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[Primary myelofibrosis with double mutation in U2AF1]. [原发性骨髓纤维化伴 U2AF1 双突变]。
Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.30
Keiko Maeyama, Keiki Nagaharu, Kazuko Ino, Yuka Sugimoto, Isao Tawara, Keiki Kawakami

A 47-year-old woman presented with subcutaneous hemorrhage. Blood tests revealed leukoerythroblastosis, anemia, and thrombocytopenia. Bone marrow biopsy led to a diagnosis of primary myelofibrosis (aaDIPSS, DIPSS-plus: intermediate-II risk). JAK2, CALR, and MPL mutations were not detected in peripheral blood, but targeted sequencing of bone marrow specimens revealed a double mutation (Q157R, S34F) in U2AF1. Allo-PBSCT was performed using an HLA-matched related donor, and post-transplantation bone marrow examination showed complete donor chimerism on day 55. Two years after allogeneic transplantation, the patient remains relapse-free. Although U2AF1 gene abnormality is known as a poor prognostic factor in primary myelofibrosis, this patient had a favorable long-term prognosis due to prompt transplantation therapy. This case highlights the importance of detailed gene mutation analysis in patients with triple-negative MF.

一名 47 岁的妇女因皮下出血就诊。血液检查显示白细胞增多、贫血和血小板减少。骨髓活检诊断为原发性骨髓纤维化(aaDIPSS,DIPSS-plus:中II级风险)。外周血中未检测到 JAK2、CALR 和 MPL 突变,但骨髓标本的靶向测序发现 U2AF1 存在双突变(Q157R、S34F)。移植后骨髓检查显示,第55天时供体出现完全嵌合。异体移植两年后,患者仍未复发。尽管U2AF1基因异常是原发性骨髓纤维化的不良预后因素,但由于及时进行了移植治疗,该患者的长期预后良好。本病例强调了对三阴性骨髓纤维化患者进行详细基因突变分析的重要性。
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引用次数: 0
Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.197
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引用次数: 0
[Pyogenic spondylitis after Corynebacterium striatum blood stream infection following allogeneic hematopoietic stem cell transplantation for malignant lymphoma]. [因恶性淋巴瘤接受异体造血干细胞移植后,因纹状体科里奈杆菌血流感染引发化脓性脊柱炎]。
Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.243
Takumi Nishikawa, Masuho Saburi, Kentaro Nagamatsu, Keiichi Uraisami, Hiroyuki Takata, Yasuhiko Miyazaki, Eiichi Ohtsuka

Patient 1 was a 70-year-old woman with refractory diffuse large B-cell lymphoma who received allogeneic peripheral blood stem cell transplantation from an HLA-haploidentical related donor. Upper back pain appeared on day63, and Th8-Th9 pyogenic spondylitis was diagnosed based on magnetic resonance imaging (MRI). Blood culture on day14 identified Corynebacterium striatum as the causative bacteria of blood stream infection (BSI). The pyogenic spondylitis resolved after treatment with daptomycin for 2 months. Patient 2 was a 65-year-old man with relapsed angioimmunoblastic T-cell lymphoma who received bone marrow transplantation from an HLA-DR single-antigen-mismatched unrelated donor. Lower back pain appeared on day30, and L4-L5 pyogenic spondylitis was diagnosed based on MRI. Blood culture was negative. Daptomycin and clindamycin were selected for treatment based on the drug susceptibility of bacteria that had caused pre-engraftment BSI (Escherichia coli on day3 and Corynebacterium striatum on day9), and the pyogenic spondylitis resolved after 6 months of this treatment. Pyogenic spondylitis should be considered in the differential diagnosis of back pain accompanied by BSI before engraftment in allogeneic hematopoietic stem cell transplant recipients.

患者1是一名70岁的女性,患有难治性弥漫大B细胞淋巴瘤,接受了HLA同种异体干细胞移植。第63天出现上背痛,根据磁共振成像(MRI)诊断为Th8-Th9化脓性脊柱炎。第 14 天的血液培养发现,纹状体棒状杆菌是血流感染(BSI)的致病菌。使用达托霉素治疗 2 个月后,化脓性脊柱炎痊愈。患者2是一名65岁的男性,患有复发性血管免疫母细胞T细胞淋巴瘤,接受了HLA-DR单抗原不匹配非亲属供者的骨髓移植。第30天出现下背部疼痛,根据核磁共振成像诊断为L4-L5化脓性脊柱炎。血液培养呈阴性。根据引起移植前 BSI 的细菌(第 3 天为大肠埃希菌,第 9 天为纹状杆菌)对药物的敏感性,选择了达托霉素和林可霉素进行治疗,经过 6 个月的治疗,化脓性脊柱炎得到缓解。异体造血干细胞移植受者在移植前出现背痛并伴有BSI时,应将化脓性脊柱炎考虑在鉴别诊断中。
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引用次数: 0
[Infection stress and a driver mutation interact to promote transformation to hematological malignancies]. [感染压力和驱动突变相互作用,促进向血液恶性肿瘤的转化]。
Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.702
Goro Sashida

Myelodysplastic syndrome (MDS) is a refractory cancer that arises from hematopoietic stem cells and predominantly affects elderly adults. In addition to driver gene mutations, which are also found in clonal hematopoiesis in healthy elderly people, systemic inflammation caused by infection or collagen disease has long been known as an extracellular factor in the pathogenesis of MDS. Wild-type HSCs have an "innate immune memory" that functions in response to infection and inflammatory stress, and my colleagues and I used an infection stress model to demonstrate that the innate immune response by the TLR-TRIF-PLK-ELF1 pathway is similarly critical in impairment of hematopoiesis and dysregulation of chromatin in MDS stem cells. This revealed that not only are MDS stem cells expanded by the TRAF6-NF-kB pathway, the innate immune response is also involved in generating MDS stem cells. In this review, I will present research findings related to "innate immune memory," one of the pathogenic mechanisms of blood cancer, and discuss future directions for basic pathological research and potential therapeutic development.

骨髓增生异常综合征(MDS)是一种由造血干细胞引起的难治性癌症,主要影响老年人。除了在健康老年人的克隆性造血中也发现的驱动基因突变外,感染或胶原病引起的全身炎症早已被认为是MDS发病机制中的细胞外因素。野生型造血干细胞具有 "先天性免疫记忆",可对感染和炎症应激做出反应。我和我的同事利用感染应激模型证明,TLR-TRIF-PLK-ELF1途径的先天性免疫反应同样是MDS干细胞造血功能受损和染色质失调的关键。这揭示了MDS干细胞不仅通过TRAF6-NF-kB途径扩增,先天性免疫反应也参与了MDS干细胞的生成。在这篇综述中,我将介绍与血癌致病机制之一的 "先天免疫记忆 "有关的研究成果,并讨论基础病理研究和潜在治疗开发的未来方向。
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引用次数: 0
[Recent findings and advances in treatment of myeloproliferative neoplasms]. [骨髓增生性肿瘤治疗的最新发现和进展]。
Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.375
Yuka Sugimoto

Many novel agents have been developed for BCR::ABL1-negaive myeloproliferative neoplasms (MPN), namely, polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). Some of these agents not only achieve hematologic complete response, reduce spleen size, and alleviate constitutional symptoms, but also induce molecular response, which means that they reduce the allele burden of driver gene mutations. These agents also prevent and alleviate fibrosis in bone marrow, which reduces the incidence of thrombotic events and disease progression and might improve prognosis. This article discusses the latest findings and promising treatments, including ongoing clinical trials, in PV, ET, and PMF.

针对BCR::ABL1-negaive骨髓增殖性肿瘤(MPN),即真性红细胞增多症(PV)、原发性血小板增多症(ET)和原发性骨髓纤维化(PMF),已开发出许多新型药物。其中一些药物不仅能获得血液学完全应答、缩小脾脏体积和缓解体征,还能诱导分子应答,即减少驱动基因突变的等位基因负荷。这些药物还能预防和缓解骨髓纤维化,从而降低血栓事件和疾病进展的发生率,并可能改善预后。本文讨论了针对骨髓增生性白血病、骨髓移植和骨髓纤维化的最新发现和有前景的治疗方法,包括正在进行的临床试验。
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引用次数: 0
Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.439
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引用次数: 0
[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
[Clostridioides difficile infection diagnosed by nucleic acid amplification test in a patient with Epstein-Barr Virus-related T-cell lymphoproliferative disorder]. [通过核酸扩增检验诊断出一名与爱泼斯坦-巴氏病毒相关的 T 细胞淋巴增生性疾病患者感染了艰难梭菌]。
Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.732
Hideshige Seki, Megumi Yasunaga, Ken Morita, Mineo Kurokawa

Steroid usage poses a risk of Clostridioides difficile infection (CDI), but high-dose corticosteroid treatment can lead to false-negative CD toxin test results. Moreover, CDI-induced nausea can complicate administration of oral antibiotics, which are typically the primary therapy for CDI. In the present case, a 43-year-old woman diagnosed with EBV-associated T-cell post-transplant lymphoproliferative disorder developed CDI during treatment with cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP). Following five cycles of CHOP, the patient presented with nausea and diarrhea. CT scans revealed swelling in the ileocecal to transverse area of the colon. While the glutamate dehydrogenase (GDH) antigen test result was positive, the CD toxin test result was negative. However, the nucleic amplification test (NAAT) result was positive, confirming the diagnosis of CDI. Oral treatment with fidaxomicin was initially impractical due to persistent nausea. Instead, treatment began with intravenous metronidazole, and was later switched to fidaxomicin pills. Symptoms improved notably within 10 days, and the patient ultimately made a complete recovery. This case underscores the significance of exploring alternative approaches to CDI management, particularly in immunosuppressed patients.

使用类固醇会带来艰难梭菌感染(CDI)的风险,但大剂量皮质类固醇治疗会导致 CD 毒素检测结果呈假阴性。此外,CDI 引起的恶心会使口服抗生素的治疗复杂化,而口服抗生素通常是 CDI 的主要治疗方法。在本病例中,一名被诊断患有 EBV 相关 T 细胞移植后淋巴组织增生性疾病的 43 岁女性在接受环磷酰胺、多柔比星、长春新碱和泼尼松龙(CHOP)治疗期间出现了 CDI。接受五个周期的CHOP治疗后,患者出现恶心和腹泻。CT 扫描显示结肠回盲部至横结肠区域肿胀。谷氨酸脱氢酶(GDH)抗原检测结果呈阳性,CD毒素检测结果呈阴性。然而,核扩增试验(NAAT)结果呈阳性,确诊为 CDI。由于持续恶心,最初无法使用非达霉素口服治疗。于是,患者开始接受甲硝唑静脉注射治疗,后来又改用非达霉素药片。症状在10天内明显改善,患者最终完全康复。该病例强调了探索其他方法治疗 CDI 的重要性,尤其是对免疫抑制患者。
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引用次数: 0
期刊
[Rinsho ketsueki] The Japanese journal of clinical hematology
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