Circulating endothelial progenitor cells and residual in vivo thromboxane biosynthesis in low-dose aspirin-treated polycythemia vera patients.
Circulating endothelial progenitor cells and residual in vivo thromboxane biosynthesis in low-dose aspirin-treated polycythemia vera patients.
复制标题
低剂量阿司匹林治疗真性红细胞增多症患者的循环内皮祖细胞和残留体内血栓素生物合成。
作者：
F. Santilli;M. Romano;A. Recchiuti;A. Dragani;A. Falco;G. Lessiani;F. Fioritoni;S. Lattanzio;D. Mattoscio;R. De Cristofaro;B. Rocca;G. Davı̀
真性红细胞增多症（PV）与血栓形成的高发病率和死亡率相关。我们推测，在PV改变敏感性阿司匹林可能与内皮修复和/或一氧化氮（NO）系统的功能障碍。对37例服用小剂量阿司匹林的PV患者和12例健康对照者进行了尿血栓素（TX）A（2）代谢物（TXM）、内皮细胞集落形成细胞（ECFC）、血浆不对称二甲基精氨酸（ADMA）和血管性血友病因子（VWF）的测定。与非阿司匹林对照组相比，患者的TXM和血浆ADMA水平中位数增加约2倍（P <0.001），而ECFC数量减少约7倍（P <0.001）。这些差异在既往有血栓形成的患者中更为明显。阿司匹林8周疗程对6例对照组ECFC无影响。VWF、TXM与ADMA呈正相关，与ECFC呈负相关。通过多元回归分析，较低的ECFC四分位数（β = -0.39; SE = 0.17; P = 0.028）和较高的VWF水平（β = 0.338，SE = 0.002，P = 0.034）是较高TXM四分位数的独立预测因子（R（2）= 0.39）。在22名患者中测得的血清TXB（2）大约是阿司匹林治疗对照组的10倍。PV患者似乎存在ECFC/NO轴失衡，血小板产生TXA 2的敏感性明显改变，所有这些都可能导致阿司匹林不敏感的TXM形成。因此，额外的抗血栓策略可能对PV有益。
Polycythemia vera (PV) is associated with high morbidity and mortality for thrombosis. We hypothesized that in PV altered sensitivity to aspirin might be related to dysfunction of the endothelial repair and/or of the nitric oxide (NO) system. Urinary thromboxane (TX) A(2) metabolite (TXM), endothelial colony-forming cells (ECFCs), plasma asymmetric dimethylarginine (ADMA) and von Willebrand factor (VWF) were measured in 37 PV patients on low-dose aspirin and 12 healthy controls. Patients showed an approximately 2-fold increase in median TXM and plasma ADMA levels (P < .001), while ECFC numbers were reduced by approximately 7-fold (P < .001) as compared with non-aspirinated control. These differences were more pronounced in patients with previous thrombosis. An 8-week course of aspirin did not affect ECFCs in 6 controls. VWF and TXM correlated directly with ADMA, and inversely with ECFCs. By multiple regression analysis, lower ECFC quartiles (beta = -0.39; SE = 0.17; P = .028) and higher VWF levels (beta = 0.338, SE = 0.002, P = .034) were independent predictors of higher TXM quartiles (R(2) = 0.39). Serum TXB(2), measured in 22 patients, was approximately 10-fold higher than aspirin-treated controls. PV patients appear to have an unbalanced ECFC/NO axis, and an apparent altered sensitivity of platelet TXA(2) production, all potentially contributing to aspirin-insensitive TXM formation. Thus, additional antithrombotic strategies may be beneficial in PV.
影响因子：
37.8
作者：
DATTA, YH;ROMANO, M;EWENSTEIN, BM
通讯作者：
EWENSTEIN, BM
影响因子：
20.3
作者：
Yoder, Mervin C.;Mead, Laura E.;Ingram, David A.
通讯作者：
Ingram, David A.