Aboulafia, D

Dezube, BJ

Früh, K

Marconi, S

Pantanowitz, L

Infectious Agents and Cancer

Harvard University - DASH 

 Pathology of rituximab-induced Kaposi sarcoma flare: role of B-celldepletion  (Article begins on next page)The Harvard community has made this article openly available.Please share how this access benefits you. Your story matters.Citation Pantanowitz, L, K Früh, D Aboulafia, S Marconi, and BJ Dezube.2009. “Pathology of rituximab-induced Kaposi sarcoma flare: roleof B-cell depletion.” Infectious Agents and Cancer 4 (Suppl 2):P33. doi:10.1186/1750-9378-4-S2-P33.http://dx.doi.org/10.1186/1750-9378-4-S2-P33.Published Version doi:10.1186/1750-9378-4-S2-P33Accessed February 17, 2015 8:33:36 AM ESTCitable Link http://nrs.harvard.edu/urn-3:HUL.InstRepos:13581177Terms of Use This article was downloaded from Harvard University's DASHrepository, and is made available under the terms and conditionsapplicable to Other Posted Material, as set forth athttp://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAABioMed  CentralPage 1 of 1(page number not for citation purposes)Infectious Agents and CancerOpen Access Poster presentationPathology of rituximab-induced Kaposi sarcoma flare: role of B-cell depletionL Pantanowitz*1, K Früh2, D Aboulafia3, S Marconi1 and BJ Dezube4Address: 1Department of Pathology, Baystate Medical Center, Tufts University School of Medicine, Springfield, Massachusetts, USA, 2Vaccine and Gene Therapy Institute, Oregon Health and Science University, Portland, Oregon, USA, 3Virginia Mason Medical Center, Seattle, Washington, USA and 4Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA* Corresponding author    BackgroundKaposi sarcoma (KS) flare (exacerbation) may occur fol-lowing therapy with corticosteroids, as part of theimmune reconstitution inflammatory syndrome seenwith highly active antiretroviral therapy (HAART), andafter rituximab therapy. The exact mechanism responsiblefor iatrogenic KS flare is unclear. Therefore, the aim of thisstudy was to investigate the pathologic features in cases ofAIDS-associated KS flare.MethodsTwo cases of AIDS-associated cutaneous KS flare wereidentified following rituximab therapy. Tissue biopsiesobtained from these KS flare lesions were compared tosimilar controls (AIDS-KS samples of similar stage frompatients who had not received rituximab) by means ofimmunohistochemistry using vascular makers (CD34,CD31), monoclonal antibodies to human Herpesvirus-8(HHV-8) gene products (LNA-1, K5), as well as B-lym-phocyte (CD20) and T-lymphocyte (CD3, CD4, CD8)markers.ResultsOne patient was a 36-year-old male, HIV-positive for 2years (CD4 T-lymphocyte count 363 cells/mm3; HIV viralload >100,000 copies/ml), and the other a 44-year-oldmale, HIV-positive for 5 years (CD4 T-lymphocyte count443 cells/mm3; HIV viral load <75 copies/ml), who hadboth received rituximab therapy for multicentric Castle-man disease. The former manifested with cutaneous KSafter 7 days, and the later patient with skin and lymphad-enopathic KS flares within 3 months of receiving rituxi-mab. In the control cases both CD3 and CD20 cells werepresent, with a preponderance of T-lymphocytes identi-fied. In the KS flare specimens, there were only T-cellspresent with a notable absence of B-lymphocytes. In allcontrol and flare KS cases T-cell subsets showed CD8 >CD4. CD20+ B-cell depletion in the KS flare case of the36-year-old patient occurred concomitantly with activa-tion of the HHV-8 immediate early gene protein K5. KSflares in both patients were successfully treated with lipo-somal doxorubicin and valganciclovir.ConclusionRituximab-induced KS flare appears to be related to amodification in the host immune system, most notablywith complete absence of B lymphocytes in the KS lesion.B-cell depletion with rituximab in patients at risk for KSdevelopment may activate HHV-8, resulting in unwantedKS flare. Effective management of iatrogenic KS flaretherefore depends upon the control of HHV-8 viremia inconjunction with specific chemotherapy for KS.from 11th International Conference on Malignancies in AIDS and Other Acquired Immunodeficiencies (ICMAOI): Basic, Epidemiologic, and Clinical ResearchBethesda, MD, USA. 6–7 October 2008Published: 17 June 2009Infectious Agents and Cancer 2009, 4(Suppl 2):P33 doi:10.1186/1750-9378-4-S2-P33<supplement> <title> <p>Proceedings of the 11th International Conference on Malignancies in AIDS and Other Acquired Immunodeficiencies (ICMAOI): Basic, Epidemiologic, and Clinical Research</p> </title> <sponsor> <note>Publication of this supplement was made possible with support from the Office of HIV and AIDS Malignancy, National Cancer Institute, National Institutes of Health.</note> </sponsor> <note>Meeting abstracts – A single PDF containing all abstracts in this Supplement is available <a href="http://www.biomedcentral.com/content/files/pdf/1750-9378-4-S2-full.pdf">here</a>.</note>  <url>http://www.biomedcentral.com/content/pdf/1750-9378-4-S2-info.pdf</url> </supplement>This abstract is available from: http://www.infectagentscancer.com/content/4/S2/P33© 2009 Pantanowitz et al; licensee BioMed Central Ltd. 

Pathology of rituximab-induced Kaposi sarcoma flare: role of B-cell depletion

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Pathology of rituximab-induced Kaposi sarcoma flare: role of B-cell depletion

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