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系统性红斑狼疮脑血管病变中的壁内血小板沉积。

Intramural platelet deposition in cerebral vasculopathy of systemic lupus erythematosus.

作者信息

Ellison D, Gatter K, Heryet A, Esiri M

机构信息

Department of Pathology, John Radcliffe Hospital, Oxford.

出版信息

J Clin Pathol. 1993 Jan;46(1):37-40. doi: 10.1136/jcp.46.1.37.

DOI:10.1136/jcp.46.1.37
PMID:8432885
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC501110/
Abstract

AIMS

To test the hypothesis that fragments of platelet thrombi and vascular endothelium are incorporated into the walls of small cerebral vessels in systemic lupus erythematosus (SLE).

METHODS

Six varied necropsy cases of central nervous system (CNS) SLE and 15 controls were studied. The controls were selected to represent a wide range of diseases in which the cerebral circulation is compromised. Tissue sections were stained by standard histochemical and immunocytochemical methods, the latter using antibodies to platelet membrane glycoprotein IIIa (CD61), and vascular endothelium (CD31).

RESULTS

In four of six cases of CNS SLE characterised by small vessel hyalinization and thickening, fragments of platelet membrane were found in the walls of small cortical and meningeal vessels. Similar findings were not evident in two other SLE cases that were characterised by relatively short clinical histories and an acute vasculitis. One control case of severe polyarteritis nodosa showed platelet fragment deposition in arteries larger than the vessels so affected in SLE.

CONCLUSIONS

Previous studies have suggested that neuropsychiatric symptoms in SLE may be related to repeated episodes of vasculitis in small cerebral vessels that are triggered by antiphospholipid antibodies. Concurrent thrombus formation might facilitate the incorporation of platelet fragments into small vessel walls. This process contributes to the thickening and irregularity of small vessels, a major feature of longstanding cases of CNS SLE.

摘要

目的

检验血小板血栓和血管内皮碎片会被纳入系统性红斑狼疮(SLE)患者大脑小血管壁这一假说。

方法

研究了6例中枢神经系统(CNS)SLE的不同尸检病例和15例对照。对照的选择代表了一系列脑循环受损的疾病。组织切片采用标准组织化学和免疫细胞化学方法染色,后者使用抗血小板膜糖蛋白IIIa(CD61)和血管内皮(CD31)的抗体。

结果

在6例以小血管玻璃样变和增厚为特征的CNS SLE病例中,有4例在皮质和脑膜小血管壁中发现了血小板膜碎片。在另外2例以相对较短的临床病史和急性血管炎为特征的SLE病例中,未发现类似结果。1例严重结节性多动脉炎对照病例显示,动脉中血小板碎片沉积,这些动脉比SLE中受影响的血管大。

结论

先前的研究表明,SLE中的神经精神症状可能与抗磷脂抗体引发的大脑小血管反复血管炎发作有关。同时形成的血栓可能会促进血小板碎片融入小血管壁。这一过程导致小血管增厚和不规则,这是CNS SLE长期病例的一个主要特征。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38da/501110/34a79b9b38dd/jclinpath00427-0049-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38da/501110/948f5fca0a33/jclinpath00427-0047-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38da/501110/d821cc5d7dea/jclinpath00427-0047-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38da/501110/403b3e40558c/jclinpath00427-0048-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38da/501110/3bd842f8a844/jclinpath00427-0048-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38da/501110/43901b22c89b/jclinpath00427-0048-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38da/501110/34a79b9b38dd/jclinpath00427-0049-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38da/501110/948f5fca0a33/jclinpath00427-0047-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38da/501110/d821cc5d7dea/jclinpath00427-0047-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38da/501110/403b3e40558c/jclinpath00427-0048-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38da/501110/3bd842f8a844/jclinpath00427-0048-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38da/501110/43901b22c89b/jclinpath00427-0048-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38da/501110/34a79b9b38dd/jclinpath00427-0049-a.jpg

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