Lippi G, Bassi A, Brocco G, Manzato F, Marini M, Guidi G
Istituto di Chimica e Microscopia Clinica, Università degli Studi di Verona, Italy.
Haematologica. 1999 Aug;84(8):726-9.
Lipoprotein(a) is an LDL-like particle displaying strong athero-thrombotic properties. Although Lp(a) plays a pivotal role in the genesis and progression of thrombosis in the arterial district, its role in promoting thrombosis in the venous district is still unclear.
To give further insight into the thrombotic potential of Lp(a), 100 potentially eligible consecutive outpatients who had suffered from previous episodes of venous thrombosis (deep vein thrombosis with or without pulmonary embolism) were enrolled into the study. Thirty-six of these patients who did not fulfil the entry criteria were then excluded from the study. The concentration of Lp(a) was thus measured in 64 patients, and compared to that of 64 control subjects, matched for sex (p=0.46), age (p=0.25) and pharmacological treatment; no subject belonging to the control group had a familial or personal history of venous thromboembolism. Exclusion criteria for both groups included: diabetes mellitus, liver or kidney diseases and malignancy, as established by both laboratory analysis and physical examination. To rule out false elevations of Lp(a) due to the presence of a concurrent acute phase response, C reactive protein (CRP) was measured in both groups using a commercial immunonephelometric assay.
No statistically significant differences were observed in the median Lp(a) concentration between patients and controls (median: 69 vs 83 mg/L, respectively; p=0.34). Neither were any significant differences found between patients who had suffered from deep venous thrombosis with (n=18) or without (n=46) pulmonary embolism (median: 73 vs 69 mg/L, respectively; p=0. 83). The concentration of CRP did not differ significantly between cases and controls (median: 1.8 vs 2.3 g/L, respectively; p=0.37).
Although there are several plausible biological mechanisms to explain the strong thrombogenicity of Lp(a) in vitro, we failed to demonstrate a convincing association between Lp(a) and thrombosis in the venous district. Besides the proven prothrombotic role of Lp(a) in some selected clinical settings, it is thus conceivable that the contribution of Lp(a) to genesis and progression of the venous thrombosis might be marginal or efficiently counterbalanced in vivo. The clinical usefulness of including the measurement of Lp(a) among the screening tests for thrombophilic patients, therefore, remains questionable.
脂蛋白(a)是一种具有强烈动脉粥样硬化血栓形成特性的低密度脂蛋白样颗粒。尽管脂蛋白(a)在动脉区域血栓形成的发生和发展中起关键作用，但其在促进静脉区域血栓形成中的作用仍不清楚。
为进一步深入了解脂蛋白(a)的血栓形成潜能，本研究纳入了100例有静脉血栓形成（有或无肺栓塞的深静脉血栓形成）既往发作史的潜在合格连续门诊患者。其中36例不符合纳入标准的患者随后被排除在研究之外。因此，对64例患者的脂蛋白(a)浓度进行了测量，并与64例性别匹配（p=0.46）、年龄匹配（p=0.25）和药物治疗匹配的对照受试者进行比较；对照组中无受试者有静脉血栓栓塞的家族史或个人史。两组的排除标准包括：经实验室分析和体格检查确定的糖尿病、肝脏或肾脏疾病以及恶性肿瘤。为排除由于同时存在急性期反应导致的脂蛋白(a)假性升高，使用商业免疫比浊法在两组中测量C反应蛋白(CRP)。
患者和对照组之间脂蛋白(a)浓度中位数无统计学显著差异（中位数分别为69和83mg/L；p=0.34）。有肺栓塞（n=18）或无肺栓塞（n=46）的深静脉血栓形成患者之间也未发现显著差异（中位数分别为73和69mg/L；p=0.83）。病例组和对照组之间CRP浓度无显著差异（中位数分别为1.8和2.3mg/L；p=0.37）。
尽管有几种合理的生物学机制可解释脂蛋白(a)在体外的强血栓形成性，但我们未能证明脂蛋白(a)与静脉区域血栓形成之间有令人信服的关联。除了在某些特定临床环境中已证实的脂蛋白(a)的促血栓形成作用外，因此可以想象，脂蛋白(a)对静脉血栓形成的发生和发展的贡献可能很小，或者在体内被有效抵消。因此，在血栓形成倾向患者的筛查试验中纳入脂蛋白(a)测量的临床实用性仍然值得怀疑。
