Abstract
Simple SummaryHodgkin lymphoma (HL) is a non-AIDS defining neoplasm, but people living with HIV (PLWH) have between a 5- and 26-fold higher risk of developing it than the general population. Epstein-Barr virus is present in almost all HIV-related HL cases, and plays an important role in its etiopathogenesis. Despite the aggressive characteristics, the prognosis of HL affecting PLWH is similar to that of the general population if patients are treated following the same recommendations. Administration of cART concomitantly with chemotherapy is highly recommended. However, this combination may be challenging due to drug–drug interactions and overlapping toxicity. Thus, interdisciplinary collaboration between hemato-oncologists and HIV specialists is crucial for the optimal treatment of both lymphoma and HIV infection.Despite widespread use of combined antiretroviral therapy (cART) and increased life expectancy in people living with HIV (PLWH), HIV-related lymphomas (HRL) remain a leading cause of cancer morbidity and mortality for PLWH, even in patients optimally treated with cART. While the incidence of aggressive forms of non-Hodgkin lymphoma decreased after the advent of cART, incidence of Hodgkin lymphoma (HL) has increased among PLWH in recent decades. The coinfection of Epstein–Barr virus plays a crucial role in the pathogenesis of HL in the HIV setting. Currently, PLWH with HRL, including HL, are treated similarly to HIV-negative patients and, importantly, the prognosis of HL in PLWH is approaching that of the general population. In this regard, effective cART during chemotherapy is strongly recommended since it has been shown to improve survival rates in all lymphoma subtypes, including HL. As a consequence, interdisciplinary collaboration between HIV specialists and hemato-oncologists for the management of potential drug–drug interactions and overlapping toxicities between antiretroviral and antineoplastic drugs is crucial for the optimal treatment of PLWH with HL. In this article the authors review and update the epidemiological, clinical and biological aspects of HL presenting in PLWH with special emphasis on advances in prognosis and the factors that have contributed to it.
Highlights
A significant reduction in CD56+ cells, CD57+ cells, CD123+ plasmocytoid dendritic cells, and B cells, have been observed [62]. These findings show the differences between the microenvironment of Classical HL (cHL) in people living with HIV (PLWH) and that of the general population and could contribute to the increased incidence of cHL among HIV-infected people [62]
Yotsumoto and colleagues, compared only Epstein–Barr virus (EBV)-positive Hodgkin lymphoma (HL) cases, most of them treated with ABVD and did not find significant differences in the complete response (CR) rate, overall survival (OS), and progression-free survival (PFS) between EBV+ HIV-positive and
The widespread use of combination antiretroviral therapy (cART) initially produced an increase in the incidence of cHL in PLWH
Summary
Since the introduction of combination antiretroviral therapy (cART) the incidence of opportunistic infections and AIDS defining cancers, such as Kaposi sarcoma (KS), aggressive B-cell non-Hodgkin lymphomas (NHL) and invasive cervical cancer, has decreased in people living with HIV (PLWH) [1,2]. Hodgkin lymphoma (HL) is a non-AIDS defining neoplasm, but PLWH have between a 5- and 26-fold higher risk of developing it than the general population. Unlike cHL affecting the general population, around 90% of cases of PLWH-related are associated with Epstein–Barr virus (EBV) infection of tumor cells, which are Hodgkin Reed–Sternberg cells (HRS) [10]. Presenting with more aggressive characteristics, PLWH with cHL have similar response rates and survival to HIV-negative patients when they are treated with the same standard therapies [9,14]. In this article the authors review and update the epidemiological, clinical, and biological aspects of cHL presenting in PLWH with special emphasis on the improvement of prognosis and the factors that have contributed to it
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