Pathology of rituximab-induced Kaposi sarcoma flare

Liron Pantanowitz, Klaus Frueh, Sharon Marconi, Ashlee Moses, Bruce J. Dezube

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Background. Kaposi sarcoma (KS) flare may occur following therapy with corticosteroids, as part of the immune reconstitution inflammatory syndrome seen with highly active antiretroviral therapy (HAART), and after rituximab therapy. The exact mechanism responsible for iatrogenic KS flare is unclear. Methods. A case of AIDS-associated cutaneous KS flare following rituximab therapy was compared to similar controls by means of immunohistochemistry using vascular makers (CD34, CD31), monoclonal antibodies to Human Herpesvirus 8 (HHV8) gene products (LNA-1, K5), as well as B-lymphocyte (CD20) and T-lymphocyte (CD3, CD4, CD8) markers. Results. CD20+ B-cell depletion with rituximab in KS flare occurred concomitantly with activation of the HHV8 immediate early gene protein K5. KS flare in this patient was successfully treated with liposomal doxorubicin and valganciclovir. Conclusion. Rituximab-induced KS flare appears to be related to HHV8 activation. Effective management of iatrogenic KS flare therefore depends upon the control of HHV8 viremia in conjunction with specific chemotherapy for KS.

Original languageEnglish (US)
Article number7
JournalBMC Clinical Pathology
Volume8
Issue number1
DOIs
StatePublished - 2008

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Kaposi's Sarcoma
Pathology
Human Herpesvirus 8
B-Lymphocytes
Immune Reconstitution Inflammatory Syndrome
Immediate-Early Proteins
Immediate-Early Genes
Rituximab
Viremia
Highly Active Antiretroviral Therapy
Blood Vessels
Adrenal Cortex Hormones
Acquired Immunodeficiency Syndrome
Therapeutics
Immunohistochemistry
Monoclonal Antibodies
T-Lymphocytes
Drug Therapy
Skin
Genes

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Pathology of rituximab-induced Kaposi sarcoma flare. / Pantanowitz, Liron; Frueh, Klaus; Marconi, Sharon; Moses, Ashlee; Dezube, Bruce J.

In: BMC Clinical Pathology, Vol. 8, No. 1, 7, 2008.

Research output: Contribution to journalArticle

Pantanowitz, Liron ; Frueh, Klaus ; Marconi, Sharon ; Moses, Ashlee ; Dezube, Bruce J. / Pathology of rituximab-induced Kaposi sarcoma flare. In: BMC Clinical Pathology. 2008 ; Vol. 8, No. 1.
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abstract = "Background. Kaposi sarcoma (KS) flare may occur following therapy with corticosteroids, as part of the immune reconstitution inflammatory syndrome seen with highly active antiretroviral therapy (HAART), and after rituximab therapy. The exact mechanism responsible for iatrogenic KS flare is unclear. Methods. A case of AIDS-associated cutaneous KS flare following rituximab therapy was compared to similar controls by means of immunohistochemistry using vascular makers (CD34, CD31), monoclonal antibodies to Human Herpesvirus 8 (HHV8) gene products (LNA-1, K5), as well as B-lymphocyte (CD20) and T-lymphocyte (CD3, CD4, CD8) markers. Results. CD20+ B-cell depletion with rituximab in KS flare occurred concomitantly with activation of the HHV8 immediate early gene protein K5. KS flare in this patient was successfully treated with liposomal doxorubicin and valganciclovir. Conclusion. Rituximab-induced KS flare appears to be related to HHV8 activation. Effective management of iatrogenic KS flare therefore depends upon the control of HHV8 viremia in conjunction with specific chemotherapy for KS.",
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AB - Background. Kaposi sarcoma (KS) flare may occur following therapy with corticosteroids, as part of the immune reconstitution inflammatory syndrome seen with highly active antiretroviral therapy (HAART), and after rituximab therapy. The exact mechanism responsible for iatrogenic KS flare is unclear. Methods. A case of AIDS-associated cutaneous KS flare following rituximab therapy was compared to similar controls by means of immunohistochemistry using vascular makers (CD34, CD31), monoclonal antibodies to Human Herpesvirus 8 (HHV8) gene products (LNA-1, K5), as well as B-lymphocyte (CD20) and T-lymphocyte (CD3, CD4, CD8) markers. Results. CD20+ B-cell depletion with rituximab in KS flare occurred concomitantly with activation of the HHV8 immediate early gene protein K5. KS flare in this patient was successfully treated with liposomal doxorubicin and valganciclovir. Conclusion. Rituximab-induced KS flare appears to be related to HHV8 activation. Effective management of iatrogenic KS flare therefore depends upon the control of HHV8 viremia in conjunction with specific chemotherapy for KS.

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