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ulceration, extensive oral KS, non-nodal visceral KS; immune system status of CD4 cell count
less than 150/µL; presence of systemic illness defined as a history of opportunistic infection or
oral thrush, presence of "B" symptoms, performance status less than 70, or other HIV-related
illness (e.g., neurologic disease, lymphoma). The "B" symptoms include: unexplained fever,
night sweats, >10% involuntary weight loss, or diarrhea persisting for more than two
weeks.[545,958] In the era of antiretroviral therapy, the CD4 count provides little prognostic
information, so that a designation of T1S1 indicates poor risk.[959]

HISTOPATHOLOGY OF KAPOSI SARCOMA.-- The histogenesis of Kaposi sarcoma
(KS) is unclear, but the spindle cells are of mesenchymal origin, with features of both
endothelium and smooth muscle. Though KS tends to be multifocal, whether involving the skin
or visceral organs, it is monoclonal in origin, similar to a true neoplasm.[556] An HIV gene
product may be instrumental for inducing neoplasia, with cellular proliferation mediated by
cytokines produced by the KS cells.[545] Kaposi's sarcoma in AIDS has three gross pathologic
patterns of skin involvement: patch, plaque, and tumor.
The early lesions of patch stage KS are clinically as well as microscopically quite
inconspicuous. These flat or macular bluish to reddish-purple lesions often resemble bruises.
Cutaneous lesions may occur anywhere on the trunk and extremities but there is a propensity for
facial involvement. Lesions on the neck, upper trunk and arms may follow the skin cleavage
lines in a dermatomal distribution pattern similar to the lesions of pityriasis rosea.[545]
The patch stage microscopically shows a superficial and perivascular proliferation of
spindle cells. The spindle cells are arranged in parallel arrays around the vessels or beneath the
epidermis. The involved vessels often appear straighter than usual and seem to cut through the
dermis. They tend to be more conspicuous in the immediate vicinity of native dermal vessels
and cutaneous appendages. Protrusion of the normal vascular structures into the lumens of
more ectatic neoplastic vascular spaces produces a promontory sign. The dermal collagen may be
invaded by slit-like vascular spaces lined by a monolayer bland, flattened endothelial cells, often
containing erythrocytes and with a variable degree of erythrocyte extravasation outside the
vascular spaces. Most often the neoplastic cells of KS are spindle-shaped, but they may also
have a fusiform to epithelioid appearance. They have an eosinophilic cytoplasm and may have
prominent round, oval, or fusiform nuclei. Atypical features of nuclear pleomorphism and
hyperchromatism may not be pronounced. In the earliest lesions red blood cells may not be seen.
There can be an inflammatory cell infiltrate of lymphocytes and plasma cells, as well as
hemosiderin-laden macrophages, most prominent around native vessels and skin adnexal
structures.[960]
Helpful findings in very early KS lesions include individually necrotic cells, a
mononuclear cell infiltrate, presence of epithelioid cells, dilated irregular vascular spaces, and
perivascular distribution. This is followed by a marked increase in spindle cells along slightly
widened spaces between the collagen bundles. With passage of time the perivascular spindle cell
proliferation becomes more prominent, and spindle cell proliferation can be observed around the
skin appendages. Red blood cells are present in the slit-like spaces in association with
occasional deposits of golden-brown hemosiderin granules either free or within
macrophages.[961]
The plaque stage is intermediate between the patch stage and the nodular or tumor stage,
and it has some features of both. In its early phase, the plaques show more diffuse dermal
vascular infiltration along with greater cellularity and occasional extension into the underlying