Blood:ADAMTS13缺陷和补体过度激活协同导致血栓性微血管病

2019-08-14 MedSci MedSci原创

血浆ADAMTS13活性重度缺陷是血栓性血小板减少性紫癜(TTP)的主要原因,而补体通过替代途径过度激活又导致了非典型溶血性尿毒症综合征(aHUS),TTP和aHUS是血栓性微血管病的两种原型。但从临床和致病机制上区别TTP和aHUS非常具有挑战性。临床报道表明补体激活可能在血浆ADAMTS13活性重度缺陷所引起的TTP发展过程中发挥作用。但目前尚无确凿的实验证据。近日,《血液》杂志上发表一篇文章

血浆ADAMTS13活性重度缺陷是血栓性血小板减少性紫癜(TTP)的主要原因,而补体通过替代途径过度激活又导致了非典型溶血性尿毒症综合征(aHUS),TTP和aHUS是血栓性微血管病的两种原型。但从临床和致病机制上区别TTP和aHUS非常具有挑战性。

临床报道表明补体激活可能在血浆ADAMTS13活性重度缺陷所引起的TTP发展过程中发挥作用。但目前尚无确凿的实验证据。

近日,《血液》杂志上发表一篇文章,研究人员发现无论是在Adamts13-/-小鼠,还是补体因子H (cfh)1206位氨基酸残基杂合突变(cfhW/R)的小鼠,都没有症状,尽管在各组织器官中偶尔存在微血管血栓。

同时携带Adamts13-/-和cfhW/R的小鼠则表现出血小板减少、低血浆结合蛋白、外周血涂片中破碎红细胞增多、血浆乳酸脱氢酶活性增强、BUN和肌酐水平增加,死亡率也升高,与血栓性微血管病变的发展相一致。此外,cfh纯合突变的小鼠(cfhR/R)无论有无携带Adamts13-/-均可发展为严重的血栓性微血管病变。Adamts13-/-cfhR/R组小鼠的死亡率明显高于cfhR/R组。

组织学免疫组织化学分析显示,在被处死或死亡的小鼠中,主要器官组织的末梢小动脉和毛细血管中存在弥散性血小板丰富的血栓。

总而言之,本研究结果证实了重度ADAMTS13缺陷和补体激活在小鼠血栓性微血管病发病机制中具有协同作用。

原始出处:

Liang Zheng, et al.Synergistic effects of ADAMTS13 deficiency and complement activation in pathogenesis of thrombotic microangiopathy. Blood 2019 :blood.2019001040; doi: https://doi.org/10.1182/blood.2019001040

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    2021-09-30 ms3000001741732165

    依然爱你呦

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    2021-08-08 ms3000001741732165

    学习了

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    2019-08-16 般若傻瓜
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    2019-08-16 mgqwxj

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