论文部分内容阅读
作者报道2例急性淋巴细胞自血病用 L-门冬酰胺酶治疗导致抗凝血酶Ⅲ的缺乏。一例为55岁的男性,在完成 L-门冬酰胺酶20,000单位/天,7天的疗程后3天,并发髂股静脉血栓形成。其在应用肝素前血浆抗凝血酶Ⅲ(AT-Ⅲ)浓度仅为56%,1个月后上升为81%。例2为58岁的男性,L-门冬酰胺酶也以20,000单位/天治疗10天。曾作过仔细观察。纤维蛋白原从100%下降至50%,AT—Ⅲ抗原从90%下降至35%,AT-Ⅲ迅速明显下降,较纤维蛋白原下降为明显,且在停药后一周数值仍低。使用 L-门冬酰胺酶常合并血浆白蛋白,纤维蛋白原、其他凝血因子及甲状晾素结合球蛋白浓度减少,其机制是由于含 L-门冬酰胺酶的蛋白质合成减少。血浆 AT-Ⅲ减少的原因也可能由于合成减少。这2例病人均没有 DIC 证据,而在 DIC 时由于抗凝血酶与释放的凝血酶复合而使 AT-Ⅲ浓度减少。静脉血栓形成也可伴抗凝血酶减少。作者最后认为使用 L-门冬酰胺酶治疗时合并症罕见的可能解释是因伴有凝血因子减少而
The authors report that 2 cases of acute lymphocytic leukemia treated with L-asparaginase resulted in a lack of antithrombin III. An example is a 55-year-old man with an iliofemoral venous thrombosis at the completion of L-asparaginase at 20,000 units / day for 3 days after a 7-day course of treatment. Its plasma antithrombin III (AT-III) concentration was only 56% before heparin was applied, and rose to 81% after 1 month. Example 2 is a 58-year-old man with L-asparaginase also treated at 20,000 units / day for 10 days. Have made careful observation. Fibrinogen decreased from 100% to 50%, AT-Ⅲ antigen decreased from 90% to 35%, AT-Ⅲ rapidly decreased significantly, compared with fibrinogen decreased significantly, and one week after stopping the value is still low. The use of L-asparaginase often associated with plasma albumin, fibrinogen, other coagulation factors and thyronin binding globulin concentration decreased, the mechanism is due to L-asparaginase-containing protein synthesis decreased. The reason for the decrease in plasma AT-III may also be due to decreased synthesis. None of the two patients had DIC evidence, whereas at DIC the concentration of AT-III was reduced due to the combination of antithrombin and released thrombin. Venous thrombosis may also be associated with decreased antithrombin. The authors conclude that the rare explanation for comorbidities when treated with L-asparaginase may be due to decreased coagulation factors