102. PROPOSAL FOR A SYNOPTIC SYSTEM FOR REPORTING OF TEMPORAL ARTERY BIOPSIES
102. PROPOSAL FOR A SYNOPTIC SYSTEM FOR REPORTING OF TEMPORAL ARTERY BIOPSIES
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102. 用于报告颞动脉活检的概要系统的提案
DOI：
10.1093/rheumatology/kez058.042
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发表时间：
2019
期刊：
影响因子：
5.5
通讯作者：
Mackie S
中科院分区：
文献类型：
--
作者：
Mackie S
背景资料：英国巨细胞动脉炎（GCA）患者使用托珠单抗需要区域中心进行病例审查和诊断确认。我们调查了不同病理学家之间报告的一致性，并提出了一个solution.Methods：（1）英国病理学家的审计进行。本文提供了9幅经苏木精和伊红（H&E）染色的颞动脉横断面数字图像，可选择4种诊断类别（正常、正在消退的动脉炎、明确的动脉炎、不确定）。(2)构建了结构化报告模板，包括病理类别（外膜、外膜侵袭性、同心双层、全动脉炎）和是否存在来自文献综述的GCA特征。此外，血管壁各层的炎症被分类为局灶性、多灶性或弥漫性。结果：（1）12名病理医师参加了本次审核，其中12名医师对来自英国GCA联盟的H&E染色切片进行了评分，并采用斯皮尔曼秩和检验（Spearman rank test）对与全动脉炎、管腔闭塞和小动脉周围淋巴细胞浸润相关的特征进行了鉴别。所有患者均报告颞动脉活检> 5年，采用横断面+/-纵切面。9例中2例诊断一致。在其余7例病例中，对诊断类别缺乏一致意见。(2)由1名病理学家对来自英国GCA联盟的88名患者的250个个体动脉切片进行评分。207/250张切片显示动脉炎。134/207例动脉炎切片具有完全发展的全动脉炎病变，与弥漫性外膜炎症相关（表）。管腔闭塞与巨细胞、巨细胞聚集体、中膜破坏、内膜增生和内膜水肿有关。动脉周围淋巴细胞浸润的存在/不存在与任何经典的组织学特征GCA.Conclusion：鉴于诊断类别之间的协议差，我们提出了一个结构化的颞动脉活检报告项目：巨细胞，弥漫性外膜炎症，炎症多层血管壁，全动脉炎，介质破坏，新生血管生成，内膜增生和内膜水肿。由于动脉周围淋巴细胞浸润或血管周围浸润与GCA的任何经典组织学特征无关，因此它们可能不是该疾病的特异性，并且不应单独依赖于临床实践中GCA的组织学诊断确认。分类外膜炎症类型局灶性多灶性弥漫性外膜14/31（45%）7/31（23%）10/31（32%）外膜浸润性2/11（18%）5/11（46%）4/11（36%）同心双层4/29（14%）3/29（10%）22/29（76%）全动脉炎7/134（5%）18/134（13%）109/134（81%）分类外膜炎症类型局灶性多灶性弥漫性外膜14/31（45%）7/31（23%）10/31（32%）外膜浸润性2/11（18%）5/11（46%）4/11（36%）同心双层4/29（14%）3/29（10%）22/29（76%）全动脉炎7/134（5%）18/134（13%）109/134（81%）
Background: Access to tocilizumab for UK patients with giant cell arteritis (GCA) requires a case review and diagnostic confirmation by regional centres. We investigated consistency of reporting between different pathologists, and propose a solution.Methods:(1) An audit of UK pathologists was conducted. 9 digital images of temporal artery transverse sections stained with haematoxylin and eosin (H&E) were presented, with a choice of 4 diagnostic categories (normal, resolving arteritis, definite arteritis, unsure).(2) A structured reporting template was constructed including pathological category (adventitial, adventitial invasive, concentric bilayer, panarteritis) and presence/absence of features of GCA derived from a literature review. In addition, inflammation in each layer of the vessel wall was categorized as focal, multifocal or diffuse. H&E stained slides from the UK GCA Consortium were scored by a pathologist using this template and Spearman rank test was used to identify features associated with panarteritis, luminal occlusion and peri-arteriolar lymphocytic infiltrates.Results:(1) 12 pathologists took part in the audit. All had been reporting temporal artery biopsies for> 5 years using transverse sections+/-longitudinal sections. There was diagnostic consensus on 2 of 9 cases. In the remaining 7 cases, there was lack of agreement about diagnostic category.(2) 250 individual arterial sections from 88 patients in the UK GCA Consortium were scored by 1 pathologist. 207/250 sections showed arteritis. 134/207 sections with arteritis had the fully-developed panarteritis lesion, which was associated with diffuse adventitial inflammation (Table). Luminal occlusion was associated with giant cells, giant cell aggregates, medial destruction, intimal hyperplasia and intimal oedema. Presence/absence of peri-arteriolar lymphocytic infiltrates was not associated with any classical histological feature of GCA.Conclusion: In view of poor agreement between diagnostic categories, we propose items for a structured (synoptic) temporal artery biopsy report: giant cells, diffuse adventitial inflammation, inflammation in multiple layers of the vessel wall, panarteritis, media destruction, neoangiogenesis, intimal hyperplasia and intimal oedema. Since peri-arteriolar lymphocytic infiltrates or infiltrates around the vasa vasorum were not associated with any classical histological feature of GCA, they may not be specific to the disease and should not be relied on alone for confirmation of histological diagnosis of GCA in clinical practice.Disclosures: National Institute for Health Research Medical Research CouncilAbstract 102 Table 1:CategoryAdventitial pattern of inflammationFocalMultifocalDiffuseAdventitial 14/31 (45%) 7/31 (23%) 10/31 (32%)Adventitial invasive 2/11 (18%) 5/11 (46%) 4/11 (36%)Concentric bilayer 4/29 (14%) 3/29 (10%) 22/29 (76%)Panarteritis 7/134 (5%) 18/134 (13%) 109/134 (81%)CategoryAdventitial pattern of inflammationFocalMultifocalDiffuseAdventitial 14/31 (45%) 7/31 (23%) 10/31 (32%)Adventitial invasive 2/11 (18%) 5/11 (46%) 4/11 (36%)Concentric bilayer 4/29 (14%) 3/29 (10%) 22/29 (76%)Panarteritis 7/134 (5%) 18/134 (13%) 109/134 (81%)