Department of Cardiologic, Thoracic, and Vascular Sciences, 2nd Chair of Internal Medicine, University of Padua Medical School, Padua, Italy.
Int J Lab Hematol. 2013 Feb;35(1):101-5. doi: 10.1111/ijlh.12003. Epub 2012 Sep 10.
Portal vein thrombosis (PVT) is caused by local and systemic prothrombotic risk factors. In this case-control study, we evaluated the use of the Factor VIIa-antithrombin complex (FVIIa-AT) complex assay as a hypercoagulability marker in patients with PVT.
Two different groups of cases were considered: (i) n = 12 noncirrhotic PVT patients, (ii) n = 33 cirrhotic patients with PVT. Controls were sex and age-matched healthy volunteers and cirrhotic subjects without PVT, respectively.
Levels of the FVIIa-AT complex were significantly higher in noncirrhotic PVT subjects (132 ± 32 pM) than in healthy volunteers (108 ± 18 pM, P = 0.04). No significant difference in FVIIa-AT complexes was seen between cirrhotic patients with (64 ± 20 pM) or without (61 ± 24 pM) PVT. A linear correlation was seen between FVIIa-AT and FVIIa in noncirrhotic PVT subjects. In cirrhotic patients, FVIIa-AT complexes depended on both FVIIa and AT.
These results confirm the utility of the FVIIa-AT assay in identifying the hypercoagulable state of noncirrhotic patients because of a previous thrombotic event.
门静脉血栓形成（PVT）是由局部和全身促血栓形成危险因素引起的。在这项病例对照研究中，我们评估了因子 VIIa-抗凝血酶复合物（FVIIa-AT）复合物测定作为 PVT 患者高凝状态标志物的用途。
考虑了两组不同的病例：（i）非肝硬化 PVT 患者 n = 12 例，（ii）肝硬化合并 PVT 患者 n = 33 例。对照组分别为性别和年龄匹配的健康志愿者和无 PVT 的肝硬化患者。
非肝硬化 PVT 患者（132 ± 32 pM）的 FVIIa-AT 复合物水平明显高于健康志愿者（108 ± 18 pM，P = 0.04）。肝硬化合并 PVT 患者（64 ± 20 pM）与无 PVT 患者（61 ± 24 pM）的 FVIIa-AT 复合物无显著差异。非肝硬化 PVT 患者中可见 FVIIa-AT 与 FVIIa 之间存在线性相关性。在肝硬化患者中，FVIIa-AT 复合物取决于 FVIIa 和 AT。
这些结果证实了 FVIIa-AT 测定在识别非肝硬化患者先前血栓形成事件后的高凝状态的有用性。
