Lanoy E, Dores GM, Madeleine MM et al.Epidemiology of nonkeratinocytic skin cancers among persons with AIDS in the United States. AIDS 23:385-393

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland 20892, USA.
AIDS (London, England) (Impact Factor: 5.55). 01/2009; 23(3). DOI: 10.1097/QAD.0b013e3283213046
Source: DOAJ


Immunosuppression may increase risk for some skin cancers. We evaluated skin cancer epidemiology among persons with AIDS.
We linked data from population-based US AIDS and cancer registries to evaluate risk of nonkeratinocytic skin cancers (melanoma, Merkel cell carcinoma, and appendageal carcinomas, including sebaceous carcinoma) in 497 142 persons with AIDS.
Standardized incidence ratios (SIRs) were calculated to relate skin cancer risk to that in the general population. We used logistic regression to compare risk according to demographic factors, CD4 cell count, and a geographic index of ultraviolet radiation exposure.
From 60 months before to 60 months after AIDS onset, persons with AIDS had elevated risks of melanoma (SIR = 1.3, 95% confidence interval 1.1-1.4, n = 292 cases) and, more strongly, of Merkel cell carcinoma (SIR = 11, 95% confidence interval 6.3-17, n = 17) and sebaceous carcinoma (SIR = 8.1, 95% confidence interval 3.2-17, n = 7). Risk for appendageal carcinomas increased with progressive time relative to AIDS onset (P trend = 0.03). Risk of these skin cancers was higher in non-Hispanic whites than other racial/ethnic groups, and melanoma risk was highest among men who have sex with men. Melanoma risk was unrelated to CD4 cell count at AIDS onset (P = 0.32). Risks for melanoma and appendageal carcinomas rose with increasing ultraviolet radiation exposure (P trend <10 and P trend = 10, respectively).
Among persons with AIDS, there is a modest excess risk of melanoma, which is not strongly related to immunosuppression and may relate to ultraviolet radiation exposure. In contrast, the greatly increased risks for Merkel cell and sebaceous carcinoma suggest an etiologic role for immunosuppression.

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    • "Approximately 20% of cases arise in the periorbital or eyelid area, 40% on an extremity, and 10% on the trunk [4]. Immunodeficiency and immunosuppression, including patients with chronic lymphoid malignancies, HIV, and renal transplants may also play an important role in the development of MCC [3] [5] [6] [7]. Once MCC becomes metastatic, it is a highly aggressive skin cancer with a median survival of only 8 to 12 months. "

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    • "MCC has been recently shown to be associated with a virus, “Merkel-cell-polyomavirus” [4]. An increased risk of MCC has been reported among solid-organ transplant recipients [5, 6] and persons with HIV/AIDS [6, 7], and some studies have reported an association between MCC and other cancers, such as chronic lymphocytic leukemia [8–11]. MCC is considered to be highly aggressive and lethal [1, 2]; in fact, more than half of the persons with non-localized MCC die within 1 year of diagnosis [11]. "
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    • "HIV patients with these skin cancers tend to present at a younger age, manifest with multiple synchronous tumors, higher recurrence rate, treatment-associated complications, and a poorer prognosis compared to their HIV-negative counterparts [54]. MCC was recently shown to harbor a novel polyomavirus, Merkel cell polyomavirus (MCPyV), in the majority of cases [58, 59]. MCPyV can be detected in MCC using polymerase chain reaction (PCR) and the CM2B4 immunohistochemical stain (Figure 4). "
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