Abstract
Patients with human immunodeficiency virus/acquired immune deficiency syndrome (HIV/AIDS) are at increased risk for developing Hodgkin's lymphoma (HL), a risk that has not decreased despite the success of combination antiretroviral therapy (cART) in the modern era. HIV-associated HL (HIV-HL) differs from HL in non-HIV-infected patients in that it is nearly always associated with Epstein-Barr virus (EBV) and more often presents with high-risk features of advanced disease, systemic “B” symptoms, and extranodal involvement. Before the introduction of cART, patients with HIV-HL had lower response rates and worse outcomes than non-HIV-infected HL patients treated with conventional chemotherapy. The introduction of cART, however, has allowed for the delivery of full-dose and dose-intensive chemotherapy regimens with improved outcomes that approach those seen in non-HIV infected patients. Despite these significant advances, HIV-HL patients remain at increased risk for treatment-related toxicities and drug-drug interactions which require careful attention and supportive care to insure the safe administration of therapy. This paper will address the modern diagnosis, risk stratification, and therapy of HIV-associated HL.
Highlights
Since the introduction of combination antiretroviral therapy in 1996, patients with human immunodeficiency virus (HIV) infection are living longer, with improved immune function and a reduced risk of developing acquired immune deficiency syndrome (AIDS) [1, 2]
These observations were replicated in the Swiss HIV Cohort Study of 9429 HIV-infected patients, where Hodgkin’s lymphoma (HL) standardized incidence was 9 times increased in the precART era, compared with 21 times increased in the early combination antiretroviral therapy (cART) era and 28 times increased in the late cART era [7]
This is consistent with multivariate analysis revealing that cART and nonnucleoside reverse transcriptase inhibitors are associated with an increased risk of developing HIV-associated HL (HIV-HL) [4]
Summary
Since the introduction of combination antiretroviral therapy (cART) in 1996, patients with human immunodeficiency virus (HIV) infection are living longer, with improved immune function and a reduced risk of developing acquired immune deficiency syndrome (AIDS) [1, 2]. HL outside of HIV is a disease characterized by a bimodal age distribution with an initial peak at age 20–30 and a second peak at age 50–65 [10], while the median age of HL presentation in HIV is in the 30s [11] The incidence of this disease in HIV-positive patients is 5–10 times higher than in the general population, and may be increasing since the introduction of cART [3,4,5,6,7,8, 12, 13]. As in advanced HIV/AIDS, may disrupt this productive relationship with the host microenvironment, resulting in a decreased incidence of HL in the setting of profound immunosuppression This may explain why the incidence of HL in HIV peaks at a modestly decreased CD4 count (150–199 cells/μL), and disease risk is associated with cART, but it is rarely seen at severely depressed CD4 counts [4, 14, 15]. Patients with HIV-HL enjoy similar response rates and progression-free and overall survivals to their stage- and risk-matched non-HIV infected counterparts
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