Pseudoepitheliomatous hyperplasia in lichen sclerosus of the vulva
Pseudoepitheliomatous hyperplasia in lichen sclerosus of the vulva
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DOI：
10.1097/00004347-200301000-00012
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发表时间：
2003-01-01
影响因子：
2.4
通讯作者：
Scurry, J
中科院分区：
文献类型：
--
作者：
Lee, ES;Allen, D;Scurry, J
在长期存在的外阴硬化性苔藓（LS）伴表皮增厚中，真皮内的小触手或鳞状细胞巢并不少见。我们最近遇到的情况下，分离巢分化良好的鳞状细胞在真皮很难区分鳞状细胞癌（SCC）。进一步的活组织检查显示类似的巢起源于每个毛囊。我们假设诊断为多灶性假上皮瘤样增生（PEH）来解释这一现象。由于我们在LS的背景下找不到PEH的参考，我们回顾了92例生殖器外和外阴LS伴或不伴癌的妇女的活检，以确定其频率和组织学表现。排除索引病例的研究人群包括10名肛门外生殖器LS女性，58名外阴LS无癌，24名外阴LS伴癌。记录PEH的存在、表皮厚度、主要真皮胶原蛋白变化、炎症程度以及纤维蛋白和红细胞的存在。记录是否存在慢性单纯性苔藓（LSC）、鳞状细胞增生（SCH）和分化的外阴上皮内瘤变（VIN）。仅在外阴LS中发现PEH，其中7/58（12.1%）例无癌女性、1/24（8.3%）例癌女性和0/10（0%）例肛门外LS女性中发现PEH。观察到两种形式的PEH：主要为表皮7/8（87.5%）和主要为滤泡1/8（12.5%）。PEH与表皮厚度增加、真皮水肿减少、真皮炎症增加、新鲜纤维蛋白和红细胞外渗相关。在所有病例中，均存在相关的LSC，但无SCH或分化的VIN。总之，PEH可以解释许多情况下，真皮触手和分离鳞状巢外阴LS与LSC。与新鲜纤维蛋白和红细胞的相关性表明PEH可能是对组织损伤的反应。PEH与SCC的区别在于其缺乏胶原蛋白，局限于异常胶原蛋白和有限的生长。病理学家在诊断LS伴表皮增厚的PEH时必须谨慎，仔细寻找基底层和上覆表皮或真皮增生中分化VIN的其他特征。我们不知道PEH是否发生在分化的VIN中，如果发生，如何将其与SCC区分开来。
Small tentacles or separated nests of squamous cells in the dermis are not uncommonly seen in long-standing vulvar lichen sclerosus (LS) associated with epidermal thickening. We recently encountered a case where separated nests of well-differentiated squamous cells in the dermis were difficult to distinguish from squamous cell carcinoma (SCC). Further biopsies showed similar nests originating from every hair follicle. We postulated a diagnosis of multifocal pseudoepitheliomatous hyperplasia (PEH) to explain this phenomenon. Because we could find no reference to PEH in the setting of LS, we reviewed the biopsies of 92 women with extragenital and vulvar LS with and without carcinoma to determine its frequency and histological appearance. The study population, which excluded the index case, comprised 10 women with extra-anogenital LS, 58 with vulvar LS without carcinoma, and 24 with vulvar LS with carcinoma. The presence of PEH, epidermal thickness, predominant dermal collagen change, degree of inflammation, and presence of fibrin and red blood cells were recorded. The presence or absence of lichen simplex chronicus (LSC), squamous cell hyperplasia (SCH), and differentiated vulvar intraepithelial neoplasia (VIN) were recorded. PEH was identified only in vulvar LS, where it was seen in 7/58 (12.1%) women without carcinoma, 1/24 (8.3%) with carcinoma, and 0/10 (0%) with extra-anogenital LS. Two forms of PEH were seen: predominantly epidermal 7/8 (87.5%) and predominantly follicular 1/8 (12.5%). PEH was associated with increased epidermal thickness, less dermal edema, more dermal inflammation, fresh fibrin, and red blood cell extravasation. In all cases, there was associated LSC, but there was no SCH or differentiated VIN. In conclusion, PEH may explain many of the cases of dermal tentacles and separated squamous nests in vulvar LS with LSC. The association with fresh fibrin and red blood cells suggests that PEH might be a reaction to tissue damage. PEH is distinguished from SCC by its lack of atypia, confinement to the abnormal collagen, and limited growth. The pathologist must be careful about making a diagnosis of PEH in LS with epidermal thickening, looking carefully for basal atypia and other features of differentiated VIN in the overlying epidermis or dermal proliferation. We do not know whether PEH occurs in differentiated VIN and, if it does, how it could be distinguished from SCC.