Iron replacement therapy and anemia associated with chronic infectious diseases in sub-Saharan Africa.

TO THE EDITOR—We read with interest the article by Minchella and colleagues, who prospectively studied anemia (baseline prevalence, 67%) in patients with tuberculosis in TheGambia [1].Although themost common etiology was immune-mediated anemia of chronic disease (ACD), iron deficiency anemia (IDA) and combined anemia (ACD + IDA) were also frequently observed. Whereas ACD typically resolved with successful tuberculosis treatment alone, IDA and ACD +IDA did not. At baseline, patients had high serum levels of hepcidin, the master regulator of iron homeostasis. Such high levels are predictive of nonresponsiveness to oral iron replacement therapy [2] due to its combined effects of inhibiting duodenal iron absorption and causing iron sequestration. However, since levels reduced to near normal after 2 months of tuberculosis treatment, the authors suggested that ironbased interventions for anemia might be effective from this time-point. The data presented by Minchella and colleagues may be informative with regard to the management of anemia associated with other chronic infectious diseases in sub-Saharan Africa, including human immunodeficiency virus (HIV). We recently reported on the prevalence of anemia among HIV-infected patients (n = 814) in South Africa and on the recovery of hemoglobin levels during antiretroviral therapy (ART) [3]. During the first year of ART, the overall prevalence of anemia decreased from 71% to 27% and the prevalence of moderate/severe anemia decreased from 43% to 8%. Thus, although ART was associated with substantial recovery of hemoglobin levels, anemia persisted in an important subset of patients. In multivariable analysis, the factor most strongly associated with persistent anemia was persistence of erythrocyte microcytosis (mean corpuscular volume <80 fL) during ART. ART is accompanied by rapid and profound reductions in systemic immune activation as plasma HIV load is suppressed and opportunistic infections resolve. Thus, in light of the data presented by Minchella and colleagues, we suspect that the hemoglobin recovery observed in our cohort was likely to be largely attributable to resolution of immune-mediated ACD and that the persistence of anemia in a subset of patients was due to IDA or ACD+ IDA.