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What are the long-term complications of pediatric ALL treatments and how can they be mitigated? Perspectives on long-term consequences of curative treatment in childhood ALL 儿科ALL治疗的长期并发症有哪些?如何减轻这些并发症?儿童ALL治疗的长期后果的观点
IF 2.1 4区 医学 Q3 HEMATOLOGY Pub Date : 2022-12-01 DOI: 10.1016/j.beha.2022.101403
Lia Gore

Despite cure rates approaching 100% for some subsets of patients, survivors of childhood acute lymphoblastic leukemia (ALL) report a multitude of short- and long-term side effects. Indeed, the long-term complications of pediatric ALL treatment regimens can be associated with significant morbidity and mortality. Identifying mitigation strategies and developing more effective, less toxic therapies is a central goal of current research.

尽管某些亚群患者的治愈率接近100%,但儿童急性淋巴细胞白血病(ALL)的幸存者报告了许多短期和长期的副作用。事实上,儿童ALL治疗方案的长期并发症可能与显著的发病率和死亡率相关。确定缓解策略和开发更有效、毒性更小的疗法是当前研究的中心目标。
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引用次数: 0
How can we design a better care model to address the acute distress of an acute leukemia diagnosis? Care models to address the acute distress of an acute leukemia diagnosis 我们如何设计一个更好的护理模式来解决急性白血病诊断的急性痛苦?护理模式,以解决急性白血病诊断的急性痛苦
IF 2.1 4区 医学 Q3 HEMATOLOGY Pub Date : 2022-12-01 DOI: 10.1016/j.beha.2022.101409
Areej El-Jawahri
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引用次数: 0
How can we intervene to mitigate post-transplantation relapse in AML? Strategies to mitigate post-transplantation relapse in AML 我们如何干预以减轻AML移植后复发?减轻AML移植后复发的策略
IF 2.1 4区 医学 Q3 HEMATOLOGY Pub Date : 2022-12-01 DOI: 10.1016/j.beha.2022.101411
Jonathan A. Gutman

Although allogeneic hematopoietic stem cell transplantation (allo-HSCT) is a curative approach for patients with acute myeloid leukemia (AML), relapse is a common occurrence. Several strategies, such as choice of conditioning regimen, donor lymphocyte infusions, pharmacologic agents, and cellular therapy approaches, are currently being developed to improve transplantation outcomes. This review outlines some important interventions and considerations to lower the burden of post-transplantation relapse in AML.

虽然同种异体造血干细胞移植是治疗急性髓系白血病(AML)的一种方法,但复发是常见的。目前正在开发几种策略,如调节方案的选择、供体淋巴细胞输注、药物制剂和细胞治疗方法,以改善移植结果。本文概述了降低AML移植后复发负担的一些重要干预措施和注意事项。
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引用次数: 1
How can we incorporate molecular data into the IPSS? 我们如何将分子数据整合到IPSS中?
IF 2.1 4区 医学 Q3 HEMATOLOGY Pub Date : 2022-12-01 DOI: 10.1016/j.beha.2022.101410
Rafael Bejar
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引用次数: 0
Consolidation chemotherapy in AML: Are we playing with a full deck of cards? AML的巩固化疗:我们是否在玩全套纸牌?
IF 2.1 4区 医学 Q3 HEMATOLOGY Pub Date : 2022-12-01 DOI: 10.1016/j.beha.2022.101408
Richard M. Stone

The safe diminution of leukemic cell numbers to a level such that the patient will not succumb to their disease has been an achievable, yet often elusive goal in AML. Disease heterogeneity based both on biological features as well as on patient characteristics such as age, exposure to prior to anti-cancer chemotherapy and co-morbidities play a role in an allowing the physician to predict which patient has a greater or lesser chance to be cured after a diagnosis of acute myeloid leukemia. Cure rates range from 95% in younger patients with non-high-risk acute promyelocytic leukemia to essentially zero in older adults with intrinsically resistant biologies such as complex karyotype and/or TP53 mutations. One unifying feature of all AMLs, however, is the notion that whatever initial therapy is used, while possible to eradicate all morphological evidence of disease in a sizeable fraction of patients, an initial cycle (or two) is not sufficient to yield a low enough disease burden to prevent eventual relapse. Thus, the application of additional chemotherapy after the initial complete remission is received (post-remission therapy generally or consolidation therapy if a myelointense approach is used) is absolutely required for the patient to have a reasonable chance at cure. The widely accepted principle of the need to provide post-remission therapy leads to multiple controversies pertaining to the appropriate intensity, drug choice, and duration of exposure to consolidation chemotherapy, which can range from repetitive cycles of non-intensive therapy, up to and including a myeloblative allogeneic stem cell transplant. In this review, both the principles and the individual strategies that can be used once remission is achieved, will be examined.

在AML中,将白血病细胞数量安全减少到患者不会死于疾病的水平是可以实现的,但往往难以实现的目标。基于生物学特征和患者特征(如年龄、接受抗癌化疗前的暴露情况和共病)的疾病异质性在医生预测哪些患者在诊断为急性髓性白血病后有更大或更小的治愈机会方面发挥了作用。治愈率范围从非高风险急性早幼粒细胞白血病的年轻患者的95%到具有内在耐药生物学(如复杂核型和/或TP53突变)的老年人基本上为零。然而,所有急性粒细胞白血病的一个统一特征是,无论使用何种初始治疗,虽然可能根除相当一部分患者的所有疾病形态学证据,但初始周期(或两个)不足以产生足够低的疾病负担以防止最终复发。因此,在最初完全缓解后,患者绝对需要额外的化疗(通常是缓解后治疗,如果使用骨髓强化方法则需要巩固治疗),以获得合理的治愈机会。广泛接受的原则是需要提供缓解后治疗,这导致了与适当的强度、药物选择和暴露于巩固化疗的持续时间有关的多重争议,巩固化疗的范围可以从重复的非强化治疗周期,一直到并包括骨髓同种异体干细胞移植。在本综述中,将审查一旦达到缓解,可以使用的原则和个别策略。
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引用次数: 0
Recent progress in acute leukemia and myelodysplasia 急性白血病和骨髓异常增生的最新进展
IF 2.1 4区 医学 Q3 HEMATOLOGY Pub Date : 2022-12-01 DOI: 10.1016/j.beha.2022.101415
Hetty E. Carraway , Daniel A. Pollyea , Eytan M. Stein

The advances and progress in the understanding and management of acute leukemia and myelodysplasia continue to occur at an exponential rate. While this has led to more therapy options, clinicians and researchers are now facing more challenges in terms of clinical decision-making and more unanswered questions. This paper has outlined some conundrums in acute leukemia and myelodysplasia, and the efforts that are underway to address these.

在对急性白血病和骨髓增生的认识和管理方面的进步和进展继续以指数速度发生。虽然这带来了更多的治疗选择,但临床医生和研究人员现在在临床决策方面面临着更多的挑战和更多未解之谜。本文概述了急性白血病和骨髓增生异常的一些难题,以及正在进行的解决这些问题的努力。
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引用次数: 0
How can we improve response assessments in MDS? Strategies to improve response assessment in MDS treatment paradigms 我们如何改进MDS的疗效评估?改善MDS治疗模式疗效评估的策略
IF 2.1 4区 医学 Q3 HEMATOLOGY Pub Date : 2022-12-01 DOI: 10.1016/j.beha.2022.101405
Rafael Bejar

Evaluating response to treatment in MDS represents a major challenge due to its associated complexity and heterogeneity. Although response criteria have been proposed by the IWG and revised on several occasions, these criteria have limitations. This review has outlined some refinements that can be used to improve response assessment and to ensure the identification of clinically meaningful endpoints.

由于其相关的复杂性和异质性,评估MDS治疗的反应是一个主要的挑战。虽然工作组提出了反应标准,并进行了多次修订,但这些标准都有局限性。本综述概述了一些可用于改善疗效评估和确保确定临床有意义的终点的改进方法。
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引用次数: 2
COVID-19 and antiphospholipid antibodies COVID-19和抗磷脂抗体
IF 2.1 4区 医学 Q3 HEMATOLOGY Pub Date : 2022-09-01 DOI: 10.1016/j.beha.2022.101402
Ayesha Butt , Doruk Erkan , Alfred Ian Lee

Antiphospholipid syndrome and the coagulopathy of COVID-19 share many pathophysiologic features, including endotheliopathy, hypercoagulability, and activation of platelets, complement pathways, and neutrophil extracellular traps, all acting in concert via a model of immunothrombosis. Antiphospholipid antibody production in COVID-19 is common, with 50% of COVID-19 patients being positive for lupus anticoagulant in some studies, and with non-Sapporo criteria antiphospholipid antibodies being prevalent as well. The biological significance of antiphospholipid antibodies in COVID-19 is uncertain, as such antibodies are usually transient, and studies examining clinical outcomes in COVID-19 patients with and without antiphospholipid antibodies have yielded conflicting results. In this review, we explore the biology of antiphospholipid antibodies in COVID-19 and other infections and discuss mechanisms of thrombogenesis in antiphospholipid syndrome and parallels with COVID-19 coagulopathy. In addition, we review the existing literature on safety of COVID-19 vaccination in patients with antiphospholipid antibodies and antiphospholipid syndrome.

抗磷脂综合征和COVID-19的凝血功能障碍具有许多共同的病理生理特征,包括内皮病变、高凝性、血小板活化、补体途径和中性粒细胞细胞外陷阱,所有这些都通过免疫血栓形成模型协同作用。在COVID-19中产生抗磷脂抗体很常见,在一些研究中,50%的COVID-19患者狼疮抗凝血剂呈阳性,非札幌标准的抗磷脂抗体也很普遍。抗磷脂抗体在COVID-19中的生物学意义尚不确定,因为这种抗体通常是短暂的,并且对有无抗磷脂抗体的COVID-19患者临床结局的研究得出了相互矛盾的结果。在这篇综述中,我们探讨了抗磷脂抗体在COVID-19和其他感染中的生物学作用,并讨论了抗磷脂综合征的血栓形成机制以及与COVID-19凝血功能障碍的相似之处。此外,我们还回顾了现有关于抗磷脂抗体和抗磷脂综合征患者接种COVID-19疫苗安全性的文献。
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引用次数: 6
Coagulopathy in COVID-19 and anticoagulation clinical trials COVID-19的凝血功能障碍和抗凝临床试验
IF 2.1 4区 医学 Q3 HEMATOLOGY Pub Date : 2022-09-01 DOI: 10.1016/j.beha.2022.101377
Heng Zhang , Qifang Lao , Jue Zhang , Jieqing Zhu

Severe acute respiratory disease coronavirus 2 (SARS-COV-2) first emerged in Wuhan, China, in December 2019 and has caused a global pandemic of a scale unprecedented in the modern era. People infected with SARS-CoV-2 can be asymptomatic, moderate symptomatic or develop severe COVID-19. Other than the typical acute respiratory distress syndrome (ARDS), patients with moderate or severe COVID-19 also develop a distinctive systemic coagulopathy, known as COVID-19-associated coagulopathy (CAC), which is different from sepsis-related forms of disseminated intravascular coagulation (DIC). Endotheliopathy or endotheliitis are other unique features of CAC. The endothelial cell perturbation can further increase the risk of thrombotic events in COVID-19 patients. In this review, we will summarize the current knowledge on COVID-19 coagulopathy and the possible mechanisms for the condition. We also discuss the results of clinical trials testing methods for mitigating thrombosis events in COVID-19 patients.

2019年12月,严重急性呼吸道疾病冠状病毒2型(SARS-COV-2)首次在中国武汉出现,并引发了现代前所未有的全球大流行。感染SARS-CoV-2的人可以无症状、有中度症状或发展为严重的COVID-19。除了典型的急性呼吸窘迫综合征(ARDS)外,中度或重度COVID-19患者还会出现独特的全身性凝血功能障碍,即COVID-19相关凝血功能障碍(CAC),这与败血症相关的弥散性血管内凝血(DIC)不同。内皮病变或内皮炎是CAC的其他独特特征。内皮细胞扰动可进一步增加COVID-19患者血栓形成事件的风险。在这篇综述中,我们将总结目前关于COVID-19凝血功能障碍的知识及其可能的机制。我们还讨论了缓解COVID-19患者血栓事件的临床试验结果。
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引用次数: 3
Dysregulation of Protein S in COVID-19 蛋白S在COVID-19中的失调
IF 2.1 4区 医学 Q3 HEMATOLOGY Pub Date : 2022-09-01 DOI: 10.1016/j.beha.2022.101376
Martha M.S. Sim , Jeremy P. Wood

Coronavirus Disease 2019 (COVID-19) has been widely associated with increased thrombotic risk, with many different proposed mechanisms. One such mechanism is acquired deficiency of protein S (PS), a plasma protein that regulates coagulation and inflammatory processes, including complement activation and efferocytosis. Acquired PS deficiency is common in patients with severe viral infections and has been reported in multiple studies of COVID-19. This deficiency may be caused by consumption, degradation, or clearance of the protein, by decreased synthesis, or by binding of PS to other plasma proteins, which block its anticoagulant activity. Here, we review the functions of PS, the evidence of acquired PS deficiency in COVID-19 patients, the potential mechanisms of PS deficiency, and the evidence that those mechanisms may be occurring in COVID-19.

冠状病毒病2019 (COVID-19)与血栓形成风险增加广泛相关,有许多不同的机制被提出。其中一种机制是获得性蛋白S (PS)缺乏,PS是一种血浆蛋白,调节凝血和炎症过程,包括补体激活和efferocytosis。获得性PS缺乏症在严重病毒感染患者中很常见,在COVID-19的多项研究中都有报道。这种缺乏可能是由于蛋白质的消耗、降解或清除,合成减少,或PS与其他血浆蛋白结合,从而阻断其抗凝血活性。本文就PS的功能、COVID-19患者获得性PS缺乏的证据、PS缺乏的潜在机制以及这些机制可能在COVID-19中发生的证据进行综述。
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引用次数: 2
期刊
Best Practice & Research Clinical Haematology
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