Initial lesions of HIV-related Kaposi's sarcoma--a histological, immunohistochemical, and ultrastructural study

• Published in: Archives of dermatological research Vol. 279; no. 8; p. 499
• Main Authors: Schulze, H J, Rütten, A, Mahrle, G, Steigleder, G K
• Format: Journal Article
• Language: English
• Published: Germany 01.01.1987
• Subjects: Acquired Immunodeficiency Syndrome - complications; Capillaries - pathology; Endothelium, Vascular - pathology; Humans; Immunoenzyme Techniques; Microscopy, Electron; Sarcoma, Kaposi - etiology; Sarcoma, Kaposi - pathology; Sarcoma, Kaposi - ultrastructure; Skin - blood supply; Skin - pathology; Skin - ultrastructure
• ISSN: 0340-3696
• 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.