In persons with HIV/AIDS (PWHAs), Hodgkin lymphoma (HL) risk is increased. However, HL incidence in PWHAs has unexpectedly increased since highly active antiretroviral therapy (HAART) was introduced. We linked nationwide HIV/AIDS and cancer registry data from 1980 through 2002. Immunity was assessed by CD4 T-lymphocyte counts at AIDS onset. Annual HL incidence rates were calculated for 4 through 27 months after AIDS onset.
IntroductionHodgkin lymphoma (HL) risk is significantly increased in persons with HIV/AIDS (PWHAs) of all ages. [1][2][3][4][5][6][7][8][9][10][11] Risks relative to the general population are increased from 5-to 15-fold. Additionally, most HL cases in PWHAs are mixed cellularity (MC) and lymphocyte-depleted (LD) subtypes, whereas the nodular sclerosing (NS) subtype predominates in young adults without HIV/AIDS. 2,12,13 That HIV/AIDS-related immunosuppression would affect HL risk and subtype distribution is not surprising. Persons with genetic conditions associated with T-lymphocyte immune dysfunction have a higher risk of HL, and patients with HL may have underlying abnormalities of T-cell immunity. 14 Few studies of HL in PWHAs have had sufficient data to examine risks in the era of highly active antiretroviral therapy (HAART). By controlling HIV replication with combination therapies, HAART improves immune function, and its use is associated with reduced incidence of Kaposi sarcoma and non-Hodgkin lymphoma (NHL), the 2 most common AIDSassociated cancers. [15][16][17][18] Unexpectedly, however, HL risk in PWHAs increased after HAART became available in 1996. 15,18 Consistent with this temporal increase, HL incidence was reported to be higher in HIV-infected persons using HAART than in those not using it. 16 To address the role of immunity in HL etiology, we examined HL risk in a large multicenter study linking HIV/AIDS and cancer registry data. Since 1990, CD4 T-lymphocyte counts have been increasingly recorded by HIV/AIDS registries, permitting prospective studies of HL incidence using this marker of immune status to stratify subjects. We also examined the relationship between CD4 count and the incidence of specific HL subtypes provided by the cancer registries.
Patients, materials, and methodsSince 1991, we have periodically linked HIV/AIDS and cancer registry data in the United States. The current linkage included the states of Connecticut, Georgia, Florida, Massachusetts, Michigan, and New Jersey, and the metropolitan areas of Los Angeles, San Diego, and San Francisco, CA; New York City, NY; and Seattle, WA. We included HIV/AIDS cases registered through 2002 and linked them to cancer diagnoses during periods when cancer registry data were considered complete. Details of the matching approach have been presented elsewhere. 6,9,11,19 Briefly, a probabilistic algorithm identified record linkages using the social security number, name, sex, race, and birth and death dates. Possible linkages were reviewed by authorized registry personnel to ensure their validity, and questionable linkages we...