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阵发性夜间血红蛋白尿症和骨髓增生异常综合征:细胞遗传学异常消失。

Paroxysmal nocturnal hemoglobinuria and myelodysplastic syndrome: Disappearance of cytogenetic abnormalities.

机构信息

Haematology Department, Vyrides Clinic, Nicosia, Cyprus; University of Nicosia Medical School, Nicosia, Cyprus.

Hematology Department-BMT Unit, G. Papanicolaou Hospital, Thessaloniki; Greece.

出版信息

Cancer Genet. 2021 Jan;250-251:1-5. doi: 10.1016/j.cancergen.2020.11.001. Epub 2020 Nov 6.

Abstract

Paroxysmal nocturnal hemoglobinuria (PNH) is a rare life-threatening disease resulting from clonal hematopoietic stem cell evolution. There is a strong link between PNH and other acquired bone marrow failure syndromes, including myelodysplastic syndrome (MDS). Cytogenetic, morphological abnormalities or both are observed in the range of MDS/PNH diagnosis. Herein, we investigate cytogenetic abnormalities in PNH patients. We found two patients with PNH clones and MDS-associated abnormalities that later disappeared. The first patient, originally diagnosed with MDS and Trisomy 6, developed a large PNH clone. At the time of PNH diagnosis, the abnormal cytogenetic clone was no longer detectable despite persistent trilineage dysplasia. In the second patient, a large PNH clone and MDS-defining abnormality were detected at diagnosis, without evidence of dysplasia. No cytogenetic abnormalities were evident after complement inhibition. Our report adds significant information on the complex link between MDS and PNH, suggesting that distinction between these entities may be difficult in some cases. Especially in transplant eligible patients, the clinical phenotype may be the leading feature for treatment decisions in the era of complement inhibition. Lastly, the transient presence of cytogenetic abnormalities is a unique characteristic of our patients' course that needs to be further elucidated in larger studies.

摘要

阵发性睡眠性血红蛋白尿症(PNH)是一种由克隆性造血干细胞演变而来的罕见危及生命的疾病。PNH 与其他获得性骨髓衰竭综合征之间存在很强的关联,包括骨髓增生异常综合征(MDS)。在 MDS/PNH 的诊断范围内观察到细胞遗传学、形态学异常或两者兼有。在此,我们研究了 PNH 患者的细胞遗传学异常。我们发现了两名患有 PNH 克隆和 MDS 相关异常的患者,这些异常后来消失了。第一例患者最初诊断为 MDS 和三体 6,随后发展出大的 PNH 克隆。在 PNH 诊断时,尽管存在三系发育不良,但异常细胞遗传学克隆不再可检测到。在第二例患者中,在诊断时检测到大的 PNH 克隆和 MDS 定义的异常,没有发育不良的证据。补体抑制后没有明显的细胞遗传学异常。我们的报告增加了 MDS 和 PNH 之间复杂联系的重要信息,表明在某些情况下,区分这些实体可能很困难。特别是在可进行移植的患者中,在补体抑制时代,临床表型可能是治疗决策的主要特征。最后,细胞遗传学异常的短暂存在是我们患者病程的一个独特特征,需要在更大的研究中进一步阐明。

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