Camilleri Eleonora, van Rein Nienke, van Vlijmen Bart J M, Biedermann Joseph S, Kruip Marieke J H A, Leebeek Frank W, van der Meer Felix J, Cobbaert Christa M, Cannegieter Suzanne C, Lijfering Willem M
Department of Clinical Epidemiology, Leiden University Medical Center, Leiden, the Netherlands.
Department of Pharmacy, Leiden University Medical Center, Leiden, the Netherlands.
Res Pract Thromb Haemost. 2023 Feb 3;7(2):100063. doi: 10.1016/j.rpth.2023.100063. eCollection 2023 Feb.
The STAtins Reduce Thrombophilia trial showed that, in patients with prior venous thrombosis, rosuvastatin decreased various coagulation factor levels.
Here, we investigated the hypothesis that statins decrease coagulation factor levels through shared mechanisms of synthesis or regulatory pathways with apolipoproteins.
We measured the levels of apolipoprotein (Apo)A-I, A-II, A-IV, (a), B-100, B-total, C-I, C-II, C-III, and E in patients (n = 126) randomized to 28 days of rosuvastatin use. We assessed the association between apolipoproteins and coagulation factors at baseline using linear regression. The mean difference in apolipoprotein levels between baseline and after 28 days of rosuvastatin use was determined through linear regression, adjusting for age, sex, and body mass index. Coagulation factors were added to this model to determine if the lowering of apolipoproteins by rosuvastatin was linked with coagulation factor levels.
At baseline, levels of all apolipoproteins, except Apo(a), were positively associated with FVII, FIX, and FXI. Apolipoproteins levels, except for ApoA-I, A-IV, and Apo(a), were decreased after 28 days of rosuvastatin. ApoB-100 showed the largest mean decrease of -0.43 g/L (95% CI = -0.46 to -0.40). The decrease in ApoC-I and C-III levels was associated with a decrease in FVII, whereas the decrease in apoA-II, B-100, and B-total was associated with a decrease in FXI. The decrease in apolipoproteins was neither associated with FVIII or vWF decrease nor with endogenous thrombin potential changes.
Rosuvastatin decreases the level of several apolipoproteins, but this decrease was associated only with a decrease in FVII and XI and not with FVIII/vWF.
他汀类药物降低血栓形成倾向试验表明，在既往有静脉血栓形成的患者中，瑞舒伐他汀可降低多种凝血因子水平。
在此，我们研究了他汀类药物通过与载脂蛋白共享合成机制或调节途径来降低凝血因子水平这一假说。
我们测定了随机接受28天瑞舒伐他汀治疗的患者（n = 126）的载脂蛋白（Apo）A-I、A-II、A-IV、（a）、B-100、总B、C-I、C-II、C-III和E的水平。我们使用线性回归评估了基线时载脂蛋白与凝血因子之间的关联。通过线性回归确定瑞舒伐他汀使用28天前后载脂蛋白水平的平均差异，并对年龄、性别和体重指数进行校正。将凝血因子添加到该模型中，以确定瑞舒伐他汀降低载脂蛋白是否与凝血因子水平相关。
在基线时，除Apo（a）外，所有载脂蛋白水平均与FVII、FIX和FXI呈正相关。瑞舒伐他汀治疗28天后，除ApoA-I、A-IV和Apo（a）外，其他载脂蛋白水平均降低。ApoB-100的平均降幅最大，为-0.43 g/L（95%CI = -0.46至-0.40）。ApoC-I和C-III水平的降低与FVII的降低相关，而ApoA-II、B-100和总B的降低与FXI的降低相关。载脂蛋白的降低与FVIII或vWF的降低无关，也与内源性凝血酶潜力变化无关。
瑞舒伐他汀可降低多种载脂蛋白水平，但这种降低仅与FVII和XI的降低相关，与FVIII/vWF无关。
