Spicka Ivan, Rihova Zuzana, Kvasnicka Jan, Cieslar Petr, Prochazka Bohumir, Klener Pavel
First Department of Internal Medicine, Department of Hematology, Charles University Hospital, U nemocnice 2, Prague 2, 128 08, Czech Republic.
Thromb Res. 2003;112(5-6):297-300. doi: 10.1016/j.thromres.2003.12.007.
Monoclonal gammopathies (MG) may be associated with unique monoclonal immunoglobulin (MIg)-induced disturbances of either primary hemostasis or plasma coagulation. We have investigated the possible interference of MIg with antithrombotic systems in 49 patients with MG. Although an increase of tissue-type plasminogen activator (t-PA) activity was the most frequent abnormality in our group, defect of anticoagulation factors was found in 26.5% of patients. The relationship between MIg type and concentration and frequency of antithrombotic factor abnormalities was not found. The risk of venous thrombosis was higher in patients with the defect in comparison with the unaffected group (46% vs. 22%), but the difference was not statistically significant. Bleeding complications were markedly less frequent in the group of patients with defect of anticoagulation mechanisms (0% vs. 17%). In conclusion, we have found abnormalities in anticoagulation and/or fibrinolytic system, analogous to well-known disturbances of hemostatic mechanisms, in more than a quarter of patients with MG. The interference of M-protein with antithrombotic pathways is supposed to be another mechanism of secondary deficiencies of antithrombin III (AT III), protein C (PC), protein S (PS), plasminogen and APC resistance. Together with other factors, it could contribute to higher risk of thromboembolism in myeloma patients.
单克隆丙种球蛋白病(MG)可能与独特的单克隆免疫球蛋白(MIg)引起的原发性止血或血浆凝血紊乱有关。我们研究了49例MG患者中MIg对抗血栓系统的可能干扰。虽然组织型纤溶酶原激活物(t-PA)活性增加是我们组中最常见的异常,但26.5%的患者存在抗凝因子缺陷。未发现MIg类型和浓度与抗血栓因子异常频率之间的关系。与未受影响的组相比,有缺陷的患者发生静脉血栓形成的风险更高(46%对22%),但差异无统计学意义。抗凝机制有缺陷的患者组中出血并发症明显较少(0%对17%)。总之,我们发现超过四分之一的MG患者存在抗凝和/或纤维蛋白溶解系统异常,类似于众所周知的止血机制紊乱。M蛋白对抗血栓途径的干扰被认为是抗凝血酶III(AT III)、蛋白C(PC)、蛋白S(PS)、纤溶酶原和活化蛋白C抵抗继发性缺陷的另一种机制。与其他因素一起,它可能导致骨髓瘤患者血栓栓塞风险更高。