The degree of anaemia increases with progression of HIV disease irrespective of other factors, including drug therapy (especially zidovudine), reticuloendothelial iron block, intercurrent infections, especially with atypical mycobacteria, marrow infiltration with lymphoma and haemophagocytic syndrome. It is unlikely that autoimmune haemolysis contributes, although a positive direct antiglobulin reaction is seen in 6-43% of HIV antibody-positive patients and may result from IgG or complement on the surface of the red cells. Although specific antibodies directed against a phospholipid antigen on the red cell could account for the positive antiglobulin test, in many patients this results from non-specific deposition of circulating immune complexes.
Reduced vitamin B12 levels have been reported in 10-35% of patients infected with HIV and, although many of these patients have gastrointestinal symptoms or late-stage HIV disease, reduced levels are also described in early, asymptomatic disease. The serum transcobalamin II cobalamin-binding capacity is significantly raised in asymptomatic patients with HIV infection, regardless of the vitamin B12 level; this suggests a stage of negative cobalamin balance.
The most likely mechanism underlying the reduced serum cobalamin in HIV disease is malabsorption. Malabsorption of cobalamin assessed by a Schilling test has been demonstrated in some patients with AIDS, and colonic and duodenal biopsies show chronic inflammation within the lamina propria. In situ hybridization of the specimens shows HIV to be present within mononuclear cells. Partial villous atrophy in the absence of enteropathogens has been shown in patients at all stages of disease, and HIV antigen p24 is present within the intestinal mucosa of patients presenting with gastrointestinal complaints. There is also some evidence that damage occurs to the gastric mucosa in patients with HIV disease, resulting in a reduced ability to secrete acid and enzymes, which may cause difficulty in releasing cobalamin from protein-binding in food. This might explain the observation that in some HIV patients with reduced cobalamin levels, the Schilling test, in which cobalamin unattached to food is presented to the intestine, is normal.
Cobalamin levels tend to fall along with CD4 cell counts in those patients progressing to AIDS and thus falling serum cobalamin levels are a predictor of disease progression.
Anaemia in HIV disease is not usually due to or compounded by vitamin B12 deficiency and would not be expected to improve with vitamin B12 therapy.
The major cause of anaemia in HIV disease is impaired erythropoiesis secondary to marrow dysfunction and impaired response to erythropoietin. The anaemia has the characteristics of the anaemia of chronic disease, usually being normochromic, normocytic with a low or normal reticulocyte count. As with other cytopenias, inhibitor cytokines play a central role. In addition, there is an inappropriately low serum level of erythropoietin for the degree of anaemia. Treatment with recombinant erythropoietin may be helpful in patients with an endogenous erythropoietin level of < 500 IU/L. For most patients with severe anaemia, however, management is with red cell transfusions when clinically indicated. An occasional patient develops chronic red cell aplasia following parvovirus infection and may be helped by infusions of intravenous immunoglobulin.
Drugs may cause or exacerbate anaemia, the main culprits being zidovudine, ganciclovir and chemotherapeutic agents, all of which lead to marrow suppression; primaquine and dapsone may provoke oxidative haemolysis in patients with glucose-6-phosphate-dehydrogenase deficiency and even, in high dose, in patients with normal enzyme levels.
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