Kaposi's sarcoma of the bone marrow presenting with fever of unknown origin

The first thrombocytopenia cases related to the human immunodeficiency virus (HIV) were described even before its isolation in 1983. Subsequently, multiple mechanisms have been proposed to elucidate the etiology of thrombocytopenia. In addition to other types of cytopenia affecting patients with HIV, thrombocytopenia is observed in about 10–50% HIV patients as one of the first clinical signs of infection. Thus, in this review we aim to summarize the mechanisms proposed for thrombocytopenia since the discovery of HIV, and especially the innovations in the field in recent years. Among the different mechanisms suggested for HIV-related thrombocytopenia, there is emphasis on the accelerated destruction of platelets (PLTs) due to the action of immune complexes, and the presence of anti-PLT and anti-HIV antibodies that cross-react with the PLT membrane. There are also secondary causes of thrombocytopenia, such as the effect of drugs and opportunistic diseases associated with HIV.

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“…There are also secondary causes of thrombocytopenia, such as the effect of drugs [53] and opportunistic diseases associated with HIV [54,55,56]. …”

Section: Mechanisms Of Hiv-related Thrombocytopeniamentioning

confidence: 99%

An Overview of the Mechanisms of HIV-Related Thrombocytopenia

Passos

Treitinger²,

Spada³

2010

Acta Haematol

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Favourable Effect of Chemotherapy on Clinical Symptoms and Human Herpesvirus-8 DNA Load in a Patient with Kaposi's Sarcoma Presenting with Fever and Anemia

Prins¹,

Sol

Renwick

et al. 1999

European Journal of Clinical Microbiology & Infectious Dise

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The case of a patient infected with human immunodeficiency virus type 1 (HIV-1) with Kaposi's sarcoma who presented with fever of unknown origin, severe anemia, thrombocytopenia and hypoalbuminemia but only limited involvement of the skin is presented. Chemotherapy directed at Kaposi's sarcoma resulted in resolution of these clinical signs and symptoms and was associated with a significant reduction in human herpesvirus-8 DNA load in serum, despite continued HIV-1 replication. Such a decreasing human herpesvirus-8 load following Kaposi's sarcoma-directed chemotherapy has not been reported previously. These findings suggest that Kaposi's sarcoma was indeed responsible for the clinical syndrome and that this neoplasm is a source of human herpesvirus-8 virus particle production, which can be inhibited by chemotherapy-induced reduction in tumor burden.

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