Anemia

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Anemia increases in incidence in HIV-infected patients as their degree of immune dysfunction worsens. The anemia is usually normochromic and normocytic with iron studies that are either normal or indicative of chronic disease. Occasionally the vitamin B₁₂ level is decreased, but true vitamin B₁₂ deficiency is uncommon; rather, transcobalamin transport may be altered and therapy with the vitamin does not lead to improved erythropoiesis. Should a low vitamin B₁₂ level be found, then a true deficiency needs to be ruled out by a Schilling test and other studies.
The Coombs’ test (antiglobulin) may be positive in the majority of patients with AIDS and in about a third of asymptomatic HIV-infected individuals. Although anti-i or other specific antibodies may occur, nonspecific binding of antiphospholipid antibodies or immune complexes to erythrocytes is more common. Immune-mediated hemolysis is unusual in HIV-infected patients as a cause of anemia.

Impaired erythropoiesis accounts for anemia in most HIV-infected individuals. Serum erythropoietin levels are often low for the degree of anemia in the patient without renal abnormalities and is of unclear origin. Parvovirus infection has been reported in HIV-infected patients and may result in red cell aplasia. Gamma globulin therapy has been reported to reverse this unusual cause of severe anemia.

AZT is associated with both dose-related and idiosyncratic suppression of erythropoiesis, whereas other antiretroviral drugs generally are not associated with anemia. Macrocytic changes occur in the erythrocytes with AZT therapy. The mechanism of impaired erythropoiesis due to the drug appears to be impairment of DNA synthesis in developing progenitors.

Recombinant erythropoietin therapy may decrease the transfusion requirement and increase the hemoglobin in anemic AIDS patients on AZT. The response to recombinant erythropoietin treatment is most clearly seen in patients with pretreatment serum erythropoietin levels below 500 mU per milliliter. Some anemic AIDS patients receiving AZT have developed red cell aplasia that does not improve with recombinant erythropoietin therapy.

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