遗传性血栓病的临床和实验室问题。

Haemostasis Pub Date : 1999-01-01 DOI:10.1159/000022491
M Samama, G Gerotziafas, J Conard, M Horellou, I Elalamy
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引用次数: 18

摘要

遗传性血栓病是一种单基因或多基因的多因子疾病,其临床表现与异质表达有关。因子V (FV) Leiden和FII基因突变比抗凝血酶、蛋白C和S缺乏更为频繁。所有的血栓患者都不一样。杂合子携带FV Leiden或FII基因突变者静脉血栓形成风险较低。前者的平均发病年龄较大,后者的复发率较高。突变的共分离显著增加了血栓形成的风险。这两种突变都具有与基因奠基者效应相关的地理和种族分布。临床表现为深静脉或浅静脉血栓形成,伴或不伴肺栓塞,异常部位血栓形成(如脑、门静脉、肠系膜)或胎儿丢失和流产发生率增加。在50%以上的患者中存在沉淀原因。动脉血栓形成的风险似乎仅限于某些蛋白S和FII基因突变。实验室诊断策略应以仔细选择患者为导向,并应考虑分析前变量。其他未确定的基因突变极有可能是遗传性血栓病异质表达的其他原因,至少是部分原因。
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Clinical aspects and laboratory problems in hereditary thrombophilia.

Hereditary thrombophilia is a multifactorial disease which is mono- or plurigenic and its clinical expression is associated with a heterogeneous expression. Factor V (FV) Leiden and FII gene mutations are more frequent than antithrombin, and protein C and S deficiencies. All thrombophilias are not the same. Heterozygous carriers of FV Leiden or FII gene mutation have a weaker risk of venous thrombosis. The mean age at the first episode is older in the former and higher rate of recurrences is observed in the latter. The cosegregation of mutations significantly increases the risk of thrombosis. Both mutations have a geographic and ethnic distribution in relation with a gene founder effect. Clinical expression consists of deep or superficial venous thrombosis with or without pulmonary embolism, thromboses at unusual sites (e.g. cerebral, portal, mesenteric) or with an increased incidence of fetal loss and abortion. A precipitating cause is present in more than 50% of patients. The risk pf arterial thromboses seems to be restricted to some protein S and FII gene mutations. Laboratory diagnosis strategy should be oriented by careful selection of patients and preanalytical variables should be considered. It is highly probable that other unindentified gene mutations are, at least partly, other causes of the heterogeneous expression of hereditary thrombophilia.

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