脂蛋白(a)升高与静脉血栓栓塞症之间的关联：一项系统评价与荟萃分析。
完整摘要 · 中文译文
背景：脂蛋白(a)[Lp(a)]升高是公认的心血管危险因素，与动脉粥样硬化形成、炎症和血栓形成相关；然而，其与静脉血栓栓塞症（VTE）的关联仍不确定，各项观察性研究的结果并不一致。 目的：系统评价Lp(a)水平升高与VTE风险之间的关联，并探讨不同研究设计间的差异。 方法：检索PubMed/MEDLINE、Embase、Scopus、Web of Science和Cochrane Library自建库至2026年1月期间评估Lp(a)与VTE的观察性研究。采用DerSimonian-Laird随机效应模型并结合Hartung-Knapp校正合并效应估计值（比值比[OR]或风险比[HR]）。采用I2和τ2评估异质性。采用ROBINS-E评估偏倚风险，采用漏斗图、Egger检验和Begg检验评估发表偏倚，并采用GRADE评估证据确定性。主要结局为VTE；次要结局包括深静脉血栓形成（DVT）、肺栓塞（PE）和复发性VTE。 结果：共纳入11项研究（6项病例对照研究、5项队列研究；63,325名参与者；3,581例VTE事件）。Lp(a)升高与VTE风险呈边缘性升高相关（合并OR/HR 1.34 [95% CI 1.00-1.80]；P = 0.049），异质性高（I2 = 77.8%），预测区间宽（0.56-3.21）。在分层分析中，病例对照研究显示存在显著关联（OR 1.88 [1.25-2.81]；I2 = 57.2%），而队列研究未显示关联（HR 0.99 [0.85-1.15]；I2 = 0%），组间差异显著（p < 0.0001）。 结论：脂蛋白(a)（Lp(a)）升高与静脉血栓栓塞症（VTE）之间的关联似乎仅限于病例对照研究，而未得到前瞻性队列数据的支持，提示可能存在偏倚或残余混杂。有必要进一步开展大规模研究和遗传学研究以阐明这一关系。
完整摘要 · 英文原文
BACKGROUND: Elevated lipoprotein(a) [Lp(a)] is an established cardiovascular risk factor linked to atherogenesis, inflammation, and thrombosis; however, its association with venous thromboembolism (VTE) remains uncertain, with inconsistent findings across observational studies. AIMS: To systematically evaluate the association between elevated Lp(a) levels and VTE risk and to examine differences by study design. METHODS: PubMed/MEDLINE, Embase, Scopus, Web of Science, and Cochrane Library were searched from inception through January 2026 for observational studies assessing Lp(a) and VTE. Effect estimates (odds ratios [ORs] or hazard ratios [HRs]) were pooled using DerSimonian-Laird random-effects models with Hartung-Knapp adjustment. Heterogeneity was assessed using I2 and τ2. Risk of bias was evaluated with ROBINS-E, publication bias with funnel plots, Egger's and Begg's tests, and certainty of evidence using GRADE. The primary outcome was VTE; secondary outcomes included deep vein thrombosis (DVT), pulmonary embolism (PE), and recurrent VTE. RESULTS: Eleven studies (6 case-control, 5 cohort; 63,325 participants; 3581 VTE events) were included. Elevated Lp(a) was associated with a borderline increased VTE risk (pooled OR/HR 1.34 [95% CI 1.00-1.80]; P = 0.049), with high heterogeneity (I2 = 77.8%) and a wide prediction interval (0.56-3.21). In stratified analyses, case-control studies showed a significant association (OR 1.88 [1.25-2.81]; I2 = 57.2%), whereas cohort studies showed no association (HR 0.99 [0.85-1.15]; I2 = 0%), with significant between-group differences (p < 0.0001). CONCLUSIONS: The association between elevated Lp(a) and VTE appears limited to case-control studies and is not supported by prospective cohort data, suggesting potential bias or residual confounding. Further large-scale and genetic studies are warranted to clarify this relationship.