Human immunodeficiency and Hodgkin lymphoma

Sissolak, Gerhard; Sissolak, Dagmar; Jacobs, Peter

doi:10.1016/j.transci.2010.01.008

« Previous Next »Transfusion and Apheresis Science
Volume 42, Issue 2 , Pages 131-139, April 2010

Human immunodeficiency and Hodgkin lymphoma

Gerhard Sissolak
- Division of Clinical Haematology, Department of Internal Medicine, Faculty of Health Sciences, Stellenbosch University, Tygerberg Academic Hospital, South Africa
Dagmar Sissolak
- Division of Clinical Haematology, Department of Internal Medicine, Faculty of Health Sciences, Stellenbosch University, Tygerberg Academic Hospital, South Africa
Peter Jacobs
- Division of Clinical Haematology, Department of Internal Medicine, Faculty of Health Sciences, Stellenbosch University, Tygerberg Academic Hospital, South Africa
- University of Cape Town, South Africa
- College of Medicine, University of Nebraska Medical Centre, South Africa
- The Department of Haematology and Bone Marrow Transplant Unit, Incorporating The Searll Research Laboratory for Cellular and Molecular Biology, Constantiaberg Medi-Clinic, Burnham Road, Plumstead, Cape Town, South Africa
- Corresponding author. Address: Constantiaberg Medi-Clinic, P.O. Box 294, Plumstead 7800, Cape Town, South Africa. Tel.: +27 21 799 2566; fax: +27 21 761 4278.

Abstract

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 1–2years. 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 1.5years 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 2years. A similar trend was seen when using the Stanford V regimen with an OS rate of 51% at 3years, 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.