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Portal vein thrombosis and prothrombotic disorders

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY 1999年第11期14卷 1051-1052页

作者： Valla, DC Hop Beaujon Serv Hepatol Paris France

Editorial. Comments on several cases of portal vein thrombosis. Cause of acute abdominal pain; Clinical features of portal vein thrombosis; Association of portal vein thrombosis with prothrombotic disorder.

关键词：急腹症/病因学抗凝药/投药和剂量诊断鉴别用药计划表门静脉蛋白质C缺乏/诊断蛋白质C缺乏/药物疗法蛋白质C缺乏/遗传学血栓形成倾向/诊断血栓形成倾向/药物疗法血栓形成倾向/遗传学血栓形成/诊断血栓形成/药物疗法血栓形成/遗传学成年人人类男(雄)性

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Prothrombotic genetic risk factors in young survivors of myocardial infarction

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BLOOD 1999年第1期94卷 46-51页

作者： Ardissino, D Mannucci, PM Merlini, PA Duca, F Fetiveau, R Tagliabue, L Tubaro, M Galvani, M Ottani, F Ferrario, M Corral, J Margaglione, M Univ Milan A Bianchi Bonomi Hemophilia & Thrombosis Ctr I-20122 Milan Italy Policlin San Matteo IRCCS Div Cardiol Pavia Italy Univ Milan Maggiore Hosp IRCCS Dept Internal Med I-20122 Milan Italy Niguarda Hosp Ca Granda Milan Italy San Camillo Hosp Rome Italy Gian Battista Morgagni Hosp Forli Italy Bentivoglio Hosp Bentivoglio Italy Reg Transfus Ctr Murcia Spain Casa Sollievo della Sofferenza IRCCS San Giovanni Rotondo Italy

It has long been thought that an individual thrombotic tendency increases the risk of myocardial infarction, especially in young adults. Several "prothrombotic" genetic factors that may influence the individual thrombotic risk have been identified. To investigate the association between the risk of myocardial infarction at a young age and genetic factors thought to be associated with an increased tendency to thrombosis (the polymorphisms 4G/5G of the PAI-1 gene, PIA1/PIA2 of the platelet glycoprotein IIIa, C3550T of the platelet glycoprotein Ib gene, G10976A of the factor VII gene, C677T of the methylenetetrahydrofolate reductase gene, G1691A of the factor V gene, and G20210A of the prothrombin gene), we performed a case-control study evaluating 200 survivors (185 men, 15 women) of myocardial infarction who had experienced the event before the age of 45 years and 200 healthy subjects with a negative exercise test, individually matched for sex, age, and geographic origin with the cases. The presence of the PIA2 polymorphic allele was the only prothrombotic genetic factor associated with the risk of myocardial infarction at a young age. The odds ratio for carriers of the PIA2 allele compared with those of the PIA1 allele was 1.84 (95% confidence intervals (CI) 1.12 to 3.03). There was a significant interaction between the presence of the PIA2 allele and smoking: with their simultaneous presence, 46% (95% confidence intervals 11% to 81%) of premature myocardial infarctions were attributable to the interaction between the two factors. In conclusion, carrying the PIA2 polymorphic allele of platelet glycoprotein IIIa was the only genetic prothrombotic factor associated with the risk of developing myocardial infarction at a young age. The clinical expression of this genetic predisposition seems to be enhanced by smoking. (C) 1999 by The American Society of Hematology.

关键词：等位基因抗原 CD/遗传学病例对照研究因子Ⅴ/遗传学因子Ⅶ/遗传学整合素β3 亚甲基四氢叶酸还原酶(NADPH) 心肌梗死/病因学心肌梗死/遗传学作用于CH-NH族供体的氧化还原酶类/遗传学纤溶酶原激活物抑制物1/遗传学血小板糖蛋白GPⅠb-Ⅸ复合物/遗传学血小板膜糖蛋白类/遗传学多态现象遗传凝血酶原/遗传学危险因素血栓形成/病因学血栓形成/遗传学成年人女(雌)性人类男(雄)性

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Genetic variation in the apolipoprotein H (β2-glycoprotein I) gene affects plasma apolipoprotein H concentrations

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HUMAN GENETICS 1999年第1-2期105卷 63-71页

作者： Mehdi, H Aston, CE Sanghera, DK Hamman, RF Kamboh, MI Univ Pittsburgh Grad Sch Publ Hlth Dept Human Genet Pittsburgh PA 15261 USA Univ Colorado Hlth Sci Ctr Dept Prevent Med & Biometr Denver CO 80262 USA

Apolipoprotein H (apoH, protein;APOH, gene) is a single chain glycoprotein that exists in plasma both in a free form and in combination with lipoprotein particles. ApoH has been implicated in several physiologic pathways, including lipid metabolism, coagulation, and the production of antiphospholipid antibodies. The wide range of interindividual variation in plasma apoH levels is thought to be under genetic control, but its molecular basis is unknown. APOH displays a common structural polymorphism with the occurrence of three common alleles (APOH*1, APOH*2, and APOH*3), the APOH*2 allele being the most frequent in all populations. The relationship between the APOH polymorphism and plasma apoH levels is unknown. In this study, we have determined the impact of this APOH polymorphism on apoH levels in 455 normoglycemic non-Hispanic Whites (220 men and 235 women) from the San Luis Valley, Colorado. Mean plasma apoH levels, determined by capture enzyme-linked immunosorbent assay, were 20.0 +/- 0.2 mg/dl (range: 3.4-31.2 mg/dl) with no significant difference between men and women. In women, but not in men, age had a significant effect on plasma apoH levels explaining 3.4% of its phenotypic variance. ApoH levels also correlated positively with cholesterol (P = 0.015), HDL-cholesterol (P = 0.044), and triglyceride (P = 0.037) in women, but not in men. An analysis of variance (ANOVA) of adjusted plasma apoH levels showed significant association with the APOH polymorphism in both men and women (P < 0.0001), and the APOH polymorphism accounted for 11.4% and 13.6% of the variation in apoH levels in men and women, respectively. Compared with the APOH*1 and APOH*2 alleles, the APOH*3 allele was associated with significantly lower plasma apoH levels. At the molecular level, APOH*3 can be further subdivided into two distinct forms, called APOH*3(W) and APOH*3(B). The APOH*3(W) form is more common in US Whites and is the result of a missense mutation at codon 316. An ANOVA for the c

关键词：心磷脂质类/遗传学胆固醇 HDL/遗传学密码子科罗拉多欧洲大陆世系人群/遗传学遗传变异基因型糖蛋白类/血液糖蛋白类/遗传学脂蛋白类 HDL/遗传学多态现象遗传性别因素血栓形成/遗传学 β2糖蛋白Ⅰ 成年人老年人女(雌)性人类男(雄)性中年人

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POSSIBILITIES OF DNA ANALYSIS FOR THE DETECTION OF PREDISPOSITION TO THROMBOTIC DISEASE

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ANNALS OF THE NEW YORK ACADEMY OF SCIENCES 1992年第1期667卷 332-342页

作者： THOMAS, AE GREEN, FR DAWSON, SJ LANE, A HENNEY, AM KELLEHER, CH WILKES, HC BRENNAN, PJ CRUICKSHANK, JK HAMSTEN, A WIMAN, B MEADE, TW HUMPHRIES, SE NATL UNIV IRELAND UNIV COLL GALWAY DEPT HLTH PROMOTGALWAYIRELAND ST BARTHOLOMEWS HOSP COLL MEDWOLFSON INST PREVENT MEDMRCEPIDEMIOL & MED CARE UNITLONDON EC1M 6BQENGLAND UNIV MANCHESTER DEPT PUBL HLTH & EPIDEMIOLMANCHESTER M13 9PTLANCSENGLAND KAROLINSKA HOSP DEPT INTERNAL MEDS-10401 STOCKHOLM 60SWEDEN KING GUSTAF V RES INST STOCKHOLMSWEDEN KAROLINSKA HOSP DEPT CLIN CHEMS-10401 STOCKHOLM 60SWEDEN

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Prothrombin and the prothrombin 20210 G to A polymorphism: their relationship with hypercoagulability and thrombosis

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BLOOD REVIEWS 1999年第4期13卷 205-210页

作者： Girolami, A Simioni, P Scarano, L Carraro, G Inst Med Semeiot I-35100 Padua Italy Univ Padua Sch Med Dept Med & Surg Sci 2nd Chair Med Padua Italy

Polymorphisms of several clotting factors have been associated during the past few years with an increased risk of both venous or arterial thrombosis. However, final proof for the existence of a pathogenetic relationship between a given polymorphism and an increased risk for thrombosis is still lacking. Particular emphasis has been placed recently on a 20210 G to A prothrombin polymorphism. A critical review of available data indicates that such an abnormality may be associated with an increased risk of venous thrombosis but not arterial thrombosis (with a possible exception for myocardial infarction). However, this conclusion is based only on retrospective cohort studies which compared the prevalence of the abnormality in a group of patients with past venous or arterial thrombosis with a normal group (with no thrombosis). No prospective study has yet to show that patients with the abnormality, given similar additional acquired risk factors, have a higher incidence of thrombotic complications as compared with controls. The mechanism whereby the abnormality might cause thrombosis has been assumed to be an increase in prothrombin levels. Since an association between two phenomena does not necessarily mean that a causal relationship exists between the same events, it is important to be cautious before claiming that such abnormality is responsible for thrombosis. Therefore, although included commonly in the investigation profile, the search for the 20210 G to A prothrombin abnormality should not be considered yet to be an essential component in the routine study of hypercoagulable and/or thrombotic conditions. (C) 1999 Harcourt Publishers Ltd.

关键词： 3'非翻译区/血液点突变多态性单核苷酸凝血酶原/遗传学血栓形成倾向/血液血栓形成倾向/遗传学血栓形成/血液血栓形成/遗传学女(雌)性人类男(雄)性

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PLATELET ANTI-THROMBIN DEFICIENCY - NEW CLINICAL ENTITY

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AMERICAN JOURNAL OF MEDICINE 1978年第3期65卷 472-478页

作者： TULLIS, JL WATANABE, K NEW ENGLAND DEACONESS HOSP DEPT MED BOSTON MA 02215 USA HARVARD UNIV SCH MED BOSTON MA 02115 USA CTR BLOOD RES BOSTON MA USA

A kindred with a history of multiple thromboses was studied for coagulant abnormalities. A deficiency of serum antithrombin III was found in approximately 1/2 of the 13 family members by coagulant or immunologic assay. No clear relationship between antithrombin III deficiency and a history of thrombosis was present. Platelet antithrombin assays were also studied in the same subjects. Ten of the 13 members were deficient. None of the remaining 3 had a history of thrombosis. The hypothesis is proposed that in some cases familial hypercoagulability may be due to a platelet antithrombin deficiency and that the serum antithrombin III deficiency in some cases is a secondary rather than a primary effect.

关键词：抗凝药/药理学抗凝血酶Ⅲ/分析抗凝血酶类/分析血液凝固试验血小板疾病/遗传学血样采集免疫扩散方法血栓形成/血液血栓形成/遗传学青少年成年人老年人女(雌)性人类男(雄)性中年人

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Prevalence of prothrombin G20210A, factor V G1691A (Leiden), and methylenetetrahydrofolate reductase (MTHFR) C677T in seven different populations determined by multiplex allele-specific PCR

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THROMBOSIS AND HAEMOSTASIS 1999年第5期81卷 733-738页

作者： Hessner, MJ Luhm, RA Pearson, SL Endean, DJ Friedman, KD Montgomery, RR Blood Ctr SE Wisconsin Inc Diagnost Lab Milwaukee WI 53233 USA

Individuals belonging to six racial groups (African American, Asian Indian, Caucasian, Hispanic, Korean, Native American), and a seventh group comprised of referred patients with thrombosis were genotyped for the prothrombin G20210A mutation, the factor V G1691A (Leiden) mutation, and the methylenetetrahydrofolate reductase (MTHER) C677T mutation by multiplexed allele-specific PCR. The prothrombin 20210A and factor V 1691A allele frequencies in the thrombosis patients, 3.2% and 9.5%, were significantly higher than those in the random Caucasians, 1.3% and 1.8%, (p = 0.043 and p <0.001, respectively). The relative risk of venous thrombosis was determined to be 2.4-fold for carriers of the prothrombin 20210A allele (odds ratio = 2.54;95% confidence interval = 0.94, 6.82) and 4.5-fold for carriers of the factor V 1691A allele (odds ratio = 5.06;95% confidence interval = 2.25, 11.36). Among the seven populations, significant differences were observed in the MTHFR 677T allele distribution, however this mutation was not determined to be a risk factor for venous thrombosis in the patient group studied, either alone or in combination with the prothrombin 20210A and/or the factor V 1691A allele(s).

关键词：等位基因大陆人口群因子Ⅴ/遗传学亚甲基四氢叶酸还原酶(NADPH) 突变作用于CH-NH族供体的氧化还原酶类/遗传学聚合酶链反应/方法凝血酶原/遗传学危险因素血栓形成/遗传学人类

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Prothrombin G20210A polymorphism and thrombophilia

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MAYO CLINIC PROCEEDINGS 2000年第6期75卷 595-604页

作者： Nguyen, A Univ Texas SW Med Sch Dept Internal Med Dallas TX 75235 USA

Recently, a single mutation in the 3'-untranslated region of the prothrombin gene was reported, resulting in a G-to-A substitution. This finding added to the growing list of genetic disorders thought to be responsible for familial thrombophilia, Although most studies generally agree about the increased risk of venous thrombosis in individuals carrying this mutation, its role in the first event of venous thromboembolism and in recurrent events is unclear, Even less clear is the role this mutation has in the formation of arterial thrombosis (including coronary artery disease and cerebral ischemia) due to contradicting results of studies. This mutation has important clinical implications since it is a common cause of genetic thrombophilia, second only to the factor V Leiden mutation. However, the mutation by itself may not be enough to trigger disease because thromboembolic disease is now generally accepted as a multifactorial disorder. Careful evaluation of this mutation will augment the clinician's ability to stratify systematically an individual's risk of developing spontaneous thrombosis.

关键词：腺苷/遗传学非洲/流行病学非洲大陆世系人群/遗传学亚洲/流行病学亚洲大陆世系人群/遗传学脑缺血/遗传学巴西/流行病学冠心病/遗传学欧洲/流行病学欧洲大陆世系人群/遗传学因子Ⅴ/遗传学基因检测鸟苷/遗传学纯合子点突变多态现象遗传患病率凝血酶原/遗传学危险因素血栓形成倾向/流行病学血栓形成倾向/遗传学血栓形成/遗传学美国/流行病学人类

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Plasminogen activator inhibitor-1 and vitronectin promote vascular thrombosis in mice

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BLOOD 2000年第2期95卷 577-580页

作者： Eitzman, DT Westrick, RJ Nabel, EG Ginsburg, D Univ Michigan Med Ctr Cardiovasc Res Ctr Ann Arbor MI 48109 USA Univ Michigan Med Ctr Dept Internal Med Div Mol Med & Human Genet Ann Arbor MI 48109 USA Univ Michigan Med Ctr Howard Hughes Med Inst Ann Arbor MI 48109 USA

Occlusive thrombosis depends on the net balance between platelets, coagulation, and fibrinolytic factors. Epidemiologic information suggests that plasminogen activator inhibitor-1 (PAI-1), a central regulator of the fibrinolytic system, plays an important role in determining the overall risk for clinically significant vascular thrombosis. Vitronectin (VN), an abundant plasma and matrix glycoprotein, binds PAI-1 and stabilizes its active conformation. This study assessed the role of PAI-1 and VN expression in the formation of occlusive vascular thrombosis following arterial or venous injury. The common carotid arteries of 17 wild-type (WT) mice and 8 mice deficient in PAI-1 were injured photochemically while blood flow was continuously monitored. WT mice developed occlusive thrombi at 52.0 +/- 3.8 minutes (mean +/- SEM) following injury;mice deficient in PAI-1 developed occlusive thrombosis at 127 +/- 15 minutes (P <.0001). Mice deficient in VN (n = 12) developed vascular occlusion 77 +/- 11 minutes after injury, intermediate between the values observed for WT mice (P <.03) and mice deficient in PAI-1 (P <.01). PAI-1 and VN also affected the time to occlusion after injury to the jugular vein. Three WT mice developed occlusive venous thrombosis an average of 39.7 +/- 1 minutes following the onset of injury, whereas the jugular veins of 4 mice deficient in PAI-1 and 4 deficient in VN occluded 56.7 +/- 5 and 58.7 +/- 2 minutes, respectively, following injury (P <.04 and P <.01 compared to WT mice). These results suggest that endogenous fibrinolysis acid its regulation by PAI-1 and VN have important roles in the development of occlusive vascular thrombosis after vascular injury.

关键词：颈动脉狭窄/血液颈动脉狭窄/遗传学颈动脉狭窄/病理生理学颈静脉小鼠近交C57BL 小鼠基因敲除纤溶酶原激活物抑制物1/缺乏纤溶酶原激活物抑制物1/遗传学纤溶酶原激活物抑制物1/生理学血栓形成/血液血栓形成/遗传学血栓形成/病理生理学静脉血栓形成/血液静脉血栓形成/遗传学静脉血栓形成/病理生理学玻连蛋白/缺乏玻连蛋白/遗传学玻连蛋白/生理学动物男(雄)性小鼠

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Evaluation of the Roche diagnostics LightCycler-factor V Leiden mutation detection kit and the LightCycler-prothrombin mutation detection kit

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CLINICAL BIOCHEMISTRY 2000年第3期33卷 213-216页

作者： Nauck, M März, W Wieland, H Univ Hosp Dept Clin Chem Freiburg Germany

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