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microvessels, hemosiderin-laden dermal macrophages, and a conspicuous superficial
perivascular lymphocytic infiltrate. Partial or complete regression may also
occur with chemotherapy.[960]
An important point to remember is that in the absence of distinct features of KS, a
conservative approach is recommended. Rather than mistakenly labeling a patient as having
AIDS, it may be wise to obtain additional clinical information regarding HIV and immune status
or defer a diagnosis of KS to a later date and repeat biopsy. A true lesion of KS will progress--
with few exceptions--to a more diagnostic stage.

OTHER SKIN NEOPLASMS.— Since the advent of antiretroviral therapy (ART), non-
AIDS defining cutaneous malignancies have become more frequent than Kaposi sarcoma among
HIV-infected persons. These include basal cell carcinoma, malignant melanoma, and squamous
cell carcinoma. Their appearance does not relate to CD4+ lymphocyte count or to use of ART.
Risk factors are similar to those persons not infected with HIV: increasing age and white
race.[969]
Squamous epithelial dysplasias and malignancies are most frequent in the perianal region,
though squamous cell carcinomas may appear elsewhere. The appearance of such lesions may
be associated with concomitant human papillomavirus (HPV) infection, usually not high-risk
subtypes, which is frequent in HIV-infected persons, particularly when there is a risk factor of
anal intercourse with other males. The presence of the precursor lesion to anal SCC, the
squamous intraepithelial lesion (SIL), has a prevalence of 36% in HIV-positive males who have
sex with males, and 14% in women who are partners of these men. Persons with AIDS have a 3-
to 5-fold increased risk of developing a nonmelanoma skin cancer. Squamous cell carcinoma
(SCC) and basal cell carcinoma (BCC) in patients with HIV infection are similar to those seen
in immunocompetent patients. The ratio of SCC to BCC in HIV-infected patients is
approximately 1:7. Cutaneous SCC may be more aggressive with concomitant HIV infection,
but BCC is not. Most BCCs are the superficial type presenting on the trunk as multiple
lesions.[970]
Melanocytic lesions have been reported in HIV-infected persons at a median age lower
than the general population. Both dysplastic nevi and melanoma may occur in HIV-infected
patients with no prior family history. There is a greater tendency for melanomas to have a
greater depth and to metastasize sooner, compared to non-HIV-infected persons. The degree of
immunosuppression, indicated by lower CD4 counts, appears to contribute to findings.[591,592]
Cutaneous T-cell lymphoma (CTCL) has been described in patients infected with HIV,
but this entity is best termed atypical or pseudo-CTCL. Pseudo-CTCL is a lymphoproliferative
disorder that appears identical to mycosis fungoides (MF), with erythematous patches, plaques,
and tumors, or as a Sézary syndrome–like picture with erythroderma and circulating convoluted
lymphocytes. Both Sézary and pseudo-Sézary syndromes have been described in HIV patients.
Pseudo-CTCL may mimic other skin diseases, including persistent generalized eruption of
erythematous papules, drug eruption, photodistributed eruption, or deep nodules and ulcers in the
skin.56 In most cases of MF or Sézary syndrome, the neoplastic cells are clonal, but in most
pseudolymphomas, the proliferation is polyclonal. The typical microscopic finding is that of a
psoriasiform, lichenoid pattern with limited infiltration of the epidermis by small lymphocytes
marking for CD4 or CD8. Since pseudo-CTCL is not a true lymphoma, chemotherapy is not
recommended and therapy may consist of topical corticosteroids or psoralen ultraviolet A
therapy.[970]