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December 2001
Parvovirus B19
Anemia is the most common hematologic disorder observed in patients infected with HIV. The incidence varies between 16-94%, depending on age, severity of HIV disease, and use of antiretroviral medications. Anemia in a patient infected with HIV can result from a variety of processes.
Decreased RBC production:
As in anemia of chronic disease, HIV infection can lead to decreased production of erythrocytes and suppression of the reticulocyte response. Anemia is further complicated by a decreased physiological response to erythropoietin and by inflammatory cytokines that inhibit erythropoiesis. Medications such as ganciclovir, acyclovir, and trimethoprim-sulfamethoxazole also can result in decreased production of red blood cells. Zidovudine (AZT) is associated with a dose-dependent macrocytic anemia. In vitro studies show that zidovudine directly suppresses hematopoietic colony formation. Chronic diarrhea, infections of the small intestine, and poor nutrition can give rise to B12 and folic acid deficiencies and anemia.
Infiltration of bone marrow by malignancies (leukemia, lymphoma, or Kaposi’s sarcoma) or infections (Mycobacterium avium complex, cytomegalovirus) will decrease the production of red blood cells. Parvovirus B19 infects pronormoblasts in the marrow, resulting in a pure red cell aplasia with minimal to absent thrombocytopenia or neutropenia. Parvovirus infection in patients infected with HIV may be due to either reactivation of latent virus or an ineffective response to newly acquired infection.
Increased RBC loss
Iron deficiency anemia can develop in patients infected with HIV. Intestinal lymphomas, Kaposi’s sarcoma and certain opportunistic infections, including cytomegalovirus, can result in gastrointestinal bleeding, giving rise to iron deficiency anemia. Difficulty feeding and decreased absorption of nutrients can further complicate this picture.
Increased RBC destruction
Significant hemolysis of red blood cells in patients infected with HIV is rare. Oxidizing medications (e.g., dapsone or trimethoprim-sulfamethoxazole) can induce hemolysis in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency. In children, it is important to rule out sickle cell disease and thalassemia as potential causes of anemia. Some HIV-infected patients develop red blood cell autoantibodies. This results in a positive Coomb’s test and shortened red blood cell survival time, although the incidence of clinically important hemolysis is low. Other diagnoses to consider include infection (hemolytic uremic syndrome) and disseminated intravascular coagulopathy or thrombotic thrombocytopenic purpura.
Treatment
In the present case, bone marrow aspiration revealed giant pronormoblasts and intranuclear inclusions, consistent with Parvovirus B19 infection. Because the patient was symptomatic (fatigue and shortness of breath), she initially received a transfusion of packed red blood cells. Six weeks later, her hemoglobin concentration and hematocrit had normalized to 13.1 gm/dL and 37.9%, respectively. Although it was not needed in this case, Parvovirus B19-associated anemia often is treated with biweekly or monthly intravenous infusions of immunoglobulin. As in the present case, spontaneous remission of anemia sometimes is observed, especially in patients with relatively well-preserved immune function (CDC immunologic category 1 or 2).
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