布-加综合征患者血浆中vWF、GMP-140变化的研究
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摘要
布—加综合征(Budd-Chiari syndrome，B-CS)系指主肝静脉出口部和(或)肝后段下腔静脉血流受阻所引起的肝后型门静脉高压症和(或)下腔静脉高压综合征。随着医学技术水平和对该病认识的不断提高，大量病例被发现，引起越来越多的临床工作者的关注，有关的病因报道多种多样。如何从众多的病因中找到最为常见的因素，具有十分重要的意义。近年的研究认为：B-CS是血栓形成及其后遗症导致的一系列病理变化临床综合征，而非先天畸形。B-CS患者的高凝状态是由许多复杂因素共同作用的结果，已知的因素包括骨髓增殖异常、红细胞生成素增多、自发红系集落形成等。血栓性疾病的研究进展发现：血管性假血友病因子(von Willebrand factor，vWF)、血小板α-颗粒膜蛋白—140(granule membrane protein-140，GMP-140)含量升高是静脉血栓形成的重要因素。vWF是反映血管内皮细胞损伤的特异性分子标志物；GMP-140是反映血小板活化与释放反应最特异的标志物。有关B-CS患者血浆中的vWF、GMP-140变化所致凝血状态异常的国内外报道很少。本实验通过测定B-CS患者血浆中的vWF、GMP-140变化情况，旨在进一步阐明导致B-CS高凝状态的主要原因，为进一步提高临床诊断和治疗水平提供理论依据。
郑州大学2004年硕士研究生毕业论文
布一加综合征患者血浆中vWF、GMP一140变化的研究
材料与方法
病材取自于2002年6月至2003年10月在河南省人民医院肝胆胰腺外科住
院的经下腔静脉造影、彩色多普勒超声、手术确诊的B一CS患者60例。其中血
栓型B一CS 42例(男31例，女11例，年龄12一56岁，平均29.6士6.9岁);膜型
B一CS18例(男8例，女10例，年龄26一49，平均犯.6士5.2岁);正常对照组为
同期在河南省人民医院肝胆胰腺外科门诊进行体检的健康人员30例(男16例，
女14例，年龄16一65岁，平均35.9士7.8岁)。B一CS患者于术前和术后2周各
取空腹外周静脉血，正常对照组于空腹体检时取外周静脉血，经抗凝处理，分离
血浆，采用酶联免疫吸附双抗体夹心法(E LlsA)定量测定血浆中vWF、GMP一140
含量;采用临床常规方法检测B一CS患者于术前和术后2周空腹外周静脉血中血
小板计数。
结果
1.术前B一CS患者血浆中vWF含量为(25 1 .67士1 18.39)%、GMP一140含量
为87.92士34.47ng/mL。其中血栓型B一CS组vWF含量为(256.73士124.49)%、
GMP一1 40含量为88.60士25.04ng/mL;膜型B一CS组vWF含量为(239.85士103.82)
%、GMP一1 40含量为86.32士56.46ng/mL;两组间相比均无显著差异(P均>0 .05)，
但二者均显著高于正常对照组(v wF为112.25士86.61%，P均<0 .01; GMP一140
为24.90士9.31ng/mL，P均<0.01)。
2.术前B一CS患者静脉血中血小板计数为(91士34) x 109与静脉血浆中的
vWF、GMP一1 40水平无相关性(r分别为一0.1641及一0.0369，P均>0.05)。
3.术后2周血栓型B一CS患者静脉血浆中vWF含量为(248.36士1 13.43)%、
GMP一1 40含量为8 1 .73士1 7.76ng/mL，与术前相比均无明显差异(P均)0.05);
膜型B一CS患者静脉血浆中vWF含量为(1 1 9.76士87.52)%、GMP一140含量为41.33
士32.30ng/mL，与术前相比均显著降低，有统计学意义(P均<0 .01)。
结论
1.术前B一es病例组vwF、GMP一1 40含量明显高于对照组(P均<0.01)，提示
郑州大学2004年硕士研究生毕业论文
布一加综合征患者血浆中vWF、GMP一140变化的研究
vWF、GMP一140水平升高可能是导致B一CS患者高凝状态的重要因素;血栓型
B一CS、膜型B一CS患者静脉血浆中vWF、GMP一140水平升高，但两组间相比均
无明显差异(P均>0.05)，提示就vWF、GMP- 140升高所致的血液高凝状态，
在两大类B一CS中无明显差异。
2.术前B一CS组血浆中vWF、GMP一140升高水平与静脉血中血小板计数不相
关，(r分别为一0.1641及一0.0369，p均>0.05)，表明B一CS患者血浆中的vwF、
GMP一140升高与血管内皮细胞的损伤和血小板活化程度有关，提示血管内皮细
胞的损伤和血小板活化是形成B一CS的一个重要因素。
3.术后血栓型B一CS组患者血浆中vWF、GMP一140水平与术前相比均无显
著差异(P均>0.05)，表明手术不改变血栓型B一cs的血液高凝状态，术后需抗凝
祛聚治疗;膜型B一CS组患者血浆vWF、GMP一140水平较术前明显降低(P均
<0.01)，说明手术可改变膜型B一CS的血液高凝状态。
Budd-Chiari syndrome (B-CS) refers to posthepatic portal hypertension (PHT) and/or inferior vena cava hypertension caused by obstruction in outlet of major hepatic veins and/or posthepatic inferior vena cava. Though many kinds of causes about B-CS have been reported, they are uncompleted and indefinite. So the investigation of the etiology in B-CS is valuable and important especially to the clinical diagnosis and treatment. In recent years, many physicians have accepted the theory that the B-CS is not inborn but the sequels from the thrombosis. The hypercoagulation of patients with B-CS caused by many different causes, such as hyper-erythropoietin, colony-forming units erythroid and myoloproliferative disorder so on. And during the research of the thrombosis many physicians draw a conclusion that the increased quantity of vWF and GMP-140 is one of the most prevalent factors, which cause vein thrombosis. vWF is the specific molecule symbol of injury vascular endothelium cell and GMP-140 is the specific symbol
of activation and release of platelets. But there have been few reports about the relation between the B-CS and the
increased quantity of vWF and GMP-140 now. To explore the causes of hypercoagulation and give theoretical support in clinical diagnosis and treatment, vWF and GMP-140 in patients with B-CS were investigated in this study.
Materials and methods:
60 patients in B-CS group including 42 patients (12~56years) with thrombus type B-CS (31 males and 11 females with the mean age of 29.6?.9 years), and 18 patients (26~49years) with membrane type B-CS (8 males and 10 females with mean age of 32.6?.2 years) were all diagnosed definitely with Color Doppler sonography and/or inferior vena cavography(IVCG) from June,2002 to Oct 2003 in Henan Provincial People's Hospital. In control group, there were 30 healthy persons (16~65years) including 16 males and 14 females, with mean age of 35.9?.8 years. Both vWF and GMP-140 were got form the vena blood plasma before and 2 weeks after the operation in B-CS group and during the health condition test in control group. The quantity of vWF and GMP-140 was measured with enzyme linked immunosorbent assay. And in B-CS group, the platelet was got from the vena blood and the number was measured with the normal method.
Results:
1. Before operation, the quantity of vWF and GMP-140 was (251.67 118.39)% and 87.92?4.47ng/mL in patients with B-CS, (256.73?124.49)% and 88.60?5.04 ng/mL in thrombus type B-CS, (239.85?03.82)%, and 86.32?6.46 ng/mL in membrane type B-CS, (112.25?6.61), and 24.90?.31 ng/mL in the controls. There was significant difference between B-CS group and control group (P0.01). The different quantity of vWF and GMP-140 between the thrombus type B-CS and the membrane type B-CS was not significant (P>0.05).
2. Before operation, in patients with thrombus type B-CS, the number of platelet was (91 3 4) 109, and there was no significant correlation between the number of platelet and the quantity of vWF and GMP-140 (r=-0.1641 and -0.0369, P>0.05 ) . Therefore it is suggested that the injury of vascular endothelium and stimulation of platelet be the important factor in the formation of B-CS.
3. Two weeks after operation, in patients with thrombus type B-CS, the quantity of vWF and GMP-140 was (248.36+113.43) % and 81.73?7.76ng/mL. There was no significant difference between the pre-operation and post-operation in patients with thrombus type B-CS (P>0.05). Therefore it is suggested that the operation should not change the hypercoagulation in patients with thrombus type B-CS. In patients with membrane type B-CS, the quantity of vWF and GMP-140 was (119.76?7.52) % and 41.33?2.30ng/mL.There was significant difference between the pre-operation and post-operation in patients with membrane type B-CS (P>0.05). Therefore it is suggested that the operation should change the hypercoagulation in patients with membrane type B-CS.
Conclusions:
1. Before operation, the patients with B-CS have higher quantity of vWF and GMP-140 than the controls, which indicate th
郑州大学2004年硕士研究生毕业论文
布一加综合征患者血浆中vWF、GMP一140变化的研究
材料与方法
病材取自于2002年6月至2003年10月在河南省人民医院肝胆胰腺外科住
院的经下腔静脉造影、彩色多普勒超声、手术确诊的B一CS患者60例。其中血
栓型B一CS 42例(男31例，女11例，年龄12一56岁，平均29.6士6.9岁);膜型
B一CS18例(男8例，女10例，年龄26一49，平均犯.6士5.2岁);正常对照组为
同期在河南省人民医院肝胆胰腺外科门诊进行体检的健康人员30例(男16例，
女14例，年龄16一65岁，平均35.9士7.8岁)。B一CS患者于术前和术后2周各
取空腹外周静脉血，正常对照组于空腹体检时取外周静脉血，经抗凝处理，分离
血浆，采用酶联免疫吸附双抗体夹心法(E LlsA)定量测定血浆中vWF、GMP一140
含量;采用临床常规方法检测B一CS患者于术前和术后2周空腹外周静脉血中血
小板计数。
结果
1.术前B一CS患者血浆中vWF含量为(25 1 .67士1 18.39)%、GMP一140含量
为87.92士34.47ng/mL。其中血栓型B一CS组vWF含量为(256.73士124.49)%、
GMP一1 40含量为88.60士25.04ng/mL;膜型B一CS组vWF含量为(239.85士103.82)
%、GMP一1 40含量为86.32士56.46ng/mL;两组间相比均无显著差异(P均>0 .05)，
但二者均显著高于正常对照组(v wF为112.25士86.61%，P均<0 .01; GMP一140
为24.90士9.31ng/mL，P均<0.01)。
2.术前B一CS患者静脉血中血小板计数为(91士34) x 109与静脉血浆中的
vWF、GMP一1 40水平无相关性(r分别为一0.1641及一0.0369，P均>0.05)。
3.术后2周血栓型B一CS患者静脉血浆中vWF含量为(248.36士1 13.43)%、
GMP一1 40含量为8 1 .73士1 7.76ng/mL，与术前相比均无明显差异(P均)0.05);
膜型B一CS患者静脉血浆中vWF含量为(1 1 9.76士87.52)%、GMP一140含量为41.33
士32.30ng/mL，与术前相比均显著降低，有统计学意义(P均<0 .01)。
结论
1.术前B一es病例组vwF、GMP一1 40含量明显高于对照组(P均<0.01)，提示
郑州大学2004年硕士研究生毕业论文
布一加综合征患者血浆中vWF、GMP一140变化的研究
vWF、GMP一140水平升高可能是导致B一CS患者高凝状态的重要因素;血栓型
B一CS、膜型B一CS患者静脉血浆中vWF、GMP一140水平升高，但两组间相比均
无明显差异(P均>0.05)，提示就vWF、GMP- 140升高所致的血液高凝状态，
在两大类B一CS中无明显差异。
2.术前B一CS组血浆中vWF、GMP一140升高水平与静脉血中血小板计数不相
关，(r分别为一0.1641及一0.0369，p均>0.05)，表明B一CS患者血浆中的vwF、
GMP一140升高与血管内皮细胞的损伤和血小板活化程度有关，提示血管内皮细
胞的损伤和血小板活化是形成B一CS的一个重要因素。
3.术后血栓型B一CS组患者血浆中vWF、GMP一140水平与术前相比均无显
著差异(P均>0.05)，表明手术不改变血栓型B一cs的血液高凝状态，术后需抗凝
祛聚治疗;膜型B一CS组患者血浆vWF、GMP一140水平较术前明显降低(P均
<0.01)，说明手术可改变膜型B一CS的血液高凝状态。
Budd-Chiari syndrome (B-CS) refers to posthepatic portal hypertension (PHT) and/or inferior vena cava hypertension caused by obstruction in outlet of major hepatic veins and/or posthepatic inferior vena cava. Though many kinds of causes about B-CS have been reported, they are uncompleted and indefinite. So the investigation of the etiology in B-CS is valuable and important especially to the clinical diagnosis and treatment. In recent years, many physicians have accepted the theory that the B-CS is not inborn but the sequels from the thrombosis. The hypercoagulation of patients with B-CS caused by many different causes, such as hyper-erythropoietin, colony-forming units erythroid and myoloproliferative disorder so on. And during the research of the thrombosis many physicians draw a conclusion that the increased quantity of vWF and GMP-140 is one of the most prevalent factors, which cause vein thrombosis. vWF is the specific molecule symbol of injury vascular endothelium cell and GMP-140 is the specific symbol
of activation and release of platelets. But there have been few reports about the relation between the B-CS and the
increased quantity of vWF and GMP-140 now. To explore the causes of hypercoagulation and give theoretical support in clinical diagnosis and treatment, vWF and GMP-140 in patients with B-CS were investigated in this study.
Materials and methods:
60 patients in B-CS group including 42 patients (12~56years) with thrombus type B-CS (31 males and 11 females with the mean age of 29.6?.9 years), and 18 patients (26~49years) with membrane type B-CS (8 males and 10 females with mean age of 32.6?.2 years) were all diagnosed definitely with Color Doppler sonography and/or inferior vena cavography(IVCG) from June,2002 to Oct 2003 in Henan Provincial People's Hospital. In control group, there were 30 healthy persons (16~65years) including 16 males and 14 females, with mean age of 35.9?.8 years. Both vWF and GMP-140 were got form the vena blood plasma before and 2 weeks after the operation in B-CS group and during the health condition test in control group. The quantity of vWF and GMP-140 was measured with enzyme linked immunosorbent assay. And in B-CS group, the platelet was got from the vena blood and the number was measured with the normal method.
Results:
1. Before operation, the quantity of vWF and GMP-140 was (251.67 118.39)% and 87.92?4.47ng/mL in patients with B-CS, (256.73?124.49)% and 88.60?5.04 ng/mL in thrombus type B-CS, (239.85?03.82)%, and 86.32?6.46 ng/mL in membrane type B-CS, (112.25?6.61), and 24.90?.31 ng/mL in the controls. There was significant difference between B-CS group and control group (P0.01). The different quantity of vWF and GMP-140 between the thrombus type B-CS and the membrane type B-CS was not significant (P>0.05).
2. Before operation, in patients with thrombus type B-CS, the number of platelet was (91 3 4) 109, and there was no significant correlation between the number of platelet and the quantity of vWF and GMP-140 (r=-0.1641 and -0.0369, P>0.05 ) . Therefore it is suggested that the injury of vascular endothelium and stimulation of platelet be the important factor in the formation of B-CS.
3. Two weeks after operation, in patients with thrombus type B-CS, the quantity of vWF and GMP-140 was (248.36+113.43) % and 81.73?7.76ng/mL. There was no significant difference between the pre-operation and post-operation in patients with thrombus type B-CS (P>0.05). Therefore it is suggested that the operation should not change the hypercoagulation in patients with thrombus type B-CS. In patients with membrane type B-CS, the quantity of vWF and GMP-140 was (119.76?7.52) % and 41.33?2.30ng/mL.There was significant difference between the pre-operation and post-operation in patients with membrane type B-CS (P>0.05). Therefore it is suggested that the operation should change the hypercoagulation in patients with membrane type B-CS.
Conclusions:
1. Before operation, the patients with B-CS have higher quantity of vWF and GMP-140 than the controls, which indicate th
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38．刘泽林．静脉血栓栓塞的基础研究与临床实践．血栓与止血学，2001，8(1)：44-48
39. Ouyang Yingchun, Liu Yingcai, Yu Qin, et al. The markers of prothrombotic state in patients with essential hypertension. J Clin Cardiol (China),2002,18(6):248-250
40．王兆钺，阮长耿．血小板的生理功能．见：王振义，李家增，阮长耿，主编．血栓与止血—基础理论与临床．上海：上海科学技术出版社，1996，1(2)：34-60
41. Calvete JJ. Glues for understanding the structure and function of a prototypic human intergin: the platelet glycoprotein Ⅱ b/ Ⅲ a complex. Thrombi Haemost, 1994,72:1-6
42. Herzberg M. Biochemistry of factor X. Blood-Rev, 1994,8(1):56-62
43．王兆钺．血栓与止血研究的进展与趋势—第十八届国际血栓与止血大会简介．中华血液病杂志，2004，25(3)：190-191
44. G Richard Lee, John F, John L, et al. Wintrobe's Clinical Hematology 10ed.Baltimore:Williams and Wilkiness, 1999,1781-1820
45．胡群，王鸿利．肺梗死与血栓．见：王鸿利，王学锋，主编．血栓病临床新技术．北京：人民军医出版社，2003(1)：435-446
46．田建国．布-加综合征．见：杨玉秀，田建国，主编．门静脉高压症．北京：北京科技出版社，1999，1(1)：289-306
47 Wu GX, Xi XD, LI PX, et al. Preparation of a monoclonal antibody SZ-51 that recognizes an α-granule membrane protein (GMP-140) on the surface of activated human plateletso Now Rev Fr Hematol, 1990,32:231-235
48. Dunlop CL, Skinner MP, Bendall LJ, et al. Characterization of GMP-140 (P-selection) as a circulating plasma protein. J Exp Med, 1992,175:1147-1150
49. Abrams CA, Ellison N, Budzynsk AI, et al. Direct detection of activated platelets and platelet-derived microparticles in human. Blood, 1990,75:128-133
50．杜同信，王自正，时宏诊，等．GMP-140与Ⅱ型糖尿病患者微血管病变关系的研究．中华核医学杂志，1995，15(4)：222-224
51．韦旭波，刘伊丽，李进，等．冠心病与风心病和外周血血小板活性的临床意义．实用医学杂志，1998，14(6)：395-396
52．周同，吴佩．细胞粘附分子与血栓形成．见：王鸿利，王学锋，主编．血栓病临床新技术．北京：人民军医出版社，2003，1(1)：67-81
53. Larsen E; Celi A, Gilbert GE, et al. Padgem protein: a receptor that mediate the interaction of activated platelets with neutrophils and monocots.
Cell,1989,59:305-309
54. De Bruijne-Admiraal LG, Modderman PW, von dem Borne AEGKR, et al. P-selection mediates Ca~(2+) dependent adhesion of activated platelets to many different types of leukocytes: detection by flow cytometry. Blood, 1992,80:134-140
55. Packham M. A role of platelet in thrombosis and homeostasis. Can J physiol pharmacol, 1994,72:278-281
56．吴兰鸥．血小板、内皮细胞及白细胞在血栓形成中的作用．昆明医学院学报，2001，21(2)：75-80
57. Isoniemi H, Hockwestedt K, Makisalo H, et al. Liver transplantation in acute liver failure can be as in chronic liver disease. Transplant at Proc, 1995,27:3517-3518
58. Hemming AW, Langer B, Greig P, et al. Treatment of Budd-Chiari syndrome with postsystemic shunt or transplantation. Am J Surg,1996,171:176-181
59．黄志平．Epo，CFUe和LAC与B-CS的关系．国外医学消化系统疾病分册，1993，13：133-135
60. Boughton BJ. Hepatic and portal vein thrombosis is closely associated with chronic myeloproliferation disorder. Balt Med J, 1991,302:192-193
61. Orloff Mj, ,Daily Poand girard B. Treatment of Budd-Chiari syndrome due to inferior vena cava occlusion by combined portal and vena cava decompression. Am J Surg, 1992,163:137-138
62. Bick RI. Sticky platelet syndrome. Clin appl Thromb Hematol, 1998, 4:1-5
63. Mammen EF. Sticky platelet syndrome. Semi Thromb Haemost,1999, 25(4):362-365
64．邹丽芳，杨景文，胡余，等．血小板在下肢深静脉血栓形成中的临床意义．上海第二医科大学学报，1997，17(2)：111-113
65. Dayal S, Pati HP, Panda GK, et al. Platelet ultrastructure study in Budd-Chiari syndrome. Eur J Hae metal, 1995,23(4):294-301
66．吴克俭，祝惠民，祖茂衡．Budd-Chiari综合征患者血小板超微结构与形态计量学改变．徐州医学院学报，2000，20(4)：269-271
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35．王淑娟．血栓前状态的实验诊断进展．中华医学检验杂志，1995，18(2)：108-110
36. Ruggeri ZM. Old concepts and new developments in the study of platelet aggregation. J Clin Invest,2000,105:699-701
37．丁起贤，孙志，李淑兰，等．vWF、Fn检测在正常妊娠及妊高症患者的临床应用．白求恩医科大学学报，1993，19(1)：107-108
38．刘泽林．静脉血栓栓塞的基础研究与临床实践．血栓与止血学，2001，8(1)：44-48
39. Ouyang Yingchun, Liu Yingcai, Yu Qin, et al. The markers of prothrombotic state in patients with essential hypertension. J Clin Cardiol (China),2002,18(6):248-250
40．王兆钺，阮长耿．血小板的生理功能．见：王振义，李家增，阮长耿，主编．血栓与止血—基础理论与临床．上海：上海科学技术出版社，1996，1(2)：34-60
41. Calvete JJ. Glues for understanding the structure and function of a prototypic human intergin: the platelet glycoprotein Ⅱ b/ Ⅲ a complex. Thrombi Haemost, 1994,72:1-6
42. Herzberg M. Biochemistry of factor X. Blood-Rev, 1994,8(1):56-62
43．王兆钺．血栓与止血研究的进展与趋势—第十八届国际血栓与止血大会简介．中华血液病杂志，2004，25(3)：190-191
44. G Richard Lee, John F, John L, et al. Wintrobe's Clinical Hematology 10ed.Baltimore:Williams and Wilkiness, 1999,1781-1820
45．胡群，王鸿利．肺梗死与血栓．见：王鸿利，王学锋，主编．血栓病临床新技术．北京：人民军医出版社，2003(1)：435-446
46．田建国．布-加综合征．见：杨玉秀，田建国，主编．门静脉高压症．北京：北京科技出版社，1999，1(1)：289-306
47 Wu GX, Xi XD, LI PX, et al. Preparation of a monoclonal antibody SZ-51 that recognizes an α-granule membrane protein (GMP-140) on the surface of activated human plateletso Now Rev Fr Hematol, 1990,32:231-235
48. Dunlop CL, Skinner MP, Bendall LJ, et al. Characterization of GMP-140 (P-selection) as a circulating plasma protein. J Exp Med, 1992,175:1147-1150
49. Abrams CA, Ellison N, Budzynsk AI, et al. Direct detection of activated platelets and platelet-derived microparticles in human. Blood, 1990,75:128-133
50．杜同信，王自正，时宏诊，等．GMP-140与Ⅱ型糖尿病患者微血管病变关系的研究．中华核医学杂志，1995，15(4)：222-224
51．韦旭波，刘伊丽，李进，等．冠心病与风心病和外周血血小板活性的临床意义．实用医学杂志，1998，14(6)：395-396
52．周同，吴佩．细胞粘附分子与血栓形成．见：王鸿利，王学锋，主编．血栓病临床新技术．北京：人民军医出版社，2003，1(1)：67-81
53. Larsen E; Celi A, Gilbert GE, et al. Padgem protein: a receptor that mediate the interaction of activated platelets with neutrophils and monocots.
Cell,1989,59:305-309
54. De Bruijne-Admiraal LG, Modderman PW, von dem Borne AEGKR, et al. P-selection mediates Ca~(2+) dependent adhesion of activated platelets to many different types of leukocytes: detection by flow cytometry. Blood, 1992,80:134-140
55. Packham M. A role of platelet in thrombosis and homeostasis. Can J physiol pharmacol, 1994,72:278-281
56．吴兰鸥．血小板、内皮细胞及白细胞在血栓形成中的作用．昆明医学院学报，2001，21(2)：75-80
57. Isoniemi H, Hockwestedt K, Makisalo H, et al. Liver transplantation in acute liver failure can be as in chronic liver disease. Transplant at Proc, 1995,27:3517-3518
58. Hemming AW, Langer B, Greig P, et al. Treatment of Budd-Chiari syndrome with postsystemic shunt or transplantation. Am J Surg,1996,171:176-181
59．黄志平．Epo，CFUe和LAC与B-CS的关系．国外医学消化系统疾病分册，1993，13：133-135
60. Boughton BJ. Hepatic and portal vein thrombosis is closely associated with chronic myeloproliferation disorder. Balt Med J, 1991,302:192-193
61. Orloff Mj, ,Daily Poand girard B. Treatment of Budd-Chiari syndrome due to inferior vena cava occlusion by combined portal and vena cava decompression. Am J Surg, 1992,163:137-138
62. Bick RI. Sticky platelet syndrome. Clin appl Thromb Hematol, 1998, 4:1-5
63. Mammen EF. Sticky platelet syndrome. Semi Thromb Haemost,1999, 25(4):362-365
64．邹丽芳，杨景文，胡余，等．血小板在下肢深静脉血栓形成中的临床意义．上海第二医科大学学报，1997，17(2)：111-113
65. Dayal S, Pati HP, Panda GK, et al. Platelet ultrastructure study in Budd-Chiari syndrome. Eur J Hae metal, 1995,23(4):294-301
66．吴克俭，祝惠民，祖茂衡．Budd-Chiari综合征患者血小板超微结构与形态计量学改变．徐州医学院学报，2000，20(4)：269-271