Abstract
Impaired hematologic status (IHS) was investigated as a determinant of immune function defined as cluster of differentiation 4 (CD4) T-helper cell count, quality of life (QOL) weight and hospitalization/mortality over 18-months among 398 adult persons living with HIV/AIDS (PLWHA) on anti-retroviral therapy. IHS was defined as having anemia at baseline (Hemoglobin: <12 g/dL for women and <13 g/dL for men), time-updated anemia or having low (<30 μg/L) or high (>200 μg/L for men and >150 μg/L for women) ferritin levels at baseline. Months-to-hospitalization/death or study-end (if no event) was calculated from enrollment. Multivariable linear-mixed models quantified associations between IHS and changes in CD4 cell-count, weight gain and QOL. Cox proportional hazards models calculated hazard ratios (HR) and corresponding 95% confidence intervals (CI) for IHS-related differences in time-to-hospitalization/death. The prevalences of anemia and high and low ferritin levels at baseline were 48.7% (n = 194), 40.5% (n = 161) and 17% (n = 68), respectively. Most patients (63.4%, n = 123) remained anemic during follow-up. Weight gained (ferritin-time interaction, p < 0.01) and QOL (anemia-time interaction, p = 0.05; ferritin-time interaction, p = 0.01) were lower for PLWHA with versus without IHS. Relative to anemia-free/normal ferritin, the risk of hospitalization/death was elevated for PLWHA with anemia (HR = 2.0; 95% CI: 1.2–3.6), low or high ferritin (HR: 1.8–1.9, 95% CI: 0.9–4.1) and those that developed new/persistent/progressive anemia (HR: 2.3–6.7, 95% CI: 1.0–12.7). Among PLWHA, IHS predicted deficits in QOL, low weight gain and a high risk of hospitalization/death. Intervention to mitigate persistent IHS may be warranted among PLWHA on long-term highly active antiretroviral therapy (HAART) to improve health outcomes.
Highlights
Impaired hematologic status (IHS)—including anemia and high or low ferritin—remains highly prevalent in chronic HIV despite highly active antiretroviral therapy (HAART) [1,2,3]
We extend current knowledge base by providing novel empirical data on the adverse impact of persistent anemia on immune recovery, hospitalization and mortality
We show that resolution of baseline anemia was associated with comparable immune recovery, quality of life (QOL) and risk of hospitalization/death over 18 months relative to persons living with HIV/AIDS (PLWHA) anemia free throughout
Summary
Impaired hematologic status (IHS)—including anemia and high or low ferritin—remains highly prevalent in chronic HIV despite highly active antiretroviral therapy (HAART) [1,2,3]. HIV infection leads to IHS through multiple mechanisms including the HIV-1 Nef protein increasing intra-macrophagic iron accumulation [4] and perturbation of acute phase proteins/hormones such as hepcidin, which regulates iron thirst in macrophages [5,6,7]. The dynamic interactions between HIV and iron create a positive feedback loop that increases the risk of iron overload, onset and persistence of non-iron deficiency anemia and may partly mediate HIV viral persistence and rebound despite HAART [8,10,11]. Persistent immune activation typical in HIV infection contributes to anemia of chronic disease (ACD) [12]. Regardless of etiology, is associated with sub-optimal immune recovery [13] and mortality [14] in persons living with HIV/AIDS (PLWHA)
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