Department of Surgery, Temple University Hospital, Philadelphia, PA, USA.
Clin Appl Thromb Hemost. 2012 Nov;18(6):594-8. doi: 10.1177/1076029612440034. Epub 2012 Apr 11.
Contrary to well-recognized bleeding diathesis in chronic liver disease, thrombotic events can occur in these patients due to reduction or loss of synthesis of anticoagulant proteins. Forty-seven consecutive patients with end-stage liver disease (ESLD) were investigated for activity of protein C, protein S, antithrombin, and factor V Leiden mutation. Forty-two (89.4%) patients had low levels of at least 1 while 33 (70.2%) patients were deficient for all anticoagulant proteins studied. Forty-six (97.9%) patients were negative for factor V Leiden mutation. The deficiencies were more marked in hepatitis C virus-positive patients and patients with model for end-stage liver disease (MELD) score >15. Six (12.8%) patients had portal vein thrombosis (PVT), and all had diminished protein S activity. In conclusions, deficiency of anticoagulant proteins occur in early phase of chronic liver disease. The severity of deficiency is proportional to the severity of liver disease. Despite the high prevalence of hypercoagulability, the incidence of PVT is low. Further studies with larger cohort of patients are needed to support these conclusions and to study other associated factors.
与慢性肝病中公认的出血倾向相反，由于抗凝蛋白的减少或丧失，这些患者可能会发生血栓事件。对 47 例终末期肝病 (ESLD) 患者进行了蛋白 C、蛋白 S、抗凝血酶和因子 V Leiden 突变的活性研究。42 例 (89.4%) 患者至少有 1 种水平降低，而 33 例 (70.2%) 患者所有研究的抗凝蛋白均缺乏。46 例 (97.9%) 患者因子 V Leiden 突变阴性。丙型肝炎病毒阳性患者和终末期肝病模型评分>15 的患者的缺乏更为明显。6 例 (12.8%) 患者发生门静脉血栓形成 (PVT)，所有患者蛋白 S 活性均降低。总之，抗凝蛋白缺乏发生在慢性肝病的早期阶段。缺乏的严重程度与肝病的严重程度成正比。尽管存在高凝状态，但 PVT 的发生率较低。需要进一步的研究，以更大的患者队列来支持这些结论，并研究其他相关因素。
