持续感染COVID-19后白血病的发展

O. Khaniukov, L. A. Pisotska, O. V. Bucharskyi, O. S. Shchukina
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引用次数: 0

摘要

本研究的目的是回顾关于COVID-19感染后健康人群白血病病例的文献,并描述我们自己的观察结果。材料和方法。使用PubMed/MEDLINE数据库对26篇关于COVID-19患者白血病过程诊断的文献来源进行回顾和分析。研究中采用了分析方法和文献语义学方法。结果和讨论。COVID-19感染的许多方面,特别是其并发症和长期健康后果,仍然未知。已经公布了COVID-19期间血液检查的各种反应性变化。白细胞增多症、白细胞减少症、中性粒细胞增多症、淋巴细胞增多症和淋巴细胞减少症、血小板减少症和罕见的血小板增多症是最常见的。检测到的变化通常在患者身上无法观察到。有报道称,最近感染COVID-19后出现了白血病。因此,研究这类患者在病毒感染期间的临床表现和造血功能的特点,以及白血病的初始表现,是有意义的。Costa B.和合著者报告了以前健康的年轻患者白血病发展过程的病例。患者年龄31-35岁,血液检查正常,在COVID-19后约2-3个月出现白血病的表现。病程均不严重。1例低色性贫血中检出轻度小红细胞增多。恶性血液病的发展,这些患者的预后不良的过程和治疗反应引起了人们的关注。这些是t细胞急性淋巴细胞白血病,骨髓增生异常综合征,急性骨髓性白血病伴骨髓三叉神经发育不良,提示既往骨髓增生异常综合征。Nekooghadam s.m.和合著者报告了一例急性髓性白血病的病例,该病例发生在一名男子从COVID-19恢复1.5个月后。感染的过程很严重。血液检查显示轻微的白细胞增多。所述白血病病例的临床表现包括胃肠病和贫血综合征。骨髓造血分析中2倍或3倍严重全血细胞减少和发育不良更为常见。低母细胞血症是一个特征。一些作者认为,SARS-Cov-2在白细胞形成中起作用。这主要归因于由病毒引起的肾素-血管紧张素系统的不平衡,这在几个机制中触发了白细胞生成。对病毒感染的异常免疫反应可引发继发性突变事件,从而导致白血病的临床发展。除了SARS-CoV-2对肾素-血管紧张素系统的影响外,其他潜在的癌症发展机制可能是其基础。特别是,COVID-19与t细胞衰竭和致癌途径的激活有关,包括JAK-STAT、MAPK和NF-kB。冠状病毒非结构蛋白通过增加rchy1介导的p53凋亡相关降解来稳定因子。我们所描述的急性白血病过程的病例的特点是快速的非典型病程,神经系统症状,住院期间外周血全血细胞减少,以及母细胞线性形态的改变。结论。根据文献,持续的COVID-19后的白血病过程更多的是急性髓系变异伴造血发育不良和严重的非典型病程。在有肿瘤病史或血液检查有变化的情况下,有必要对COVID-19患者进行血液学监测。建议在2-3个月后控制血象
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Development of Leukemia after a Sustained COVID-19 Infection
The purpose of the study was to review the literature on cases of leukemia in healthy people after the COVID-19 infection with a description of our own observation. Materials and methods. 26 literature sources were reviewed and analyzed using the PubMed/MEDLINE database regarding diagnosis of the leukemic process in patients after COVID-19. Analytical and bibliosemantic methods were used in the research. Results and discussion. Many aspects of the COVID-19 infection, especially its complications and long-term health consequences, are still unknown. Various reactive changes in blood tests during COVID-19 have been published. Leukocytosis, leukopenia, neutrophilia, lymphocytosis and lymphocytopenia, thrombocytopenia and rarely thrombocytosis were most often detected. The detected changes were usually not observable in patients. There are reports of leukemia after a recent COVID-19. Therefore, studying the features of the clinical picture and hematopoiesis in such patients during a viral infection, as well as at the initial manifestations of leukemia, is relevant. Costa B. and co-authors report cases of the development of the leukemic process in previously healthy young patients. Patients are aged 31-35 years with normal blood tests, in whom the manifestation of leukemia appeared approximately 2-3 months after COVID-19. The course of COVID-19 was not severe in all. Mild microcytaria was detected in one case of hypochromic anemia. The development of malignant hematological diseases in these patients with an unfavorable prognosis for the course and response to treatment attracts attention. These was T-cell acute lymphoblastic leukemia, myelodysplastic syndrome, acute myeloid leukemia with trigeminal dysplasia in the bone marrow, suggesting previous myelodysplastic syndrome. Nekooghadam S. M. and co-authors presented a case of acute myeloid leukemia in a man after recovery from COVID-19 after 1.5 months. The course of the infection was severe. The blood test showed slight leukocytosis. Manifestations of the described cases of leukemia included clinical gastroenteropathy and anemic syndrome. Two- or three-fold severe pancytopenia and dysplasia were more common in the analysis of bone marrow hematopoiesis. Low blastemia was a feature. Some authors suggest that SARS-Cov-2 plays a role in leukogenesis. The leading role in this is attributed to the imbalance of the renin-angiotensin system caused by the virus, which triggers leukogenesis in several mechanisms. An abnormal immune response to a viral infection can trigger secondary mutational events, contributing to the clinical development of leukemia. In addition to the effect of SARS-CoV-2 on renin-angiotensin system, other mechanisms of the potential development of cancer may underlie it. In particular, COVID-19 has been associated with T-cell exhaustion and activation of oncogenic pathways, including JAK-STAT, MAPK, and NF-kB. The coronavirus non-structural protein stabilizes factors by increasing RCHY1-mediated apoptosis-associated degradation of p53. The case of an acute leukemic process described by us was distinguished by a rapid atypical course, neurological symptoms, pancytopenia in peripheral blood during hospitalization, and a changed linear morphology of blast cells. Conclusion. According to the literature, the leukemic process after a sustained COVID-19 more often has an acute myeloid variant with hematopoietic dysplasia and a severe atypical course. Hematological monitoring of patients who have undergone COVID-19 in the presence of an oncology history or changes in the blood test during recovery from it is necessary. It is advisable to have a control of the hemogram after 2-3 months
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