Inverse Relationship of Serum Hepcidin Levels with CD4 Cell Counts in HIV-Infected Patients Selected from an Indonesian Prospective Cohort Study

Wisaksana, Rudi; Mast, Quirijn de; Alisjahbana, Bachti; Jusuf, Hadi; Sudjana, Primal; Indrati, Rini; Sumantri, Rachmat; Swinkels, Dorine W.; Crevel, Reinout van; Ven, André van der

doi:10.1371/journal.pone.0079904

Cited by 32 publications

(48 citation statements)

References 37 publications

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“…Iron sequestration within bone marrow macrophages, suggestive of hepcidin activity, inversely correlates with secondary infections and mortality in HIV-1 infection (13), and altered iron status (independently of anemia) correlates with HIV-associated mortality and morbidity, even after accounting for confounders including CD4 count (14)(15)(16)(17)(18). Hepcidin inversely correlates with CD4 counts in individuals with advanced HIV-1 (19). However, hepcidin levels in the crucial acute phase of HIV-1 infection, which dictate later events in the disease (20), are unexplored.…”

mentioning

confidence: 99%

Distinct patterns of hepcidin and iron regulation during HIV-1, HBV, and HCV infections

Armitage

Stacey

Giannoulatou

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

100

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Significance Altered iron levels correlate with disease progression in HIV type-1 (HIV-1) infection, and cellular iron promotes HIV-1 replication. In chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infections, increased liver iron levels contribute to disease. The peptide hormone hepcidin controls iron distribution. We find that hepcidin increases during the acute phase of HIV-1 infection, early hepcidin predicts later plasma viral set-point, and hepcidin remains high even in chronically infected individuals receiving antiretroviral therapy. Conversely hepcidin is not induced, and blood iron is not decreased, during the acute response to HBV and HCV. Therefore, the nature of iron redistribution during the response to infections is a pathogen-specific phenomenon; furthermore, the deleterious effects of chronic infection on hepcidin and iron appear to be established early in infection.

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confidence: 99%

Distinct patterns of hepcidin and iron regulation during HIV-1, HBV, and HCV infections

Armitage

Stacey

Giannoulatou

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

100

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“…This gender difference became smaller with increasing age and was no longer significant at the age of 1.5 and 4 mo, respectively. Significant differences in hepcidin concentrations between males and females have been previously reported in adults (12,16) and 6-mo-old Kenyan infants (17). In these infants, lower hepcidin concentrations in males were mainly explained by the lower overall iron status in males, and higher CRP concentration in females (17).…”

Section: Articlesmentioning

confidence: 75%

“…Studies on hepcidin in preterm infants are few (8,25) and to our concern, none investigated diurnal variation in hepcidin. In adults, lowest hepcidin concentrations have been observed in the early morning, and concentrations steadily increase throughout the day before declining during the evening hours (16). This pattern was neither influenced by food intake (11), nor by the sleep-wake cycle (26).…”

Section: Articlesmentioning

confidence: 97%

Serum hepcidin in infants born after 32 to 37 wk of gestational age

et al. 2015

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Background: Preterm infants are at risk of iron deficiency (ID). Hepcidin has been suggested as a good additional indicator of ID in preterm infants, next to ferritin. Methods: In a prospective observational study, we analyzed serum hepcidin in 111 infants born after 32+0 to 36+6 wk gestational age during the first 4 mo of life. results: Hepcidin concentrations decreased during the first 4 mo of life, and concentrations were lower in infants with ID compared to those without ID. Infants who developed ID at the age of 4 mo had already significantly lower levels of hepcidin at 1.5 mo of age, while ferritin was already significantly lower at the age of 1 wk. conclusion: Hepcidin concentrations of late preterm infants decrease during the first 4 mo of life. This decrease, which parallels a decrease of ferritin concentration, we interpret as a physiological response, aiming to increase iron availability. Hepcidin concentrations are lower in infants with ID compared with those without ID, with a notable change already observed at 1.5 mo of age. Hepcidin can be used as an early marker of ID, although an additive value of hepcidin over ferritin in the diagnosis of ID is not present.

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“…For example, when hepcidin levels are high, the absorption of dietary iron and release of macrophage iron to serum are blocked as protection, resulting in a relative hypoferremia and an increase iron into the macrophages, which is thought to be anti-infective. Consequently during malaria or TB infection or immune deficiency with low CD4 counts, hepcidin levels are increased (32, 33). Among children in Malawi, including children with HIV, our group previously reported low hepcidin levels (34).…”

Section: Discussionmentioning

confidence: 99%

Hepcidin and conventional markers to detect iron deficiency in severely anaemic HIV-infected patients in Malawi

Huibers

Calis

Allain

et al. 2019

Preprint

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phone: +265(0)883699070/ +31(0)616193631 35 Abstract 36 37 Introduction: Iron deficiency is a treatable cause of severe anaemia in low-and-middle-38 income-countries (LMIC). Diagnosing it remains challenging as peripheral blood markers 39 poorly reflect bone-marrow iron deficiency (BM-ID), especially in the context of HIV-40 infection.41 Methods: Severe anaemic (haemoglobin ≤70g/l) HIV-infected adults were recruited at 42 Queen Elizabeth Central Hospital, Blantyre, Malawi. BM-ID was evaluated. Accuracy of 43 blood markers including hepcidin alongside mean corpuscular volume, mean cellular 44 haemoglobin concentration, serum iron, serum ferritin, soluble transferrin receptor 45 (sTfR), sTfR -index, sTfR -ratio to detect BM-ID was valued by ROC area under the curve 46 (AUC ROC ).47 Results: Seventy-three patients were enrolled and 35 (48.0%) had BM-ID. Hepcidin and 48 MCV performed best; AUC ROC of 0.593 and 0.545. Other markers performed poorly 49 (ROC<0.5). The AUC ROC of hepcidin in males was 0.767 (sensitivity 80%, specificity 78%) 50 and in women 0.490 (sensitivity 60%, specificity 61%).51 Conclusion: BM-ID deficiency was common in severely anaemic HIV-infected patients 52 and is an important and potential treatable contributor to severe anaemia. Hepcidin was 53 the best, though still suboptimal, marker of BM-ID. Hepcidin, which is directly linked to 54 iron absorption, is a very promising marker to guide curative iron supplementation 55 policies in severely anaemic HIV-infected patients. 56 57 59 Introduction 60 Anaemia affects approximately a third of the world's population and substantially reduces the 61 disability-adjusted life years worldwide (1). Iron deficiency contributes to development of 62 anaemia and is diagnosed in more than half of all anaemic persons (2). Consequently, iron 63 supplements remain the backbone of prevention and treatment protocols for anaemia. 64Anaemia has an extensive list of potential causes. In sub-Saharan Africa, where this 65 condition is most common, its aetiology is even more complex and in these setting 66 aetiologies commonly co-incide requiring a multifactorial approach (3, 4). HIV may be the 67 cause of anaemia by its direct effect on BM cells, but can also increase the range of 68 aetiological factors to encompass opportunistic viral, bacterial and parasitic infections, 69 drugs such as Zidovudine and co-trimoxazole, micronutrient deficiencies and neoplastic 70 diseases (5, 6). 71The exact role of iron deficiency, one of the few potentially preventable and 72 treatable causes of anaemia, remains unclear due to its diagnostic challenges in HIV-73 infected patients in low resource settings (3, 4, 7). Peripheral blood markers, including 74 erythrocyte indices, serum iron, ferritin, and soluble transferrin receptor (sTfR), have 75 been evaluated but their accuracy is often negatively affected by inflammatory states and 76 renal and liver conditions, which are common in both the African and HIV-infected 77 populations (8-11). Previous studies therefore concluded that the ...

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Inverse Relationship of Serum Hepcidin Levels with CD4 Cell Counts in HIV-Infected Patients Selected from an Indonesian Prospective Cohort Study

Cited by 32 publications

References 37 publications

Distinct patterns of hepcidin and iron regulation during HIV-1, HBV, and HCV infections

Distinct patterns of hepcidin and iron regulation during HIV-1, HBV, and HCV infections

Serum hepcidin in infants born after 32 to 37 wk of gestational age

Hepcidin and conventional markers to detect iron deficiency in severely anaemic HIV-infected patients in Malawi

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