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Reference Manager
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-
1.
World Health Organization. Vitamin and Mineral Nutrition Information System (VMNIS): Micronutrient Database. Geneva, Switzerland: WHO. Available at: http://www.who.int/vmnis/database/en/. Accessed December 4, 2015.
-
2.
McLean E, Cogswell M, Egli I, Wojdyla D, de Benoist B, 2009. Worldwide prevalence of anaemia, WHO Vitamin and Mineral Nutrition Information System, 1993–2005. Public Health Nutr 12: 444–454.
-
3.
Grantham-McGregor S, Cheung YB, Cueto S, Glewwe P, Richter L, Strupp B; International Child Development Steering Group, 2007. Developmental potential in the first 5 years for children in developing countries. Lancet 369: 60–70.
-
4.
GBD 2015 Disease and Injury Incidence and Prevalence Collaborators, 2016. Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet 388: 1545–1602.
-
5.
Engle PL, Black MM, Behrman JR, Cabral de Mello M, Gertler PJ, Kapiriri L, Martorell R, Young ME; International Child Development Steering Group, 2007. Strategies to avoid the loss of developmental potential in more than 200 million children in the developing world. Lancet 369: 229–242.
-
6.
Lozoff B, Beard J, Connor J, Barbara F, Georgieff M, Schallert T, 2006. Long-lasting neural and behavioral effects of iron deficiency in infancy. Nutr Rev 64: S34–S43; discussion S72–S91.
-
7.
WHO, 2001. Iron Deficiency Anaemia: Assessment, Prevention and Control: A Guide for Programme Managers. Geneva, Switzerland: World Health Organization.
-
8.
WHO/Centers for Disease Control and Prevention, 2007. Assessing the Iron Status of Populations: Including Literature Reviews: Report of a Joint World Health Organization/Centers for Disease Control and Prevention Technical Consultation on the Assessment of Iron Status at the Population Level. Geneva, Switzerland: World Health Organization.
-
9.
Swingler S, Zhou J, Swingler C, Dauphin A, Greenough T, Jolicoeur P, Stevenson M, 2008. Evidence for a pathogenic determinant in HIV-1 Nef involved in B cell dysfunction in HIV/AIDS. Cell Host Microbe 4: 63–76.
-
10.
Belperio PS, Rhew DC, 2004. Prevalence and outcomes of anemia in individuals with human immunodeficiency virus: a systematic review of the literature. Am J Med 116 (Suppl 7A): 27S–43S.
-
11.
Clark TD, Mmiro F, Ndugwa C, Perry RT, Jackson JB, Melikian G, Semba RD, 2002. Risk factors and cumulative incidence of anaemia among human immunodeficiency virus-infected children in Uganda. Ann Trop Paediatr 22: 11–17.
-
12.
Mocroft A, Kirk O, Barton SE, Dietrich M, Proenca R, Colebunders R, Pradier C, dArminio Monforte A, Ledergerber B, Lundgren JD, 1999. Anaemia is an independent predictive marker for clinical prognosis in HIV-infected patients from across Europe. EuroSIDA study group. AIDS 13: 943–950.
-
13.
Frosch AE, Odumade OA, Taylor JJ, Ireland K, Ayodo G, Ondigo B, Narum DL, Vulule J, John CC, 2017. Decrease in numbers of naive and resting B cells in HIV-infected Kenyan adults leads to a proportional increase in total and Plasmodium falciparum-specific atypical memory B cells. J Immunol 198: 4629–4638.
-
14.
Marconi A, Balestrieri M, Comastri G, Pulvirenti FR, Gennari W, Tagliazucchi S, Pecorari M, Borghi V, Marri D, Zazzi M, 2009. Evaluation of the Abbott Real-Time HIV-1 quantitative assay with dried blood spot specimens. Clin Microbiol Infect 15: 93–97.
-
15.
World Health Organization, 2011. Serum Ferritin Concentrations for the Assessment of Iron Status and Iron Deficiency in Populations: Vitamin and Mineral Nutrition Information System. Geneva, Switzerland: World Health Organization.
-
16.
Ramco Laboratories Inc, 2016. An In Vitro Enzyme Immunoassay for Quantifying Human Transferrin Receptor in Serum or Plasma as an Aid in the Diagnosis of Iron Deficiency Anemia, Particularly in the Presence of Other Disease States. St. Ingbert, Germany: Ramco Laboratories Inc.
-
17.
Chiari MM, Bagnoli R, De Luca PD, Monti M, Rampoldi E, Cunietti E, 1995. Influence of acute inflammation on iron and nutritional status indexes in older inpatients. J Am Geriatr Soc 43: 767–771.
-
18.
McDermid JM, Jaye A, Schim van der Loeff MF, Todd J, Bates C, Austin S, Jeffries D, Awasana AA, Whittlex AA, Prentice A, 2007. Elevated iron status strongly predicts mortality in West African adults with HIV infection. J Acquir Immune Defic Syndr 46: 498–507.
-
19.
Choi JW, 2005. Sensitivity, specificity, and predictive value of serum soluble transferrin receptor at different stages of iron deficiency. Ann Clin Lab Sci 35: 435–439.
-
20.
Armitage AE et al. 2014. Distinct patterns of hepcidin and iron regulation during HIV-1, HBV, and HCV infections. Proc Natl Acad Sci USA 111: 12187–12192.
-
21.
McDermid JM, Hennig BJ, van der Sande M, Hill AV, Whittle HC, Jaye A, Prentice AM, 2013. Host iron redistribution as a risk factor for incident tuberculosis in HIV infection: an 11-year retrospective cohort study. BMC Infect Dis 13: 48.
-
22.
Kim DK et al. 2014. Inverse agonist of estrogen-related receptor gamma controls Salmonella typhimurium infection by modulating host iron homeostasis. Nat Med 20: 419–424.
-
23.
Sazawal S et al. 2006. Effects of routine prophylactic supplementation with iron and folic acid on admission to hospital and mortality in preschool children in a high malaria transmission setting: community-based, randomised, placebo-controlled trial. Lancet 367: 133–143.
-
24.
Kortman GA, Boleij A, Swinkels DW, Tjalsma H, 2012. Iron availability increases the pathogenic potential of Salmonella typhimurium and other enteric pathogens at the intestinal epithelial interface. PLoS One 7: e29968.
-
25.
Lounis N, Truffot-Pernot C, Grosset J, Gordeuk VR, Boelaert JR, 2001. Iron and Mycobacterium tuberculosis infection. J Clin Virol 20: 123–126.
-
26.
Murray MJ, Murray AB, Murray MB, Murray CJ, 1978. The adverse effect of iron repletion on the course of certain infections. Br Med J 2: 1113–1115.
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Iron Deficiency is Prevalent among HIV-Infected Kenyan Adults and is Better Measured by Soluble Transferrin Receptor than Ferritin
Iron deficiency (ID) and human immunodeficiency virus (HIV) infection frequently coexist. Little data exist on ID in HIV-infected individuals, partly because the iron marker ferritin is altered by inflammation common in HIV infection. We measured iron biomarkers (ferritin, soluble transferrin receptor [sTfR], hepcidin) and red cell indices (hemoglobin, mean corpuscular volume [MCV]) in newly diagnosed, antiretroviral therapy-naive, HIV-infected (N = 138) and uninfected (N = 52) Kenyan adults enrolled in a study of the immune response to malaria. We compared markers between infected and uninfected groups with t test and Wilcoxon Rank–Sum, used Spearman correlation to determine the association between iron and inflammatory markers, and applied logistic regression to determine which markers best predicted anemia. HIV-infected individuals had lower hemoglobin (P < 0.001), lower MCV (P < 0.001), higher sTfR (P = 0.003), and a greater prevalence of ID (sTfR > 8.3 mg/L) than uninfected individuals. Ferritin was elevated in HIV-infected individuals and was more strongly correlated with C-reactive protein (ρ = 0.43, P < 0.001) and hepcidin (ρ = 0.69, P < 0.001) than with hemoglobin. The best predictor of anemia in HIV-infected participants was sTfR, with a one log-unit increase in sTfR associated with a 6-fold increase in the odds of anemia (odds ratio = 6.3, 95% confidence interval: 1.8–21.8). These data suggest a significant burden of ID among treatment-naive HIV-infected Kenyan adults. Soluble transferrin receptor may be a reliable marker of ID in HIV-mediated inflammation.
Author Notes
Deceased.
Financial support: Research reported in this publication was supported by the University of Minnesota Developmental Center for AIDS Research Grant, the American Society of Tropical Medicine and Hygiene Centennial Award, the National Center for Advancing Translational Sciences of the National Institutes of Health Award Number UL1TR000114, and the National Institute of Allergy and Infectious Diseases Award Numbers 2T32AI055433-06A1 and F32 AI109808-01.
Authors’ addresses: Anne E. P. Frosch, Division of Infectious Diseases and International Medicine, Department of Medicine, University of Minnesota, Minneapolis, MN, E-mail: park0587@umn.edu. George Ayodo, Kenyan Medical Research Institute, Kisumu, Kenya, and Department of Public Health, Jaramogi Oginga Odinga University of Science and Technology, Bondo, Kenya, E-mail: gayodo@gmail.com. Eliud O. Odhiambo, Kenyan Medical Research Institute, Kisumu, Kenya, E-mail: eliudonyango@gmail.com. Kathleen Ireland, University of Minnesota Medical School, Academic Health Center, University of Minnesota, Minneapolis, MN, E-mail: irela033@umn.edu. Sarah E. Cusick, Division of Global Pediatrics, Department of Pediatrics, University of Minnesota, Minneapolis, MN, E-mail: scusick@umn.edu.