Dermatology

British Medical Journal, March 25, 2000 by Peter A Foley

Kaposi's sarcoma and human herpesvirus 8

The recently discovered Kaposi's sarcoma associated herpesvirus or human herpesvirus 8 has been detected in all forms of Kaposi's sarcoma, including the classic sporadic form (fig 3), the form associated with AIDS, the form not associated with HIV immunosuppression, the African endemic form, and the rare familial forms. It has therefore been regarded as a causative factor in the

pathogenesis of Kaposi's sarcoma. Human herpesvirus 8 has also been associated with body cavity based lymphoma (often coinfected with Epstein-Barr virus) and multicentric Castelman's disease, which are also commonly associated with HIV infection. Human herpesvirus 8 contains three potential oncogenes that can transform cell lines in vitro. Human herpesvirus 8 DNA has been localised to the nuclei of tumour cells within Kaposi's sarcoma lesions, and the virus has been detected in peripheral blood mononuclear cells in over half of HIV positive patients with Kaposi's sarcoma.[17-19]

[Figure 3 ILLUSTRATION OMITTED]

Between 70% and 100% of patients with Kaposi's sarcoma have antibodies to human herpesvirus 8 (compared with 1%-5% of the general population). Seroconversion may occur several months before the clinical appearance of the disease, supporting a causative role for herpesvirus in Kaposi's sarcoma. In countries such as southern Italy and Uganda, where classic and endemic Kaposi's sarcoma are relatively common, human herpesvirus 8 is also more widespread.[17 18]

Androgenetic alopecia

Androgenetic alopecia (or male pattern baldness) begins with recession of the frontal hairline. This is followed by thinning over the vertex and then, eventually, complete loss of hair over the crown. It is partially mediated by circulating and locally produced androgens, including testosterone and 5-dihydrotestosterone, combined with a genetic susceptibility, possibly inherited in an autosomal dominant fashion with variable penetrance.[20] Men who have been castrated before puberty and homozygotes for 5 [Alpha]-reductase type II deficiency do not develop androgenetic alopecia.[20 21] 5 [Alpha]-Reductase is the enzyme that converts testosterone to 5-dihydrotestosterone. On the scalp of patients who are predisposed to the condition, androgens lead to miniaturisation, a switch from terminal to vellus or vellus-like follicles, and a reduction in the duration of anagen.[20 22] The concentration of androgen receptor and 5 [Alpha]-reductase activities in frontal hair follicles is greater than in occipital follicles.[23] Higher activities of aromatase, a bifunctional enzyme involved in converting testosterone to oestradiol, are found in occipital hair follicles.[23] This may explain the loss of hair in the frontal area in androgenetic alopecia, while occipital hair is retained. In women, in whom androgenetic alopecia expression is less severe and often spares the frontal hair line, lower concentrations of androgen receptors and 5[Alpha]-reductase activities are found in the frontal hair follicles, and aromatase activities are higher.[23]