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Altered Fibrinolysis in Hematological Malignances
Seminars in Thrombosis and Hemostasis ( IF 5.7 ) Pub Date : 2021-05-31 , DOI: 10.1055/s-0041-1725099
Søren Thorgaard Bønløkke 1, 2 , Hans Beier Ommen 2, 3 , Anne-Mette Hvas 1, 3
Affiliation  

Bleeding and thrombosis are well-known complications to hematological malignancies, and changes in fibrinolysis impact both these issues. In the present systematic review, we provide an overview and discussion of the current literature in regards to clinical manifestations, diagnosis, and treatment of altered fibrinolysis in patients suffering from hematological malignancies, beyond acute promyelocytic leukemia. We performed a systematic literature search employing the databases Pubmed, Embase, and Web of Science to identify original studies investigating fibrinolysis in hematological malignancies. Studies investigating fibrinolysis in acute promyelocytic leukemia or disseminated intravascular coagulation were excluded. We identified 32 studies fulfilling the inclusion criteria. A majority of the studies were published more than two decades ago, and none of the studies examined all available markers of fibrinolysis or used dynamic clot lysis assays. In acute leukemia L-asparaginase treatment induced a hypofibrinolytic state, and prior to chemotherapy there seemed to be little to no change in fibrinolysis. In studies examining fibrinolysis during chemotherapy results were ambiguous. Two studies examining multiple myeloma indicated hypofibrinolysis prior to chemotherapy, and in another plasma cell disease, amyloid light chain-amyloidosis, clear signs of hyperfibrinolysis were demonstrated. In myeloproliferative neoplasms, the studies reported signs of hypofibrinolysis, in line with the increased risk of thrombosis in this disease. Only one study regarding lymphoma was identified, which indicated no alterations in fibrinolysis. In conclusion, this systematic review demonstrated that only sparse, and mainly old, evidence exists on fibrinolysis in hematological malignancy. However, the published studies showed a tendency toward hypofibrinolysis in myeloproliferative disorders, an increased risk of hyperfibrinolysis, and bleeding in patients with AL-amyloidosis, whereas studies regarding acute leukemias were inconclusive except with regard to L-asparaginase treatment, which induced a hypofibrinolytic state.



中文翻译:

血液系统恶性肿瘤中纤维蛋白溶解的改变

出血和血栓形成是血液系统恶性肿瘤众所周知的并发症,纤维蛋白溶解的变化会影响这两个问题。在目前的系统评价中,我们对当前的文献进行了概述和讨论,这些文献涉及除急性早幼粒细胞白血病之外的血液系统恶性肿瘤患者的纤溶改变的临床表现、诊断和治疗。我们使用 Pubmed、Embase 和 Web of Science 数据库进行了系统的文献搜索,以确定研究血液系统恶性肿瘤中纤维蛋白溶解的原始研究。研究急性早幼粒细胞白血病或弥散性血管内凝血的纤溶研究被排除在外。我们确定了 32 项符合纳入标准的研究。大多数研究发表于二十多年前,并且没有一项研究检查了所有可用的纤溶标志物或使用动态凝块溶解测定。在急性白血病中,L-天冬酰胺酶治疗诱导了低纤维蛋白溶解状态,而在化疗之前,纤维蛋白溶解似乎几乎没有变化。在检查化疗期间纤维蛋白溶解的研究中,结果模棱两可。两项检查多发性骨髓瘤的研究表明,化疗前纤维蛋白溶解不足,而在另一种浆细胞疾病中,淀粉样蛋白轻链-淀粉样变性,显示出明显的纤维蛋白溶解过度迹象。在骨髓增殖性肿瘤中,研究报告了纤维蛋白溶解不足的迹象,这与该疾病血栓形成的风险增加一致。仅确定了一项关于淋巴瘤的研究,表明纤维蛋白溶解没有改变。综上所述,该系统评价表明,关于血液系统恶性肿瘤中的纤维蛋白溶解的证据很少,而且主要是陈旧的。然而,已发表的研究表明,AL-淀粉样变性患者在骨髓增殖性疾病中存在纤维蛋白溶解不足的趋势、纤维蛋白溶解过度的风险增加和出血,而关于急性白血病的研究尚无定论,除了 L-天冬酰胺酶治疗导致纤维蛋白溶解不足状态.

更新日期:2021-06-01
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