KAPOSI'S SARCOMA: PATHOGENESIS, ULTRASTRUCTURE AND EPIDEMIOLOGY

Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.

KAPOSI'S SARCOMA: PATHOGENESIS, ULTRASTRUCTURE AND EPIDEMIOLOGY

Diss Abstr Int [C]; 52(1):99 1991. Unique Identifier : AIDSLINE ICDB/91676166
Dictor MR; Lunds Universitet, Sweden

Abstract: Kaposi's sarcoma is an abnormal proliferation of lymphatic and venous endothelium beginning at the capillary level. Coupling between lymphatics and veins is suggested histologically by glomeruloid structures at the capillary level and radial venolymphatics during orthograde progression of the lesion along veins. Abnormal lymphatics show a fragmentary or absent basal lamina, no Weibel-Palade bodies and only a few poorly formed cell junctions. Proliferation of endothelium of blood capillaries and venules is accompanied by dissolution of basal lamina, rudimentary cell junctions, reduced numbers of Weibel-Palade bodies and loss of pericyte processes with frequent exaggeration of the irregular projections on endothelial luminal and abluminal surfaces. Ultrastructural signs of disturbed endothelial differentiation, thus, include endothelial tubes surrounded by a pericyte sheath but lacking basal lamina and endothelial tubes with complete basal lamina but no pericyte processes. Faulty differentiation is further indicated by changing immunohistochemical reactivity for endothelial markers during lesional development, which suggests phenotypic instability. Gaps in endothelial vessels of all types can account for lymphaticovenous shunting. The possibility of direct connections between lymphatics and veins must also be considered. Comparison of angiosarcoma and Kaposi sarcoma by DNA flow cytometry shows frequent aneuploidy in the former but relative genomic stability of spindle-cells in the latter until the appearance of nuclear hyperchromasia and irregularity. Analysis of 529 cases of KS in Sweden between 1958 and 1982 prior to the AIDS epidemic indicates a more than twofold increase in incidence beginning in the early 1970's. A transient shift in age specific incidence rates towards younger age groups was suggested. Most cases occurred in the elderly, and women consistently showed poorer survival although death was not attributed to KS. Lymphoproliferative disease was 2.5 times more common than expected, specifically in women.

Keywords: Adult Age Factors Aged Endothelium/ULTRASTRUCTURE Female Human Male Middle Age Sarcoma, Kaposi's/EPIDEMIOLOGY/ETIOLOGY/*ULTRASTRUCTURE Sex Factors THESIS
912130
M91C4079

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