Corticosteroid therapy in a patient with cerebral amyloid angiopathy-related inflammation.

Corticosteroid therapy in a patient with cerebral amyloid angiopathy-related inflammation.
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DOI:
10.1186/1742-2094-10-39
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发表时间:
2013-03-16
影响因子:
9.3
通讯作者:
Inuzuka T
Inuzuka T
中科院分区:
医学1区
文献类型:
--
作者:
Kimura A;Sakurai T;Yoshikura N;Hayashi Y;Takemura M;Takahashi H;Inuzuka T

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本文研究了1例淀粉样脑血管病相关炎症患者经激素治疗后脑脊液中抗A-β抗体、A-β蛋白和IL-8水平的动态变化。CAA-ri的诊断是通过脑活检来确定的。检测8个月病程中23个时间点脑脊液中抗Aβ42抗体、Aβ40、Aβ42和IL-8水平。脑脊液标本分为口服糖皮质激素治疗前(n=12)和治疗后(n=11)两组。我们比较了治疗前和治疗后的脑脊液样本的这些水平。慢性再障患者口服糖皮质激素治疗前脑脊液中抗Aβ-42抗体和IL-8水平明显高于治疗后。患者脑脊液中抗Aβ42抗体水平与IL-8水平呈正相关。口服糖皮质激素治疗前后脑脊液中Aβ40和Aβ42的平均水平无显著差异。提示抗Aβ42抗体和IL-8的自身炎症过程可能参与了CAARI的发病过程,糖皮质激素治疗直接影响抗Aβ42抗体和IL 8的水平。综上所述,CAA-ri脑病是一种复发性或进行性疾病,可以通过适当的免疫抑制治疗来治疗。脑脊液中抗A-β-42抗体是监测CAARI疗效的有用生物学指标。
We studied longitudinal changes of the levels of anti-amyloid β (anti-Aβ) antibody, amyloid β (Aβ) protein, and interleukin 8 (IL-8) in cerebrospinal fluid (CSF) of a patient with cerebral amyloid angiopathy-related inflammation (CAA-ri) in whom steroid treatment resulted in clinical improvement. The diagnosis of CAA-ri was established with brain biopsy. Levels of anti-Aβ 42 antibody, Aβ 40, Aβ 42 and IL-8 in CSF were measured in the CAA-ri patient at 23 time points in the 8-month clinical course. These CSF samples were divided into 2 groups: those obtained before (n = 12) and those after (n = 11) oral corticosteroid therapy was started. We compared these levels between CSF samples obtained before and after therapy. The mean levels of anti-Aβ 42 antibody and IL-8 were significantly higher in CSF samples of the CAA-ri patient before oral corticosteroid therapy than those after therapy. A positive correlation was noted between levels of anti-Aβ 42 antibodies and IL-8 in CSF of this patient. There were no significant differences of mean levels of Aβ 40 and Aβ 42 between CSF samples obtained before and after oral corticosteroid therapy. It was possible that the autoinflammatory process with anti-Aβ 42 antibodies and IL-8 may have been involved in the pathogenesis of CAA-ri, and that corticosteroid therapy directly affected levels of anti-Aβ 42 antibody and IL-8. In summary, CAA-ri encephalopathy is a relapsing or progressive disorder and may be treatable by adequate immunosuppressive therapy. The anti-Aβ 42 antibody in CSF is a useful biological marker for therapeutic monitoring of CAA-ri.
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