Hematology/Oncology in AIDS

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A signature abnormality of human immunodeficiency virus (HIV) infection is the decline in the number of CD4 lymphocytes over time. However, other cytopenias also are seen in advanced disease, with anemia reported in 60%, thrombocytopenia in 40%, and neutropenia in 50% of patients with acquired immunodeficiency syndrome (AIDS). These cytopenias occur in conjunction with progressive deterioration of immune function and are less common in the earlier stages of HIV infection or in patients responding to antiretroviral medications. Thrombocytopenia is the exception and may constitute a manifestation of HIV infection during the asymptomatic phases.

Multiple contributing factors frequently are operative in the cytopenia in advanced HIV infection, including direct and indirect effects of HIV; opportunistic infections; neoplasms; and toxic antiretroviral, antimicrobial, or antitumor chemotherapy. Evaluation of patients with low blood counts should focus on infectious processes and attendant myelotoxic effects of therapy. 

In addition to the usual laboratory approaches to cytopenia based on impaired production, excess consumption, and/or sequestration, a number of other diagnostic studies should be considered. These include blood isolator cultures for fungi and mycobacteria, and serum assessment for cytomegalovirus (CMV) antigen or IgM antibody to parvovirus.

Although the utility of bone marrow aspirate and biopsy in an HIV-infected patient with low blood counts has been debated, morphologic changes such as giant pronormoblasts in parvovirus infection and special stains for mycobacteria and fungi may hasten identification of a reversible cause of myelosuppression. Marrow sampling is not more sensitive, however, than routine microbiologic tests in diagnosing these abnormalities.

Morphologic abnormalities of myeloid and erythroid lineages often are present in the bone marrow of patients with HIV disease in the absence of infection or neoplasm. These changes are nonspecific and include hypercellularity, dysplasia with frequent megaloblastosis, lymphoid aggregates, and increased plasma cells and reticulin. The pathogenetic mechanisms for these morphologic abnormalities and the associated impaired hematopoiesis are not well defined. Laboratory studies of hematopoiesis in HIV infection have yielded variable and differing results. The bulk of evidence suggests that HIV does not directly infect early progenitors but may alter the proliferative capacity of progenitors by two possible mechanisms: (1) induction of inhibitory factors in the marrow microenvironment, or (2) interaction with the progenitor cell surface and induction of cell death (apoptosis) without infecting stem cells.

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