内脏利什曼病患者的临床结果、外周血和骨髓细胞形态学特征之间的关系。

Maria Aline Ferreira De Cerqueira, Alaíde Maria Rodrigues Pinheiro, Dorcas Lamounier Costa, Carlos Henrique Nery Costa
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引用次数: 0

摘要

导言:内脏利什曼病是一种细胞内单核吞噬细胞寄生虫,主要分布在骨髓和脾脏。全血细胞计数(CBC)显示贫血、白细胞减少和血小板减少的发病机制尚不清楚。我们的研究旨在比较全血细胞计数与骨髓细胞形态学特征及其与临床结果的关联,以澄清这一相关问题:方法:由两名血液学专家对 118 名患者的血细胞计数和骨髓进行描述,并比较两者之间的关系和死亡率:结果:外周血细胞减少是常见的结果,尤其是贫血,几乎在所有患者中都可见到。血红蛋白、中性粒细胞和血小板计数与死亡结果之间没有关系。61.9%的病例骨髓细胞正常。骨髓增生异常的情况很常见,49.1%的样本存在粒细胞生成障碍。此外,72%的重度贫血患者出现红细胞增生。骨髓细胞减少、红细胞增多和红细胞生成障碍的患者似乎患病风险更高:研究结果表明,内脏利什曼病患者的骨髓对炎症事件表现出一种反应模式,从而调节细胞因子和其他集落生长因子。这种代偿反应可能是发育不良和无效的,并产生不同程度的外周细胞减少症。需要进一步研究以明确其中涉及的信号通路,这些通路将来可能被用作治疗工具。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Association between clinical outcomes, peripheral blood and cytomorphologic features of bone marrow in visceral leishmaniasis.

Introduction: An intracellular parasite of mononuclear phagocytes, mainly distributed in the bone marrow and the spleen, causes visceral leishmaniasis. Complete blood count (CBC) reveals the poorly understood pathogenesis of anemia, leukopenia and thrombocytopenia. Our study aimed to compare the CBC with bone marrow cytomorphological features and their association with clinical outcomes to clarify this relevant issue.

Methods: The CBC and bone marrow of 118 patients were described by two hematologists and compared to check their association with each other and mortality.

Results: Peripheral cytopenias were common findings, particularly anemia, as seen in almost all patients. No relationship was found between values of hemoglobin, neutrophils and platelet count with fatal outcomes. The bone marrow was normocellular in 61.9% of the cases. Dysplasia figures were frequent and 49.1% of the samples had dysgranulopoiesis. Additionally, erythroid hyperplasia was found in 72% of the patients with severe anemia. Patients with reduced bone marrow cellularity, erythroid hypercellularity and dyserythropoiesis seem to have a riskier disease.

Conclusion: The study results suggest that the bone marrow of patients with visceral leishmaniasis manifests a reactional pattern to the inflammatory event, thereby modulating cytokines and other colony growth factors. This compensatory response may be dysplastic and ineffective and generate peripheral cytopenias of varying intensity. Further studies are needed to clarify the signaling pathways involved, which may be used as therapeutic tools in the future.

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