gms | German Medical Science

27th German Cancer Congress Berlin 2006

German Cancer Society (Frankfurt/M.)

22. - 26.03.2006, Berlin

HIV-associated Malignancies: Kaposi`s Sarcoma

Meeting Abstract

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  • corresponding author presenting/speaker Stefan Esser - Universitätsklinikum Essen, Klinik für Dermatologie und Venerology, Deutschland
  • Stephan Grabbe - Universitätsklinikum Essen, Klinik für Dermatologie und Venerology

27. Deutscher Krebskongress. Berlin, 22.-26.03.2006. Düsseldorf, Köln: German Medical Science; 2006. DocIS028

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dkk2006/06dkk028.shtml

Published: March 20, 2006

© 2006 Esser et al.
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Outline

Text

Kaposi`s sarcoma (KS) is a multifocal systemic neoplasia that originates from the vascular endothelium and is due to infection with human herpes virus-8 (HHV-8), which is mainly sexually transmitted. Clinical course of the disease is variable. Initially solitary, or a few asymptomatic purple macules or nodules can appear on any area of the skin or mucous membranes. Further progression of the tumor leads to central necrosis and ulceration. The KS can bleed easily. Plaque-like and nodular KS lesions, often become confluent and can be accompanied by massive edema. In HIV-infected patients, epidemic KS is an AIDS-defining illness. HIV-associated KS ranges from indolent skin lesions to aggressive, disseminated disease with lymph node and visceral involvement (particular lung and gastrointestinal tract). Lethal outcomes within one year after KS was diagnosed, have been observed in HIV patients with severe and untreated immunodeficiency. Since the introduction of high active antiretroviral Therapy (HAART) in 1996, the frequency of KS in HIV-infected patients has decreased and the clinical course of disease has improved significantly. If KS is diagnosed in HIV-infected patients who have not yet been treated with antiretroviral drugs, HAART should be started to reduce HIV viral load and to achieve immune reconstitution with an increase in the CD4 T cell count. In many cases, stabilization or complete remission of KS is possible with immune reconstitution and reduction of the HIV viral load. In addition, different treatment methods are available depending on the size, on the locations of KS, on the development of progression and on the clinical stage of KS. As KS is a multifocal systemic disease, local treatment is limited to excisional biopsies for diagnosis, palliative removal of small tumors in cosmetically disturbing areas and early stages of KS. Interferon-α combined with HAART is another treatment option. HIV-associated KS should be treated by chemotherapy in the presence of clinical symptoms, rapid progression and/or visceral involvement. The chemotherapeutics that achieve the highest remission rates for KS are liposomal anthracyclines. The combination of pegylated liposomal doxorubicin with HAART was substantially more effective than HAART alone. Should they fail, paclitaxel or combination chemotherapy (ABV regimen) can be used. Interactions between chemotherapy and HAART drugs and increase of their toxicities need very careful monitoring in HIV-patients.