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[Rinsho ketsueki] The Japanese journal of clinical hematology最新文献

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[Overview]. [概述]。
Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.341
Takahiro Yamauchi
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引用次数: 0
[Advances in the treatment of thrombotic thrombocytopenic purpura]. [治疗血栓性血小板减少性紫癜的进展]。
Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.567
Masahito Uchihara, Masayuki Kubo, Masanori Matsumoto

Thrombotic thrombocytopenic purpura (TTP) is a fatal thrombotic disease caused by a marked decrease in the activity of ADAMTS13, a von Willebrand factor cleaving protease. In congenital TTP, ADAMTS13 activity is decreased by an abnormality in ADAMTS13, and in acquired TTP, by anti-ADAMTS13 autoantibody. Death from thrombosis in the acute phase has been an issue with conventional treatment of acquired TTP by plasma exchange or immunosuppressive therapy. However, the advent of caplacizumab, an anti-VWF nanobody, has made it possible to suppress thrombus formation and is expected to improve survival rates. In addition, some case series have shown the efficacy of caplacizumab without plasma exchange for acquired TTP, and this approach is being investigated in clinical trials. Fresh-frozen plasma is transfused to supply ADAMTS13 for congenital TTP, but frequent transfusions over a long period of time can lead to problems such as infection and allergic reactions. Novel therapies such as recombinant ADAMTS13 products and gene therapy are now under development, and show promise for future clinical use.

血栓性血小板减少性紫癜(TTP)是一种致命的血栓性疾病,起因是冯-威廉因子裂解蛋白酶 ADAMTS13 的活性明显降低。在先天性 TTP 中,ADAMTS13 活性因 ADAMTS13 异常而降低;在获得性 TTP 中,则因抗 ADAMTS13 自身抗体而降低。通过血浆置换或免疫抑制疗法对获得性 TTP 进行传统治疗时,急性期血栓形成导致的死亡一直是个问题。然而,抗 VWF 纳米抗体 Caplacizumab 的出现使抑制血栓形成成为可能,有望提高存活率。此外,一些病例系列显示,卡普拉珠单抗在不进行血浆置换的情况下对获得性 TTP 有一定疗效,这种方法正在临床试验中进行研究。先天性 TTP 需要输注新鲜冷冻血浆来提供 ADAMTS13,但长期频繁输注血浆会导致感染和过敏反应等问题。重组 ADAMTS13 产品和基因疗法等新型疗法目前正在开发中,有望在未来应用于临床。
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引用次数: 0
[Fulminant Clostridioides difficile infection during treatment with FLT3 inhibitor for acute myeloid leukemia]. [在使用 FLT3 抑制剂治疗急性髓性白血病期间出现难辨梭状芽孢杆菌感染】。]
Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.153
Jotaro Yamamoto, Otoya Watanabe, Takashi Sako, Shinsuke Takagi, Daisuke Kaji, Yuki Taya, Aya Nishida, Hisashi Yamamoto, Yuki Asano-Mori, Go Yamamoto, Hideki Araoka, Naoyuki Uchida

An 80-year-old man with FLT3-TKD mutation-positive acute myeloid leukemia (AML) relapsed during consolidation therapy with venetoclax/azacitidine and was started on gilteritinib as salvage therapy. On the day after treatment initiation, febrile neutropenia was observed, but the fever resolved promptly after initiation of antimicrobial therapy. On the fifth day after completion of antimicrobial therapy, the patient experienced fever and watery diarrhea over 10 times a day, and a diagnosis of Clostridioides difficile infection (CDI) was made based on stool examination. The patient was treated with intravenous metronidazole, but renal dysfunction, hypotension, and hypoxemia developed, and a CT scan showed pleural and intraperitoneal effusion, significant intestinal wall thickening, and intestinal dilatation. Fidaxomicin was started under general monitoring in the intensive care unit and response was achieved. The patient was discharged from the intensive care unit on the 18th day after the onset of CDI. We report this case not only due to the rarity of fulminant CDI during AML treatment, but also because it is a valuable example of effective treatment of fulminant CDI with fidaxomicin.

一名患有FLT3-TKD突变阳性急性髓性白血病(AML)的80岁男性患者在接受文尼替克/阿扎胞苷巩固治疗期间复发,并开始接受吉特替尼作为挽救治疗。在开始治疗的第二天,患者出现发热性中性粒细胞减少症,但在开始抗菌治疗后,发热迅速缓解。在完成抗菌治疗后的第五天,患者出现发热和每天10次以上的水样腹泻,根据粪便检查确诊为艰难梭菌感染(CDI)。患者接受了甲硝唑静脉注射治疗,但出现了肾功能不全、低血压和低氧血症,CT 扫描显示胸腔和腹腔积液、肠壁明显增厚和肠道扩张。在重症监护室的全身监测下开始服用非达霉素,并取得了反应。患者于 CDI 发病后第 18 天从重症监护室出院。我们之所以报告该病例,不仅是因为急性髓细胞白血病治疗期间发生暴发性CDI的情况非常罕见,还因为它是用菲达霉素有效治疗暴发性CDI的一个宝贵实例。
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引用次数: 0
[Supporting career development of female physicians and researchers]. [支持女医生和女研究员的职业发展]。
Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.769
Mariko Eguchi

The proportion of female doctors among younger generations has increased in recent years, and support for reemployment after childbirth and childcare leave is important for maintaining stability of local healthcare. We conducted a questionnaire with doctors in the Department of Pediatrics at Ehime University School of Medicine and it's affiliated hospitals to identify issues in the career development of female doctors. Although many female physicians want to pursue career development by obtaining subspecialty qualifications and PhD degrees, a high percentage have not actually obtained them. This is not only due to interruptions in work caused by childbirth and childcare but also because they are busy with housework, childcare, and daily work, and lack sufficient information about career development. In this regard, it appears that beyond improving work-life balance, female doctors must always keep in mind their career design and future goals, as well as their social mission as a physician. For administrators of these departments, acceptance of diversity, providing adequate support for female physicians to return to work after maternity/childcare leave, and balancing childcare and work are important for expanding female doctors' opportunities and career development.

近年来,年轻一代中女医生的比例有所上升,而对生育和育儿假后再就业的支持对于保持当地医疗的稳定性非常重要。我们对爱媛大学医学院儿科系及其附属医院的医生进行了问卷调查,以了解女医生职业发展中存在的问题。尽管许多女医生都希望通过获得亚专科资格和博士学位来谋求职业发展,但实际上有很大比例的女医生并未获得这些资格和学位。这不仅是因为生育和育儿导致工作中断,还因为她们忙于家务、育儿和日常工作,缺乏足够的职业发展信息。由此看来,除了改善工作与生活的平衡,女医生还必须时刻牢记自己的职业设计和未来目标,以及作为医生的社会使命。对于这些科室的管理者来说,接受多样性、为女医生在产假/育儿假后重返工作岗位提供足够的支持以及平衡育儿和工作对于扩大女医生的机会和职业发展非常重要。
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引用次数: 0
[Allogeneic transplantation as a therapeutic option for atypical chronic myeloid leukemia]. [异基因移植作为非典型慢性髓性白血病的一种治疗方案]。
Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.967
Hidehiro Itonaga

Atypical chronic myeloid leukemia (aCML) is a rare disease classified as a myelodysplastic/myeloproliferative neoplasm (MDS/MPN). Recent advances in gene mutational profiling have clarified the characteristics of aCML as a disease entity relative to other MDS/MPNs. Although some studies suggest the efficacy of DNA demethylating agents and tyrosine kinase inhibitors, data about these agents are limited due to the small number of patients. Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is only therapeutic option that can provide durable remission for aCML and other MDS/MPNs. Retrospective studies from Europe and Japan revealed the clinical results of allo-HSCT for aCML. This review summarizes the pathogenesis of aCML and the development of allo-HSCT and other therapeutic options.

非典型慢性髓性白血病(aCML)是一种罕见疾病,被归类为骨髓增生异常/骨髓增生性肿瘤(MDS/MPN)。基因突变分析的最新进展阐明了 aCML 作为一种疾病实体相对于其他 MDS/MPN 的特征。尽管一些研究表明 DNA 去甲基化药物和酪氨酸激酶抑制剂具有疗效,但由于患者人数较少,有关这些药物的数据十分有限。异基因造血干细胞移植(allo-HSCT)是唯一能为 aCML 和其他 MDS/MPNs 带来持久缓解的治疗方案。欧洲和日本的回顾性研究揭示了异基因造血干细胞移植治疗 aCML 的临床效果。本综述概述了 aCML 的发病机制以及 allo-HSCT 和其他治疗方案的发展。
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引用次数: 0
[Pathogenesis and treatment of acute myeloid leukemia with FLT3 mutations]. [FLT3突变的急性髓性白血病的发病机制和治疗]。
Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.945
Yuichi Ishikawa

FLT3 mutations are the most frequently identified genetic abnormalities in adult acute myeloid leukemia (AML) patients, accounting for approximately 30%. FLT3-ITD mutation specifically is considered as a poor prognostic factor in AML, and allogeneic hematopoietic cell transplantation in first remission is recommended for younger patients. The recent clinical introduction of FLT3 inhibitors has been reported to improve the prognosis of patients with FLT3 mutation-positive AML. In Japan, alongside monotherapy with gilteritinib or quizartinib for relapsed/refractory patients, combination of quizartinib with intensive chemotherapy was approved in 2023 for untreated FLT3-ITD mutation-positive AML. Studies to date have demonstrated the utility of measurable/minimal residual disease evaluation targeting FLT3 mutations and the efficacy of maintenance therapy after allogeneic transplantation. However, emergence of additional genetic mutations associated with treatment resistance has been observed. Thus, FLT3 mutations are utilized not only as a prognostic factor in AML but also as a target for treatment and for response assessment. Furthermore, the development of new treatment strategies involving FLT3 inhibitors is highly anticipated to improve clinical outcomes for patients with FLT3 mutation-positive AML.

FLT3 突变是成人急性髓性白血病(AML)患者中最常发现的基因异常,约占 30%。FLT3-ITD突变被认为是急性髓细胞白血病的不良预后因素,建议年轻患者在首次缓解期进行异基因造血细胞移植。据报道,近期临床引入的FLT3抑制剂可改善FLT3突变阳性急性髓细胞性白血病患者的预后。在日本,除了对复发/难治患者使用吉特替尼或奎沙替尼单药治疗外,奎沙替尼联合强化化疗也于2023年获批用于未经治疗的FLT3-ITD突变阳性急性髓细胞白血病患者。迄今为止的研究已经证明了针对FLT3突变的可测量/最小残留病评估的实用性以及异基因移植后维持治疗的疗效。不过,也观察到出现了与耐药性相关的其他基因突变。因此,FLT3 突变不仅是急性髓细胞性白血病的预后因素,也是治疗和反应评估的目标。此外,涉及 FLT3 抑制剂的新治疗策略的开发有望改善 FLT3 突变阳性急性髓细胞性白血病患者的临床疗效。
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引用次数: 0
[The novel in vivo platelet activation marker, soluble CLEC-2]. [新型体内血小板活化标记--可溶性 CLEC-2]。
Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.1106
Katsue Suzuki-Inoue

Unlike for anticoagulants, no good monitoring methods exist for antiplatelet agents, and their monitoring is considered unnecessary. In the platelet aggregation test, which is the standard test for platelet function, aggregation is evaluated by adding a platelet activator to platelets in a cuvette. Therefore, it provides information on the maximum potential of platelets to induce aggregation, but not the actual in vivo degree of platelet activation. In vivo platelet activation markers are not widely used because they require a special blood collection method, although some tests are covered by insurance. My colleagues and I identified the platelet activation receptor C-type lectin-like receptor 2 (CLEC-2) and found that CLEC-2 is cleaved and released during platelet activation. We established a plasma-soluble CLEC-2 (sCLEC-2) assay system with the aim of using it as a marker of in vivo platelet activation. Elevation of sCLEC-2 has been reported in various thrombotic diseases. The multi-center prospective cohort study CLECSTRO is now underway to investigate the usefulness of sCLEC-2 for diagnosis, typing, and prognostic estimation in acute ischemic stroke.

与抗凝剂不同,抗血小板药物没有很好的监测方法,因此没有必要对其进行监测。血小板聚集试验是血小板功能的标准检测方法,通过向比色皿中的血小板添加血小板活化剂来评估血小板聚集情况。因此,它提供的信息是血小板诱导聚集的最大潜力,而不是血小板在体内的实际活化程度。体内血小板活化标记物需要特殊的采血方法,因此并未得到广泛应用,不过有些检测项目属于保险范围。我和我的同事确定了血小板活化受体 C 型凝集素样受体 2(CLEC-2),并发现 CLEC-2 在血小板活化过程中会被裂解和释放。我们建立了血浆可溶性 CLEC-2(sCLEC-2)检测系统,目的是将其用作体内血小板活化的标志物。各种血栓性疾病中都有 sCLEC-2 升高的报道。目前正在进行多中心前瞻性队列研究 CLECSTRO,研究 sCLEC-2 在急性缺血性中风的诊断、分型和预后评估中的作用。
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引用次数: 0
Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.1341
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引用次数: 0
[Overview]. [概述]。
Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.1276
Masatoshi Sakurai
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引用次数: 0
[Future prospects for the development of novel agents for acute myeloid leukemia]. [开发治疗急性髓性白血病新型药物的未来前景]。
Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.353
Naoko Hosono

For nearly 40 years, combination therapy with cytarabine and anthracycline has been the standard of care for acute myeloid leukemia (AML). The cytogenetics and molecular biology of AML are now understood, and the treatment of AML has undergone dramatic changes in Japan with the launch of drugs such as FLT3 inhibitors, Bcl2 inhibitors, and hypomethylating agents since 2018. However, AML remains very difficult to cure, with a high relapse rate. Here, we review novel agents that have not yet been approved in Japan (CPX-351, IDH inhibitors, menin inhibitors, and oral azacitidine) as potential treatments for AML, as well as therapeutic antibodies (BiTEs, DARTs, immune checkpoint inhibitors) currently under investigation in clinical trials or in development. These novel agents are being investigated not only as monotherapy but also as combination therapy with intensive chemotherapy or azacitidine/venetoclax. The new era of AML treatment is expected to support a variety of goals, including leukemic cell elimination, long-term remission, and improved quality of life.

近 40 年来,阿糖胞苷和蒽环类药物联合疗法一直是治疗急性髓性白血病(AML)的标准疗法。目前,人们对急性髓细胞白血病的细胞遗传学和分子生物学已经有所了解,随着FLT3抑制剂、Bcl2抑制剂和低甲基化药物等药物自2018年起在日本上市,急性髓细胞白血病的治疗也发生了巨大变化。然而,急性髓细胞白血病仍然很难治愈,复发率很高。在此,我们回顾了作为急性髓细胞白血病潜在治疗方法的尚未在日本获批的新型药物(CPX-351、IDH 抑制剂、menin 抑制剂和口服阿扎胞苷),以及目前正在临床试验或开发中的治疗性抗体(BiTE、DART、免疫检查点抑制剂)。这些新型药物不仅可作为单药治疗,还可作为与强化化疗或阿扎胞苷/韦尼妥类药物的联合疗法进行研究。新时代的急性髓细胞性白血病治疗有望实现各种目标,包括消灭白血病细胞、长期缓解和提高生活质量。
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引用次数: 0
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[Rinsho ketsueki] The Japanese journal of clinical hematology
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