Hodgkin lymphoma in the Swiss HIV Cohort Study

Clifford, Gary M.; Rickenbach, Martin; Lise, Mauro; Maso, Luigino Dal; Battegay, Manuel; Bohlius, Julia; Amari, Emmanuelle Boffi El; Karrer, Urs; Jundt, Gernot; Bordoni, Andrea; Ess, Silvia; Franceschi, Silvia

doi:10.1182/blood-2009-02-204172

Cited by 96 publications

(92 citation statements)

References 34 publications

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“…2 In the Swiss HIV Cohort Study, HL risk was 3-fold higher in the cART era compared with the pre-cART era in an analysis of the first 18 cases, 7 but this was not statistically significant and no increment in the cART era was found in an updated analysis of 47 HL cases. 8 Increased HL in the cART era has been postulated to be related to the actual use of cART, with a potential role for immunologic mechanisms. 2,4,9 Some support for an effect of cART on HL risk was provided by the British and initial Swiss studies, but these findings were marginally significant and were adjusted little or not at all for immune deficiency.…”

Section: Introductionmentioning

confidence: 99%

“…In the 2009 report from the Swiss study, HL risk was inversely related to CD4/CD8 lymphocyte ratio 1-2 years before diagnosis, whereas within 1 year of diagnosis, the overwhelming correlate of risk was T-cell and total lymphopenia. 8 Within-subject changes in blood counts and effects of initiating cART were not evaluated. 8 Relatively abrupt changes occurring with cART initiation could, in the short term, tip the balance to increase HL risk.…”

Section: Introductionmentioning

confidence: 99%

“…8 Within-subject changes in blood counts and effects of initiating cART were not evaluated. 8 Relatively abrupt changes occurring with cART initiation could, in the short term, tip the balance to increase HL risk. In addition to a rapid decrease in HIV load and a more gradual, clinically beneficial increase in CD4 count, the initiation of cART induces marked decreases in circulating levels of activated CD4 and CD8 cells.…”

Section: Introductionmentioning

confidence: 99%

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HIV-associated Hodgkin lymphoma during the first months on combination antiretroviral therapy

Lanoy

Rosenberg

Fily

et al. 2011

Blood

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Hodgkin lymphoma (HL) incidence with HIV infection may have increased with the introduction of combination antiretroviral therapy (cART), suggesting that immune reconstitution may contribute to some cases. We evaluated HL risk with cART during the first months of treatment. With 187 HL cases among 64 368 HIV patients in France, relative rates (RRs) and 95% confidence intervals (CIs) of HL were estimated using Poisson models for duration of cART, CD4 count, and HIV load, with and without adjustment for demographic/ clinical covariates. HL risk was unrelated to cART use overall, but it was related to time intervals after cART initiation (P ‫؍‬ .006). Risk was especially and significantly elevated in months 1-3 on cART (RR 2.95, CI 1.64-5.31), lower in months 4-6 (RR 1.63), and null with longer use (RR 1.00). CD4 count was strongly associated with HL risk (P < 10 ؊6 ), with the highest HL incidence at 50-99 CD4 cells/mm 3 . With adjustment for CD4 count and covariates, HL risk was elevated, but not significantly (RR 1.42), in months 1-3 on cART. HIV load had no added effect. HL risk increased significantly soon after cART initiation, which was largely explained by the CD4 count. IntroductionHodgkin lymphoma (HL) incidence is significantly elevated in the HIV-infected population. [1][2][3] In addition, since the advent of combination antiretroviral therapy (cART) in 1996, studies in the United States 4 and the United Kingdom 5 have reported an increase in the incidence of HL compared with the pre-cART era. For example, among people with AIDS in the United States, the incidence of HL was shown to be elevated 8-fold compared with the general population during the pre-cART era, and this increased significantly to 13-fold during the cART era. 1 Excess risk of HL in a second US population and among the HIV-infected population in France was shown to be very high during the pre-cART era. 2,6 In the French study, HL incidence increased even more (by 1.4-fold) during the cART era compared with the pre-cART era. 2 In the Swiss HIV Cohort Study, HL risk was 3-fold higher in the cART era compared with the pre-cART era in an analysis of the first 18 cases, 7 but this was not statistically significant and no increment in the cART era was found in an updated analysis of 47 HL cases. 8 Increased HL in the cART era has been postulated to be related to the actual use of cART, with a potential role for immunologic mechanisms. 2,4,9 Some support for an effect of cART on HL risk was provided by the British and initial Swiss studies, but these findings were marginally significant and were adjusted little or not at all for immune deficiency. 5,7 The British study also suggested that the excess risk of HL might specifically relate to the use of non-nucleoside reverse transcriptase inhibitors (NNRTIs). 5 Immune perturbation, and its control by cART, is likely to be integral to the development of HIV-associated HL. The relative risk (RR) of HIV-associated HL is 3.5-fold higher after AIDS onset, 10 and a lower CD4 lymphocyte count generally ...

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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HIV-associated Hodgkin lymphoma during the first months on combination antiretroviral therapy

Lanoy

Rosenberg

Fily

et al. 2011

Blood

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“…An increasing number of other neoplastic disorders including HL, testicular seminoma and lung cancer are still described as non-AIDS defining [12], [13] and [14]. Of note is a long-running Swiss study showing no increase in this particular lymphoma in recent years and also not among persons infected with the human immunodeficiency virus [15]. The same workers find no evidence of any increasing risk with improving immunity.…”

Section: Introductionmentioning

confidence: 99%

Human immunodeficiency and Hodgkin lymphoma

Sissolak

Jacobs

2010

Transfusion and Apheresis Science

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Presentation of Hodgkin lymphoma (HL) is distinctive in the infected individual being more advanced, accompanied by B symptoms and the presence of extranodal disease particularly lymphadenopathy of the head and neck. Bone marrow involvement may be found in over 50% of cases. Virtually all co express gamma-herpesvirus. Phenotypically there is prominence of the mixed-cellularity and lymphocyte depleted histopathologic subtypes that define an aggressive clinical course in comparison to other variants. Prior to the induction of cART, median survival was only 1-2 years. Notably the first chemotherapy trial using ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine) in 21 patients, without treating the viral infection, resulted in a 43% complete remission rate accompanied by severe haematological toxicities but did not extend median survival with this being 1.5 years matching the negative cases.Significant change accompanied concomitant anti-retroviral therapy that could be given safely even with dose intensive regimens exemplified by BEACOPP (bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine, and prednisone) in 12 patients or the Stanford V regimen (doxorubicin, vinblastine, mechlorethamine, etoposide, vincristine, bleomycin, prednisone) coupled with involved-field radiation for bulky disease studied in 59 patients. BEACOPP extended overall survival (OS) to 83% at 2 years. A similar trend was seen 1 when using the Stanford V regimen with an OS rate of 51% at 3 years, disease-free survival (DFS) of 68% and freedom from progression (FFP) in 60%. Additional benefits accrued from supportive care with stimulatory peptides such as G-CSF and when combined with bacterial prophylaxis results approached that found in the uninfected reference group. Current consensus holds this particular lymphoma as still among the non-AIDS defining cancers being lung, stomach, liver or anal despite these having recently gained more attention as several of these neoplasms may be occurring more commonly in the era of cART.While the relative risk of developing a non-AIDS-defining neoplasm in HIV-infected persons on the average is 2-3 times, the risk for developing HL in HIV-infected cases impressively ranges between 5 and 25 times when compared to the general population. Based on the precedent in which Kaposi sarcoma and the non-Hodgkin lymphomas distinctively alter the course of this retroviral infection in a way indistinguishable from concurrent Hodgkin lymphoma we propose that this entity be similarly regarded and the hypothesis tested in large randomised prospective study.

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“…However, classical Hodgkin lymphoma is observed more frequently 1 and HIV patients have a 9.4-fold increased risk of developing classical Hodgkin lymphoma compared with the general population. 2,3 Although HIV-related classical Hodgkin lymphoma occurs at any CD4 blood count, it is most frequently observed in patients with a moderate immune deficiency and CD4 blood counts of 150-249 cells/ml. 2,4 As Hodgkin-and Reed-Sternberg cells, the tumor cells in classical Hodgkin lymphoma, usually constitute a small subpopulation of the cells in affected lymph nodes; it is likely that the microenvironment, largely composed of CD4 þ T regulatory 1 cells, has an essential role in the pathophysiology of the disease.…”

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confidence: 99%

Spindle-shaped CD163+ rosetting macrophages replace CD4+ T-cells in HIV-related classical Hodgkin lymphoma

et al. 2013

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Combination antiretroviral therapy is highly effective in HIV infection, leading to decreased incidences of AIDSdefining neoplasms. However, HIV patients still have a 10-fold increased risk of developing classical Hodgkin lymphoma compared with the general population. As Hodgkin-and Reed-Sternberg cells represent only a minority in the tumor infiltrate, the aim of the present study was to characterize the microenvironment of HIV-related classical Hodgkin lymphoma and compare it with classical Hodgkin lymphoma cases of immunocompetent individuals. The major morphologic differences were the presence of necrotic foci and the absence of epithelioid cell formation in HIV-related Hodgkin lymphoma. We observed a significantly decreased number of CD4 þ T-cells and a significantly increased number of CD163 þ macrophages in HIVrelated Hodgkin lymphoma. Cases exhibiting a 'sarcomatoid' pattern of the reactive infiltrate exhibited significantly greater numbers of macrophages, associating the 'sarcomatoid' pattern to the presence of spindle-shaped macrophages. Whereas, rosetting of CD4 þ T-cells around Hodgkin-and Reed-Sternberg cells was frequently observed in classical Hodgkin lymphoma in immunocompetent persons; rosetting in a subset of HIV-related Hodgkin lymphoma cases appeared to involve cytoplasmic protrusions of spindle-shaped macrophages. HIV-related Hodgkin lymphoma, therefore, is characterized by unique morphologic features, which should be recognized by pathologists.

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Hodgkin lymphoma in the Swiss HIV Cohort Study

Cited by 96 publications

References 34 publications

HIV-associated Hodgkin lymphoma during the first months on combination antiretroviral therapy

HIV-associated Hodgkin lymphoma during the first months on combination antiretroviral therapy

Human immunodeficiency and Hodgkin lymphoma

Spindle-shaped CD163+ rosetting macrophages replace CD4+ T-cells in HIV-related classical Hodgkin lymphoma

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