Altered Iron Metabolism in Children With Human Immunodeficiency Virus Disease

James, Ellen Butensky; Harmatz, Paul; Lee, Marion; Kennedy, Christine; Petru, Ann; Wara, Diane W.; Miaskowski, Christine

doi:10.1080/08880010902754826

Cited by 11 publications

(7 citation statements)

References 41 publications

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“…31 Iron deficiency is highly prevalent (18.0-44.3%) in developing countries, 3,29 but not in this study. The high prevalences of IDA in other studies might be the result of the inclusion of children with poorer nutritional status and more severe clinical stage of HIV.…”

Section: Discussionmentioning

confidence: 83%

“…32 Serum ferritin is an acute phase reactant that may be increased in chronic inflammatory diseases such as HIV infection. 31,33 High levels of serum ferritin have been reported in AIDS patients; the more advanced the stage of disease, the higher the serum ferritin level. 34 However, in this study, we enrolled HIV-infected children with moderate immunosuppression, with a generally low incidence of opportunistic infections, and excluded children with acute illness.…”

Section: Discussionmentioning

confidence: 99%

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Prevalence of Anemia and Underlying Iron Status in Naive Antiretroviral Therapy HIV-Infected Children with Moderate Immune Suppression

Kosalaraksa

Bunupuradah

Saphonn³

et al. 2012

AIDS Research and Human Retroviruses

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Anemia is common in HIV-infected children and iron deficiency is thought to be a common cause. This study investigates the prevalence of anemia, thalassemia, and underlying iron status in Thai and Cambodian children without advanced HIV disease to determine the necessity of routine iron supplementation. Antiretroviral (ARV)-naive HIV-infected Asian children aged 1-12 years, with CD4 15-24%, CDC A or B, and hemoglobin (Hb) ‡ 7.5 g/dl were eligible for the study. Iron studies, serum ferritin, Hb typing, and C-reactive protein were assessed. Anemia was defined as Hb < 11.0 g/dl in children < 5 years of age or < 11.5 g/dl in children 5-12 years. We enrolled 299 children; 57.9% were female and the mean (SD) age was 6.3 (2.9) years. The mean (SD) CD4% and HIV-RNA were 20% (4.6) and 4.6 (0.6) log 10 copies/ml, respectively. The mean (SD) Hb and serum ferritin were 11.2 (1.1) g/dl and 78.3 (76.4) lg/liter, respectively. The overall iron deficiency anemia (IDA) prevalence was 2.7%. One hundred and forty-eight (50%) children had anemia, mostly of a mild degree. Of these, 69 (46.6%) had the thalassemia trait, 62 (41.8%) had anemia of chronic disease (ACD), 9 (6.1%) had thalassemia diseases, 3 (2.0%) had iron deficiency anemia, and 5 (3.4%) had IDA and the thalassemia trait. The thalassemia trait was not associated with increased serum ferritin levels. Mild anemia is common in ARV-naïve Thai and Cambodian children without advanced HIV. However, IDA prevalence is low; with the majority of cases caused by ACD. A routine prescription of iron supplement in anemic HIV-infected children without laboratory confirmation of IDA should be discouraged, especially in regions with a high prevalence of thalassemia and low prevalence of IDA.

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Prevalence of Anemia and Underlying Iron Status in Naive Antiretroviral Therapy HIV-Infected Children with Moderate Immune Suppression

Kosalaraksa

Bunupuradah

Saphonn³

et al. 2012

AIDS Research and Human Retroviruses

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“…The above suggestions are certainly true of infections caused by influenza A (Visseren et al 2002) (see also Akaike et al 1996; Beck et al 2004), herpes simplex virus (Gennero et al 2010; Lamey and Biagioni 1995; Romeo et al 2001), hepatitis C (Alavian and Tabatabaei 2009; Alla and Bonkovsky 2005; Ameli et al 2008; Bassett 2007; Batts 2007; Bonkovsky 2002; Bonkovsky et al 2006; Desai et al 2008; Di Marco et al 2008; Drakesmith and Prentice 2008; Fargion et al 2002; Ferrara et al 2009; Franchini et al 2008; Fujita et al 2007a, b; Fujita and Takei 2007; Girelli et al 2009; Gürkan et al 2005; Guyader et al 2007; Hayashi and Yano 2002; Heathcote 2004; Kaito 2007; Kaito et al 2006; Kato et al 2001, 2007; Ko et al 2007; Mahmoud et al 2008; Mueller et al 2006; Nahon et al 2008; Nishina et al 2008; Otogawa et al 2008; Price and Kowdley 2009; Rigamonti et al 2005; Sebastiani and Walker 2007; Sikorska et al 2010; Sugimoto et al 2009; Tanaka et al 2007; Tanaka and Kiyosawa 2004; Trinder et al 2008; Tung et al 2003; Valenti et al 2008; Venturini et al 2010; Won et al 2009) and HIV (Boelaert et al 1996; Butensky James et al 2009; de Monyé et al 1999; Debebe et al 2007; Drakesmith and Prentice 2008; Georgiou et al 2000; Gordeuk et al 2001, 2006; Kagu et al 2007; Ketonen et al 1996; McDermid et al 2007; McDermid and Prentice 2006; McDermid et al 2009; Meyer 2006; Northrop-Clewes 2008; Rawat et al 2008; Savarino et al 1999; Schreck et al 1992; Szajerka and Jablecki …”

Section: Virusesmentioning

confidence: 99%

Towards a unifying, systems biology understanding of large-scale cellular death and destruction caused by poorly liganded iron: Parkinson’s, Huntington’s, Alzheimer’s, prions, bactericides, chemical toxicology and others as examples

2010

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Exposure to a variety of toxins and/or infectious agents leads to disease, degeneration and death, often characterised by circumstances in which cells or tissues do not merely die and cease to function but may be more or less entirely obliterated. It is then legitimate to ask the question as to whether, despite the many kinds of agent involved, there may be at least some unifying mechanisms of such cell death and destruction. I summarise the evidence that in a great many cases, one underlying mechanism, providing major stresses of this type, entails continuing and autocatalytic production (based on positive feedback mechanisms) of hydroxyl radicals via Fenton chemistry involving poorly liganded iron, leading to cell death via apoptosis (probably including via pathways induced by changes in the NF-κB system). While every pathway is in some sense connected to every other one, I highlight the literature evidence suggesting that the degenerative effects of many diseases and toxicological insults converge on iron dysregulation. This highlights specifically the role of iron metabolism, and the detailed speciation of iron, in chemical and other toxicology, and has significant implications for the use of iron chelating substances (probably in partnership with appropriate anti-oxidants) as nutritional or therapeutic agents in inhibiting both the progression of these mainly degenerative diseases and the sequelae of both chronic and acute toxin exposure. The complexity of biochemical networks, especially those involving autocatalytic behaviour and positive feedbacks, means that multiple interventions (e.g. of iron chelators plus antioxidants) are likely to prove most effective. A variety of systems biology approaches, that I summarise, can predict both the mechanisms involved in these cell death pathways and the optimal sites of action for nutritional or pharmacological interventions.

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“…Clinical and experimental evidences have indicated that the metabolism of iron is altered in HIV‐patients and that several steps in the HIV‐1 replicative cycle require iron [Traoré and Meyer, ; James et al, ; Rawat et al, ; Nekhai et al, ]. In HIV‐patients, iron deficiency is common and elevated iron stores are associated with faster disease progression.…”

Section: Introductionmentioning

confidence: 99%

Serum hepcidin levels in women infected with HIV-1 under antiviral therapy

2014

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Accumulating data suggest that iron may have a role in the regulation of HIV-infection. In the present study, we determined by radioimmunoassay the levels of hepcidin, a key regulator of iron homeostasis, in sera of 182 women infected with HIV-1 under highly active antiretroviral therapy (HAART). In the total cohort, hepcidin levels were lower in individuals infected with HIV than in controls (3.20 ± 3.06 vs. 5.68 ± 3.66 nmol/L, P = 0.009). Serum hepcidin concentrations were strongly correlated positively with iron, ferritin, urea, and uric acid. In the total cohort of patients with abnormal viral load and CD4 cell count <500 cells/mm(3) , a strong positive correlation was found between hepcidin and viral load. Hepcidin level was significantly higher in HIV-patients with high viremia than in patients with undetectable viral load. Iron level was significantly lower in HIV-patients with high viral load compared with patients with undetectable viral load. This study suggests that hepcidin controls serum iron, especially in response of iron utilization by HIV for viral replication. The possibility of using inhibitors of hepcidin expression as adjunct therapy for HIV-patients is discussed.

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Altered Iron Metabolism in Children With Human Immunodeficiency Virus Disease

Abstract: These data indicate that alterations in iron metabolism are common even in the HAART era and warrant further study to identify individuals at risk for these alterations.

Cited by 11 publications

References 41 publications

Prevalence of Anemia and Underlying Iron Status in Naive Antiretroviral Therapy HIV-Infected Children with Moderate Immune Suppression

Prevalence of Anemia and Underlying Iron Status in Naive Antiretroviral Therapy HIV-Infected Children with Moderate Immune Suppression

Towards a unifying, systems biology understanding of large-scale cellular death and destruction caused by poorly liganded iron: Parkinson’s, Huntington’s, Alzheimer’s, prions, bactericides, chemical toxicology and others as examples

Serum hepcidin levels in women infected with HIV-1 under antiviral therapy

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