关系。
     2.如何根据血脂的水平估计形成下肢深静脉血栓的危险性,以更好的预防下肢深静脉血栓的形成。
     【方法】
     1.首先在我院随机选择骨牵引患者120例,作为实验组,再随机选择同期同等条件下的非牵引患者100例,作为对照组,分别统计出实验组和对照组患者出现下肢深静脉血栓的发病率,对两组患者的下肢深静脉血栓的发病率进行统计学分析,得出结果,进而了解骨牵引对下肢深静脉血栓形成是否有的影响。
     2.将108例外伤后卧床制动2周内形成下肢深静脉血栓的患者(实验组)分为两组:牵引组(B1组)和非牵引组(B2组),再将100例未出现下肢深静脉血栓的患者(对照组)也分为两组:牵引组(A1组)和非牵引组(A2组)。分别对其外伤卧床制动后1天,1周和2周的血脂水平进行回顾性分析,包括:胆固醇、甘油三酯、低密度脂蛋白、高密度脂蛋白、氧化型低密度脂蛋白和脂蛋白(a)。首先进行组内比较,以了解牵引是否对实验结果有影响;再通过组间比较,了解血脂的各项指标与下肢深静脉血栓的关系。
     【结果】
     1.在骨牵引组的120例患者当中,出现下肢深静脉血栓的患者为20例,其血栓发病率为16.7%,而在非牵引组的100例患者当中,出现下肢深静脉血栓的患者为15例,其血栓发病率为15.0%。通过χ~2检验,测得χ~2值为0.113(P>0.05),尚不能认为两组患者的血栓发病率不同。
     2.通过A1组与B1组和A2组与B2组的比较表明:胆固醇和甘油三酯各时段水平,实验组与对照组均无差异;而氧化型低密度脂蛋白在外伤卧床制动后各时段水平,实验组均明显高于对照组;低密度脂蛋白、高密度脂蛋白在外伤卧床制动后2周时的水平,实验组明显高于和低于对照组;脂蛋白(a)在外伤卧床制动后1周和2周时的水平,实验组均明显高于对照组。
     【结论】
     1.骨牵引不能作为下肢深静脉血栓形成的诱发因素,没有对下肢深静脉血栓形成造成影响。
     2.胆固醇和甘油三酯水平的升高对与下肢深静脉血栓的形成无影响。
     3.氧化型低密度脂蛋白、脂蛋白(a)、低密度脂蛋白和高密度脂蛋白水平的升高对下肢深静脉血栓的形成有着明显的相关性,尤其是氧化型低密度脂蛋白是下肢深静脉血栓的形成的重要因素,对静脉血栓形成有重要意义。
     4.对于氧化型低密度脂蛋白水平升高的患者应积极预防下肢深静脉血栓的形成,以免造成肺栓塞等严重后果,危及生命。而脂蛋白(a)、低密度脂蛋白和高密度脂蛋白水平可以作为指导预防和治疗下肢深静脉血栓形成的辅助指标。
[Objective]
     To explore the relationship between the lipid indexes and deep vein thrombosis (DVT) of lower extremity by the study of the lipid indexes between 108 patients of DVT of lower extremity and 100 patients as compared group.
     1. To understand the relationship between every indexes of the lipid such as: CHOL, TRIG, LDL, HDL, LDL and ox-Lp (a), and DVT of lower extremity.
     2. How to evaluate the danger of DVT of lower extremity and to carry out it better according to the level of the lipid indexes.
     [Methods]
     1. First 120 patients of traction was random selected in hospital, as experimental group; and 100 patients of non-traction was random selected in the same time and condition, as control group. Than the incidence of DVT of lower extremity of the two groups was analyzed statically, draw the conclusion, and then understand if traction can affect the incidence of DVT of lower extremity.
     2.108 patients who were in bed after injury formed DVT of lower extremity within two weeks, were divided into two groups (experimental group): traction group (B1) and non-traction group (B2), and there were 100 patients who didn't form DVT of lower extremity were divided into two groups (control group): traction group (A1) and non-traction group (A2). The lipid level of these patients who were in bed after injury one day, one week and two weeks were analyzed retrospectively, including: CHOL, TRIG, LDL, HDL, ox-LDL and Lp(a). First, we can understand the affection of traction by compare between the group Al and A2 and group B1 and B2, than we can understand the relationship by compare differences of lipids in the various indicators of between the various groups.
     [Results]
     1. Among the 120 patients of group traction there were 20 patients suffer from DVT of lower extremity, incidence of DVT of lower extremity was 16.7%; Among the 100 patients of group non-traction there were 15 patients suffer from DVT of lower extremity, incidence of DVT of lower extremity was 15%. By chi square test, X~2=0.113(P>0.05), so we can't consider incidence of DVT of lower extremity of the two groups is different.
     2. Compared between group A1 and B1 and between group A2 and B2 showed that: CHOL and TRIG, there were no different between the experimental group and the control group; but level of ox-LDL of the experimental group was significantly higher than the control group, the experimental group; level of LDL and HDL of the experimental group after two weeks was significantly higher and lower than the level of the control group; level of Lp (a) of the experimental group after one week and two weeks was significantly higher than the control group.
     [Conclusions]
     1. It is not regarded induced factor of DVT of lower extremity that bone was tracked, and it doesn't affect DVT of lower extremity.
     2. CHOL and TRIG have no relevance with DVT of lower extremity.
     3. The increase of Ox-LDL, LDL, HDL and Lp (a) levels have relevance with DVT of lower extremity, in particular ox-LDL have significantly relevance with DVT of lower extremity, it is an important factor in the formation of venous thrombosis and has great significance .
     4. To higher Ox-LDL level patients elevated should actively prevent the formation of DVT of lower extremity, so as to avoid serious consequences, such as pulmonary embolism, a life-threatening. And LDL, HDL and Lp (a) levels can be used as auxiliary indicator to the prevention of DVT of lower extremity.
引文
[1]陈松鹤,张国祯,诸俊仁.高脂血症和血小板高反应性[J].国外医学心血管病分册.1999,16(5):2571.
    [2]Drew AF,Davenport P,Apostolopoulos J,et al.Tissue factor pathway inhibitor expression in atherosclerosis[J].Lab Invest.2003,77(2):291-298.
    [3]Sandset PM.Tissue factor pathway inhibitor(TFPI)an update[J].Haemostasis,2003,26(3):154-165.
    [4]Wang C,Fneg Y,Zong Y,et al.Rapid isolation of large amount of plasma VLDL and LDL by a two step ultracentrifugation[J].Tongji MedUniv,1999,15(5):198-200.
    [5]Sambrook J,Fritsch EF,Maniatis T.Molecular Cloning:ALaboratory Manual[J].Cold Spring Harbor Laboratory Press,2002,55(1):123-125.
    [6]Chomczynshi P,Sacchi N.Single step method of RNA isolation by guanidinium thiocyanate phenol chloroform extraction[J].Anal Biochem,2001,162(5):156-159.
    [7]Yla-Herttuala S,Palinski W,Rosenfeld ME,et al.Presence of oxidatively modified low density lipoprotein in atherosclerotic lesions of rabbit and man[J].Clin Invest,2000,84(5):1086-1095.
    [8]王国平,倪娟,夏春枝,等.内皮脂质过氧化损伤增强静脉平滑肌细胞表达细胞周期素D[J].中国血管杂志,2004,22(5):208-211.
    [9]许文亮,郭新贵,徐延路,等.下肢深静脉血栓形成患者血浆胆固醇与内皮素C反应蛋白及血小板可溶性P选择素相关性研究新医学[J],2004,35(2):125-126.
    [10]Kent RS,Kitchell BB,Shand DG,et al.The ability of vascular tissue to produce prostacyclin decreases with age[J].Prostaglandins,1999,21(3):4831.
    [11]Steinberg D,Parthasarathy S,Carew TE,et al.Beyand cholesterol modifications of low density lipoprotein that increase its atherogenicity[J].N Engl J Med,2002,320(8):915-924.
    [12]Aviram M.LDL-platelet interaction under oxidative stress induces macrophage foam cell formation[J].Thromb Haemost,2003,74(5):560-564.
    [13]Zhao B,Rickert CH,Filler TJ,et al.Adhesion of washed blood platelets in vitro is advanced,accelerated,and enlarged by oxidized low density lipoprotein[J].Am J Hematol,2005,49(3):177-182.
    [14]MahfouzMM,Kummerow FA.Oxysterols and TBARS are among the LDLoxidation products which enhance thromboxane A synthesis by platelets[J].Prostaglandins Other Lipid Mediat,2004,56(2):197-217.
    [15]Zhao B,Dierichs R,Harrach - Ruprecht B,et al.Oxidized LDL induces serotonin release from blood platelets[J].Am J Hematol,2000,48(1):285-287.
    [16]Takahashi Y,Fuda H,Yanai H,et al.Significance of membrane glycoproteins in platelet interaction with oxidized low density lipoprotein[J].Semin Thromb Hemost,2001,24(6):251-253.
    [17]许贻白,王贤军,诸金水,等.氧化型低密度脂蛋白和一氧化氮的相互作用及其在静脉血栓发病中的作用[J].中华心血管杂志,2002,32(1):40-42.
    [18]Bruckdorfer KR,Naseem KM,Mohammadi B,et al.The influence of oxidized lipoproteins,oxidation products and antioxidants on the release of nitric oxide from the endothelium and the response of platelets to nitric oxide[J].Biofactors,2003,6(5):191-199.
    [19]Liao JK,Shin WS,Lee WY,et al.Oxidized low - density lipoprotein decreases the expression of endothelial nitric oxide synthase[J].J Biol Chem,2005,270(8):319-324.
    [20]Zhao B,Dierichs R,Miller FN,et al.Oxidized low density lipoprotein inhibits platelet plasma membrane Ca~(2+)-ATPase[J].Cell Calcium,2006,19(5):453-458.
    [21]杨丹,曾珊,刘文兰,等.溶血性磷脂酰胆碱诱导血小板活化及蛋白质酪氨酸激酶和蛋白激酶C的作用[J].中国药理学与毒理学杂志,1999,13(1):49-52.
    [22]Fyrnys B,Claus R,Wolf G,et al.Oxidized low density lipoprotein stimulates protein kinase C(PKC)activity and expression of PKC-isotypes via prostaglandin-H-synthase in P388D1 cells[J].2003,28(5):456-458.
    [23]Wilson BD,Pitas RE,Rodgers GM.Regulation of endothelial cell protein C activation by native and oxidized low density lipoprotein[J].Semin Thromb Hemost,2002,18920:11-17.
    [24]Weis JR,Pitas RE,Wilson BD,et al.Oxidized low-density lipoprotein increases cultured human endothelial cell tissue factor activity and reduces protein C activation[J].FASEB J,2001,45(2):459-465.
    [25]Lewis JC,Bennett-Cain AL,De Mars CS,et al.Procoagulant activity after exposure of monocyte - derived macrophages to minimally oxidized low density lipoprotein. Co - localization of tissue factor antigen and nascent fibrin fibers at the cell surface [J]. Am JPathol, 2005,147(3):1029-1040.
    [26] Sato N, Kokame K, Miyata T, et al. Lysophosphatidylcholine decreases the synthesis of tissue factor pathway inhibitor in human umbilical vein endothelial cells [J]. Thromb Haemost, 2006,79(5) :217-221.
    [27] Tremoli E. Increased sythesis of plasminogen activator inhibitor-synthesis by cultured human endothelial cells exposed to native and modified LDLs. An LDL receptor independent phenomenon [J]. Arterioscler Thromb , 2003,13(5):338-346.
    [28] Allison BA, Nilsson L, Karpe F, et al. Effects of native , triglyceride-enriched, and oxidatively modified LDL on plasminogen activator inhibitor-1 expression in human endothelial cells [J]. Arterioscler Thromb Vasc Biol ,1999,19(6): 1354-1360.
    [29] Latron Y, Chautan M, Anfosso F , et al. Stimulating effect of oxidized low density lipoproteins on plasminogen activator inhibitor-synthesis by endothelial cells [J]. Arterioscler Thromb , 1999,11 (2): 1821 -1829.
    [30] Chautan M, Latron Y, Anfosso F , et al. Phosphatidylinositol turnover during stimulation of plasminogen activator inhibitor-secretion induced by oxidized low density lipoproteins in human endothelial cells [J]. J Lipid Res, 2000, 34(11): 101- 110.
    [31] Galle J, Wanner C. Oxidized LDL and Lp (a). Preparation, modification, and analysis [J]. Methods Mol Biol, 2001,108(5): 119-130.
    [32] Kramer-Guth A, Greiber S, Pavenstadt H, et al. Interaction of native and oxidized lipoprotein (a) with human mesangial cells and matrix [J]. Kidney Int, 2000,49(2): 1250-1261.
    [33] Chin JH, Azhar S, Hoffman BB. Inactivation of endothelial derived relaxing factor by oxidized lipoproteins [J]. J Clin Invest, 2002 ,89(3): 10-18.
    [34] Li D, Yang B, Mehta JL. Ox-LDLinduces apoptosis in human coronary artery endothelial cells : role of PKC , PTK, bcl-2 ,and Fas [J]. Am J Physiol, 1998,275(3): 568-576.
    [35] Ishii H, Kizaki K, Horie S, et al. Oxidized low density lipoprotein reduces thrombomodulin transcription in cultured human endothelial cells through degradation of the lipoprotein in lysosomes [J]. J Biol Chem,20066,271(8): 458-465.
    [36] Jovinge S, Ares MP, Kallin B, et al. Human monocytes macrophages release TNF-alpha in response to Ox-LDL [J]. Arterioscler Thromb Vasc Biol, 2004,16(1): 1573-1579.
    [37] Chen LY, Mehta P, Mehta JL. Oxidized LDL decreases L-arginine uptake and nitric oxide synthase protein expression in humanplatelets : relevance of the effect of oxidized LDLon platelet function[J]. Circulation, 2006,93(6): 1740-1746.
    [38] Uittenbogaard A, Shaul PW, Yuhanna IS , et al. High density lipoprotein prevents oxidized low density lipoprotein induced inhibition of endothelial nitric oxide synthase localization and activation incaveolae[J]. J Biol Chem, 2000,275 (2): 11278-11283.
    [39] Yuhanna IS , Zhu Y, Cox BE , et al. High density lipoprotein binding to scavenger receptor BI activates endothelial nitric oxide synthase[J]. Nat Med , 2001,7(1):853-857.
    [40] Shaul PW. Endothelial nitric oxide synthase , caveolae and the devel opment of atherosclerosis[J]. J Physiol, 2003,547(5):212-233.
    [41] Mineo C , Yuhanna IS , Quon MJ, et al. High density lipoprotein induced endothelial nitric oxide synthase activation is mediated by Akt and MAP kinases [J]. J Biol Chem, 2003,278(5):9142-9149.
    [42] Cominacini L, Rigoni A, Pasini AF, et al. The binding of oxidized low density lipoprotein (ox-LDL) to ox-LDL receptor-1 reduces the intracellular concentration of nitric oxide in endothelial cells through an increased production of superoxide [J]. J Biol Chem, 200 ,276(2): 13750-13755.
    [43] Spector M, Rader DJ . The role of high density lipoproteins in thrombosis[J]. Scientific World Journal, 2002,2(2):89-95.
    [44] Tamagaki C, Monica G, Guido F. Endothelial protection by high density lipoproteins: from bench to bedside[J]. Aterioscler Thromb Vasc Biol, 2003,23(4): 1724-1731.
    [45] Oravec AD, Chapman MJ. Inflammation, bioactive lipids and atherosclerosis : potential roles of a lipoprotein associated phospholi pase A, platelet activating factor acetylhydrolase [J] .AtherosclerSuppl, 2002,3(1):57-68.
    [46]Blann LA,Fless GM,Scanu AM,et al.Interaction of HDL with plasminogen binding sites on cell[J].Thromb Haemost,2005,73(4):458-465.
    [47]Griffin JH,Kojima K,Banka CL,et al.High density lipoprotein enhancement of anticoagulant activities of protein S and activated protein C[J].J Clin Invest,1999,103(8):219-227.
    [48]Ren S,Shen GX.Impact of antioxidants and HDL on glycated LDL induced generation of fibrinolytic regulators from vascular endothelial cells[J].Aterioscler Thromb Vase Biol,2000,20(4):1688-1693.
    [49]Berg K.A new serum type system in men-the lipop rotein system[J].Acta patholMicrobiol Scand,1999,59(5):369-382.
    [50]Eaton A,Mclean T,Fujimoto N,et al.Lp(a)Lipoproten as a risk factor for deep vein thrombosis[J].Atherosclerosis,2000,59(2):199-204.
    [51]Shintani S,Kikuchi S,Hamaguchi H,et al.High serumlip protein(a)levels are an independent risk factor for deep vein thrombosis[J].Stroke,2004,24(7):965-969.
    [52]张炳峰,只野寿太郎,山本匡介.脂蛋白(a)是最敏感的急性时相蛋白[J].中华医学检验杂志,1997,20(3):167-169.
    [53]Boerwinkle E,Leffert CC,L in J,et al.Apolipoprotein(a)gene accounts for greater than 90%of the variation in plasma lipop rotein(a)concentrations[J].J Clin Invest,2002,90(1):52-60.
    [54]Kagawa A,Azuma H,AkaikeM,et al.Asp irin reduces apolipop rotein(a)[apo (a)]production in human hepatocytes by supp ression of apo(a)gene transcription[J].J Biol Chem 1999,274(48):34111-4115.
    [55]Kochl S,Fresserf,Lobentanz E,et al.Novel interaction of apolipoprotein(a)with beta glycoprotein Ⅰ mediated by the kringle Ⅳ domain[J].Blood,2003,90(4):1482-1489.
    [56]张丽霞,高三阳,王学荣,等.下肢深静脉血栓脂蛋白(a)、血小板、蛋白激酶变化[J].中华医学检验杂志,1998,21(5):269-271.
    [57]Kraft HG,Lingenhel A,Kochl S,et al.Apoliporotein(a)kringle Ⅳ repeat number predicts risk for deep vein thrombosis[J].Arterioscler Thromd Vase Bion,2001,16(6):713-719.
    [58]Edelstein C,Italia JA,Klezovitch O,et al.Functional and metabolic differences between elastase generated fragments of human lipoprotein(a) and apolipoprotein(a) [J]. J Lipid Res ,2006,37(8): 1786-1801.
    [59] Romanic AM, Arleth AJ, Willette RN, et al. Factor XIIIa cross links lipoprotein (a) with fibrinogen and is present in human atherosclerotic lesions[J]. Circ Res ,2005,83(3):264-269.
    [60] Anglescano E. Structural basis for the pathophysiology of lipoprotein (a) in the athero thrombotic process [J].Braz J Med Res,1997, 30(11):1271-1280.
    [61] AkaikeM,Azuma H, Kagawa A, et al. Effect of asp irintreatment on serum concentrations of lipop rotein (a) inpatients with atherosclerotic diseases [J]. Clin Chem ,2002,48(9): 1454-1459.
    [1]RoBert B,Ford R.Vascular surgery[M].北京:人民卫生出版社,第一版,2002:1937-1941.
    [2]Camillettia,Morettin,Giacchetti G,et all.Decreased nitric oxide levels and increased calcium content in platelets of hypertensive patients Am J Hypertens[J],2005,14(41):382-386.
    [3]Enrico Bernadi.Extended versus rapid analysis of the leg veinsystem:a multicenter ultrasound study[J].Pathophysiol H aem ostThromb,2004,33:314-318.
    [4]Lip GY,Blant A.Does hypertension confer a prethromboticstate virchows triad revisited[J].Circulation,2006,101(3):2182-2201.
    [5]Yamazaki M,Uchiyama S,Iwata M.Measurement of platelet fibrinogen binding and pselectin expression by flow cytometry in patients with cerebral infarction[J].ThrombRes,2005,104(3):197-205.
    [6]Preston RA,J imenez JJ,et all.Effects of severe hypertension on endothelial and platelet microparticles-1 Hypertension,2003,41(2):2112-2171
    [7]关永源,林默君.一氧化氮的药理学作用新医学[J],1999,130(1):552-571.
    [8]王淑娟.关于选择血栓前状态实验诊断指标的建议[J].中华医学检验杂志,2004,21(5):305-307.
    [9]许文亮,郭新贵,徐延路,等.下肢深静脉血栓形成患者血浆胆固醇与内皮素C反应蛋白及血小板可溶性P选择素相关性研究[J].新医学,2004,35(2):587-590.
    [10]万仑,胡豇,刘仲前.骨水泥对全髋置换术后深静脉血栓形成的影响[J].四川医学,2002,23(8):798-799.
    [11]Ross GM,McMillan TJ,Wilcox P,et al.The single cell microgel elect rophoresis assay(comet assay):technical aspects and applications.Report on the 5th LH Gray TrustWorkshop,Institute of Cancer Research[J],Mutat Res,2005,337(1):57-60.
    [12]Wen F,Yu SZ.A study on the content ofCSF vWF in patient s with cerebral infarction at different location[J].ThrombHaemost,2006,88(6):1067-1068.
    [13]Loscalzo J Nitric oxide insufficiency,platelet activation,and arterial thrombosis[J].Circ Res,2005,88(8):756-762.
    [14]中国高血压防治指南起草委员会中国高血压防治指南[J].高血压杂志,2000,8(1):941.
    [15]Minguez Y,Rubio C,Bernal A,et al.The impact of endometriosis incouples undergoing intracytoplasmic sperm injection because of male infertility[J].Hum Reprod,2004,12(10):2282-2285.
    [16]Christie J,Burnett R,Potts HR,et al.Echocardiography of transtrial embolism during cemented and uncemented hemiartheroplasty of the hip[J].JBone Joint Surg Br,2005,76(3):409-412.
    [17]Kaedel U,Paul R,Winkler F,et al.Lack of endothelial nitric oxide synthase aggravates murine pneumococcal meningitis.J Neuropathol.Exp Neurol,2005,60:1041-1050.
    [18]孙英信,时德,向志,等.急性下肢静脉血栓形成148例的治疗[J].第四军医大学学报,2005,23(9):813-814.
    [19]Murohara T,Scalia R,Lefer AM.Lysophosphatidylcholine promotes P selectin expression in platelets and endothelial cells.Possible involvement of protein kinase C activation and its inhibition by nitric oxide donors[J].Circ Res,2004,78(5):892-897.
    [20]Omi H,Okayama N,Shinizu M,et al.Cilostazol inhibits high glucose mediated endothelialneutrophil adhesion by decreasing adhesion mole cule exp ression via NO production[J].Microvascular Research,2004,68(2):119-125.

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