Inbal Aida, Muszbek László, Lubetsky Aharon, Katona Eva, Levi Itai, Kárpáti Levente, Nagler Arnon
Institute of Thrombosis and Hemostasis and Bone Marrow Transplantation Department, Sheba Medical Center, Tel Hashomer, and Sackler Faculty of Medicine, Tel Aviv University, Israel.
Blood Coagul Fibrinolysis. 2004 Apr;15(3):249-53. doi: 10.1097/00001721-200404000-00009.
Factor XIII subunit A (FXIII A) is synthesized by megakaryocytes, and monocytes/macrophages. In addition, the liver has been reported as an extrahaematopoietic source of FXIII A. At present, the extent of contribution of either haematopoietic or extrahaematopoietic sources to the plasma FXIII A level is unknown. We studied the effect of bone marrow aplasia due to high-dose chemotherapy followed by autologous peripheral blood stem cell transplantation (ASCT) on plasma FXIII A activity and concentration in 20 patients with haematological or solid tumour malignancies. A multiple linear regression model was used to assess the effect of gender, age, malignancy and treatment types, platelet and monocyte counts, abnormal liver function tests, prothrombin time, and number of platelet transfusions on FXIII activity measured in plasma before and following ASCT. Significant correlation between platelet counts and FXIII A activity in plasma was observed (r = 0.51, P = 0.0001), which remained after the adjustment for the aforementioned parameters (multiple R = 0.52, P = 0.0001). In contrast, no significant correlation between FXIII A levels and monocyte counts was observed (r = 0.19), and this lack of correlation persisted after the adjustment. These results suggest that in the ASCT model, following myeloablation, platelets but not monocytes are the haematopoietic cells that contribute significantly to plasma FXIII A levels. In addition, extra-haematopoietic sources of FXIII synthesis may also contribute to FXIII levels in plasma.
凝血因子 XIII A 亚基(FXIII A)由巨核细胞以及单核细胞/巨噬细胞合成。此外,有报道称肝脏是 FXIII A 的造血外来源。目前,造血或造血外来源对血浆 FXIII A 水平的贡献程度尚不清楚。我们研究了大剂量化疗后自体外周血干细胞移植(ASCT)导致的骨髓再生障碍对 20 例血液系统或实体肿瘤恶性肿瘤患者血浆 FXIII A 活性和浓度的影响。采用多元线性回归模型评估性别、年龄、恶性肿瘤类型、治疗方式、血小板和单核细胞计数、肝功能检查异常、凝血酶原时间以及血小板输注次数对 ASCT 前后血浆中 FXIII 活性的影响。观察到血小板计数与血浆中 FXIII A 活性之间存在显著相关性(r = 0.51,P = 0.0001),在对上述参数进行调整后该相关性依然存在(复相关系数 R = 0.52,P = 0.0001)。相比之下,未观察到 FXIII A 水平与单核细胞计数之间存在显著相关性(r = 0.19),且调整后这种缺乏相关性的情况仍然存在。这些结果表明,在 ASCT 模型中,骨髓清除后,对血浆 FXIII A 水平有显著贡献的造血细胞是血小板而非单核细胞。此外,FXIII 合成的造血外来源也可能对血浆中的 FXIII 水平有贡献。