HIV-associated Hodgkin's disease. Biologic and clinical aspects.

The incidence of HD appears to have increased in HIV-infected individuals, with HIV-seropositive intravenous drug users most likely to develop the disorder. All groups at risk for HIV, however, may develop HD. The pathologic spectrum of HD in the setting of HIV infection is distinct from that seen in "de novo" HD in the United States, with the majority of patients diagnosed with the mixed cellularity subtype, as opposed to the more usual occurrence of nodular sclerosis in "de novo" disease. The presence of fibrohistiocytic stromal cells within involved tissues is also a distinct characteristic of HIV-associated HD. Epstein-Barr viral genome has been detected within tumor cell nuclei, and it may be involved in the pathogenesis of disease. Clinically, patients often present with systemic "B" symptoms and widely disseminated extranodal disease, seen in 75% to 90%. Bone marrow is involved in 40% to 50% of cases at diagnosis. Complete remission may be achieved in approximately 50% of patients after use of combination chemotherapy, but median survival is short, in the range of 12 to 18 months. Death is often due to bacterial or opportunistic infection (or both), often occurring in the setting of chemotherapy-induced neutropenia.