DEFICIENCIES OF COAGULATION-INHIBITING AND FIBRINOLYTIC PROTEINS IN OUTPATIENTS WITH DEEP-VEIN THROMBOSIS

DEFICIENCIES OF COAGULATION-INHIBITING AND FIBRINOLYTIC PROTEINS IN OUTPATIENTS WITH DEEP-VEIN THROMBOSIS
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DOI:
10.1056/nejm199011293232202
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发表时间:
1990-11-29
影响因子:
158.5
通讯作者:
TENCATE, JW
TENCATE, JW
中科院分区:
医学1区
文献类型:
--
作者:
HEIJBOER, H;BRANDJES, DPM;TENCATE, JW

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背景:单独缺乏抗凝血酶III、蛋白C、蛋白S和纤溶酶原已被认为是深静脉血栓形成的原因之一。据推测,复发性、家族性或青少年血栓患者很可能有这种缺陷。方法:我们研究了277例经静脉造影证实急性深静脉血栓形成的连续门诊患者中孤立性缺乏这些蛋白的患病率,并与138例年龄匹配和性别匹配的无深静脉血栓形成的对照组进行了比较,并计算了复发性、家族性或青少年性静脉血栓栓塞史对这种缺乏的阳性预测值。结果:静脉血栓患者中任何一种蛋白质缺乏的总体发生率为8.3%(277例患者中的23例)(95%置信区间,5.4至12.4),而对照组(138例受试者中的3例)为2.2%(95%置信区间,0.5至6.1;组间比较P < 0.05)。复发性、家族性或青少年性深静脉血栓患者存在分离性蛋白缺乏的阳性预测值分别为9%、16%和12%,定义为临床发现有一种或多种蛋白缺乏的患者比例。结论:绝大多数(91.7%)门诊患者急性静脉血栓形成的原因不能用凝血抑制蛋白和纤溶蛋白异常来解释。从病史中获得的关于复发性或家族性静脉血栓形成的信息或在年轻时发病的信息对识别蛋白质缺乏症患者没有用处。
Background: Isolated deficiencies of antithrombin III, protein C, protein S, and plasminogen have been implicated as a cause of deep-vein thrombosis. It is assumed that patients with recurrent, familial, or juvenile thrombosis are very likely to have such a deficiency. Methods: We studied the prevalence of isolated deficiencies of these proteins in 277 consecutive outpatients with venographically proved acute deep-vein thrombosis, as compared with 138 age-matched and sex-matched controls without deep-vein thrombosis, and calculated the positive predictive value of a history of recurrent, familial, or juvenile venous thromboembolism for the presence of such a deficiency. Results: The overall prevalence of deficiencies of any of these proteins in the patients with venous thrombosis was 8.3 percent (23 of 277 patients) (95 percent confidence interval, 5.4 to 12.4), as compared with 2.2 percent in the controls (3 of 138 subjects) (95 percent confidence interval, 0.5 to 6.1; P < 0.05 for the comparison between groups). The positive predictive values for the presence of an isolated protein deficiency in patients with recurrent, familial, or juvenile deep-vein thrombosis, defined as the proportion of patients with the clinical finding who had a deficiency of one or more of the proteins, were 9, 16, and 12 percent, respectively. Conclusions: The cause of acute venous thrombosis in most outpatients (91.7 percent) cannot be explained by abnormalities of coagulation-inhibiting and fibrinolytic proteins. The information obtained from the medical history concerning recurrent or familial venous thrombosis or the onset of the disease at a young age is not useful for the identification of patients with protein deficiencies.