Kim Sunzoo, Jun Jae Hun, Kim Jeongshik, Kim Do Won, Jang Yong Hyun, Lee Weon Ju, Chung Ho Yun, Lee Seok-Jong
Department of Pathology, Kyungpook National University Hospital, Kyungpook National University School of Medicine Daegu, South Korea.
Int J Clin Exp Pathol. 2013 Nov 15;6(12):2912-8. eCollection 2013.
Intravascular papillary endothelial hyperplasia (IPEH) is histopathologically characterized by endothelium-lined papillary structures encircling an acellular fibrin core. The process of IPEH pathogenesis is unclear. The purpose of our study was to identify histopathological and immunohistochemical characteristics of IPEH to better understand the pathogenesis of this disease. After reviewing microscopic and medical records from Kyungpook National University Hospital, we selected 16 cases of IPEH. Masson's trichrome and immunohistochemical staining as well as hematoxylin-eosin staining for 16 cases of IPH were performed. Immunohistochemical studies included CD31, CD68, mast cell tryptase, hypoxia-inducible factor-1 (HIF-1α), and vascular endothelial growth factor (VEGF). Sections from all our cases showed three distinct histological regions including a papillary portion with hyalinized fibrous or fibroblastic cores, an area containing an unorganized thrombus, and organization area with an ingrowth of endothelial cells, myofibroblasts, and fibroblasts. In the organization area, HIF-1α-positive cells were identified in the loose connective tissue. Endothelial cells forming vascular channels were negative for HIF-1α while VEGF was highly expressed in both interstitial mononuclear and endothelial cells. In the papillary portion, the cellular cores were strongly positive for both HIF-1α and VEGF, but the acellular cores were negative. Our investigation confirmed that IPEH is a reactive lesion that incidentally arises during the organization process of older thrombi. It was also found that HIF-1α and VEGF expression was dependent on the thrombus remodeling stage in cases of IPEH.
血管内乳头状内皮增生(IPEH)在组织病理学上的特征是内皮细胞衬里的乳头状结构围绕无细胞纤维蛋白核心。IPEH的发病机制尚不清楚。我们研究的目的是确定IPEH的组织病理学和免疫组化特征,以更好地理解这种疾病的发病机制。在回顾庆北国立大学医院的显微镜和病历后,我们选择了16例IPEH病例。对16例IPH进行了Masson三色染色、免疫组化染色以及苏木精-伊红染色。免疫组化研究包括CD31、CD68、肥大细胞类胰蛋白酶、缺氧诱导因子-1(HIF-1α)和血管内皮生长因子(VEGF)。我们所有病例的切片显示出三个不同的组织学区域,包括一个具有透明变性纤维或成纤维细胞核心的乳头状部分、一个含有无组织血栓的区域以及一个有内皮细胞、肌成纤维细胞和成纤维细胞向内生长的机化区域。在机化区域,在疏松结缔组织中发现了HIF-1α阳性细胞。形成血管通道的内皮细胞HIF-1α呈阴性,而VEGF在间质单核细胞和内皮细胞中均高表达。在乳头状部分,细胞核心HIF-1α和VEGF均呈强阳性,但无细胞核心呈阴性。我们的研究证实,IPEH是一种在陈旧血栓机化过程中偶然出现的反应性病变。还发现,在IPEH病例中,HIF-1α和VEGF的表达取决于血栓重塑阶段。