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抗磷脂抗体、先兆子痫和系统性红斑狼疮患者胎盘组织中膜联蛋白A5、C3b、C4d和C5b-9无明显免疫组化分布。

Absence of Distinct Immunohistochemical Distribution of Annexin A5, C3b, C4d, and C5b-9 in Placentas From Patients With Antiphospholipid Antibodies, Preeclampsia, and Systemic Lupus Erythematosus.

作者信息

Matrai Cathleen E, Rand Jacob H, Baergen Rebecca N

机构信息

Department of Pathology and Laboratory Medicine, New York Presbyterian Hospital-Weill Cornell Medical College, New York, New York.

出版信息

Pediatr Dev Pathol. 2019 Oct;22(5):431-439. doi: 10.1177/1093526619836025. Epub 2019 Mar 28.

DOI:10.1177/1093526619836025
PMID:30922166
Abstract

INTRODUCTION

In pregnancy, the presence of preeclampsia (PEC), systemic lupus erythematosus (SLE), and/or antiphospholipid antibody syndrome (APLS) is characterized by poor obstetric outcomes, with potential adverse effects for both mother and fetus. Although the histopathologic changes observed in these entities have been well established, the pathogenic mediators associated with tissue injury are poorly understood.

METHODS

Forty placentas were evaluated, including 10 patients with preeclampsia, 9 with SLE, 11 with APLS, and 10 disease-free controls. Each case was subjected to a panel of immunohistochemical markers including C3b, C4d, Annexin A5, and C5b-9. Staining was graded on intensity and distribution.

RESULTS

C4d staining was distinctly different among disease groups and controls. Moreover, 6/10 PEC cases, 3/9 SLE cases, and 4/11 APLS cases showed at least focal staining for C4d. All controls were negative. Annexin A5 (AnxA5) staining showed intrinsic variability in all disease groups, while 10/10 controls showed diffuse, strong staining (2+ or 3+). C3b staining was heterogeneous among groups.

DISCUSSION

Previously, antiphospholipid antibody (aPLA)-associated pregnancy complications have been thought to be a consequence of a unique aPLA-mediated pathogenic mechanism. However, the immunohistochemical similarity (increased complement and decreased AnxA5 staining) observed in placentas from patients with APLS, PEC, and SLE suggests that aPLA-associated pregnancy complications may reflect a more general autoimmune mechanism.

摘要

引言

在妊娠期间,子痫前期(PEC)、系统性红斑狼疮(SLE)和/或抗磷脂抗体综合征(APLS)的存在以不良产科结局为特征,对母亲和胎儿均有潜在不良影响。尽管在这些疾病中观察到的组织病理学变化已得到充分证实,但与组织损伤相关的致病介质却知之甚少。

方法

评估了40个胎盘,包括10例子痫前期患者、9例系统性红斑狼疮患者、11例抗磷脂抗体综合征患者和10例无疾病对照。对每个病例进行一组免疫组织化学标记物检测,包括C3b、C4d、膜联蛋白A5和C5b-9。根据强度和分布对染色进行分级。

结果

疾病组和对照组之间C4d染色明显不同。此外,10例子痫前期病例中有6例、9例系统性红斑狼疮病例中有3例、11例抗磷脂抗体综合征病例中有4例至少有局灶性C4d染色。所有对照均为阴性。膜联蛋白A5(AnxA5)染色在所有疾病组中均显示出内在变异性,而10例对照中有10例显示弥漫性强染色(2+或3+)。C3b染色在各组之间存在异质性。

讨论

以前,抗磷脂抗体(aPLA)相关的妊娠并发症被认为是独特的aPLA介导的致病机制的结果。然而,在抗磷脂抗体综合征、子痫前期和系统性红斑狼疮患者的胎盘中观察到的免疫组织化学相似性(补体增加和AnxA5染色减少)表明,aPLA相关的妊娠并发症可能反映了一种更普遍的自身免疫机制。

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