Schulze H J, Rütten A, Mahrle G, Steigleder G K
Department of Dermatology, University of Cologne, Federal Republic of Germany.
Arch Dermatol Res. 1987;279(8):499-503. doi: 10.1007/BF00413279.
Kaposi's sarcoma (KS) in human immunodeficiency virus infection (HIV) has become a rather frequent manifestation of the previously rare disease with fatal outcome. Initial lesions of KS were studied by means of histopathology, immunohistology, and electron microscopy in order to define the earliest alterations. The histopathological changes of initial lesions were distinct, consisting of (1) discrete proliferation of capillary vessels, (2) dissection of collagen by proliferating spindle cells which formed slits, (3) atypical spindle cells arranged in an Indian file pattern, and (4) the lack of any inflammatory cellular infiltrate. Double staining with antibodies against vimentin and immunohistochemical markers for endothelial cells revealed that slits forming vimentin-positive spindle cells displayed laminin, factor VIII, and PAL-E. Atypical vimentin-positive spindle cells arranged in an Indian file pattern inconsistently expressed laminin and factor VIII, but not PAL-E. KS cells rarely stained with the lectin UEA I, not even in case of less advanced dedifferentiation. Electron microscopy showed gradual transformation between spindle cells forming slits and those having lost the ability to form incomplete vessel walls. The present findings support the view that KS develops from the endothelial cells of the blood vessels. The proliferation of atypical endothelial cells as early as in initial lesions and the lack of inflammation favors the primary neoplastic genesis of KS.
卡波西肉瘤(KS)在人类免疫缺陷病毒感染(HIV)中已成为这种先前罕见疾病较为常见的一种表现形式,且预后致命。通过组织病理学、免疫组织学和电子显微镜对KS的初始病变进行研究,以确定最早的改变。初始病变的组织病理学变化明显,包括:(1)毛细血管离散性增生;(2)增殖的梭形细胞将胶原纤维分隔形成裂隙;(3)非典型梭形细胞呈单列排列;(4)缺乏任何炎性细胞浸润。用抗波形蛋白抗体和内皮细胞免疫组化标记物进行双重染色显示,形成波形蛋白阳性梭形细胞的裂隙显示有层粘连蛋白、因子VIII和PAL - E。呈单列排列的非典型波形蛋白阳性梭形细胞不一致地表达层粘连蛋白和因子VIII,但不表达PAL - E。KS细胞很少被凝集素UEA I染色,即使在分化程度较低的情况下也是如此。电子显微镜显示,形成裂隙的梭形细胞与那些已失去形成不完全血管壁能力的梭形细胞之间存在逐渐转变。目前的研究结果支持KS起源于血管内皮细胞的观点。早在初始病变中就出现的非典型内皮细胞增殖以及缺乏炎症,支持了KS的原发性肿瘤发生。