Evaluation of the First Commercial Hepcidin ELISA for the Differential Diagnosis of Anemia of Chronic Disease and Iron Deficiency Anemia in Hospitalized Geriatric Patients

Geerts, Inge; Vermeersch, Pieter; Joosten, Etienne

doi:10.5402/2012/567491

Cited by 29 publications

(27 citation statements)

References 10 publications

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“…The hepcidin concentration samples were stored at -80°C for 5 to 10 months before analysis. Serum hepcidin-25 isoform measurements were performed by using a specific ELISA kit (DRG INTERNATIONAL Inc. 1167 U.S Highway 22 East, Mountainside, NJ 07092 USA) according to the manufacturer’s instructions [19]. …”

Section: Methodsmentioning

confidence: 99%

Serum hepcidin: indication of its role as an “acute phase” marker in febrile children

Kossiva

Soldatou

Gourgiotis³

et al. 2013

Ital J Pediatr

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BackgroundHepcidin is classified as a type II acute phase protein; its production is a component of the innate immune response to infections.ObjectiveTo evaluate the alterations of serum hepcidin in children during and following an acute febrile infection.Materials and methods22 children with fever of acute onset (< 6 hours) admitted to the 2nd Department of Pediatrics-University of Athens. Based on clinical and laboratory findings our sample formed two groups: the viral infection group (13 children) and the bacterial infection group (9 children). Hepcidin, ferritin and serum iron measurements were performed in all subjects.ResultsSerum hepcidin values did not differ notably between children with viral and bacterial infection, but a significant reduction of hepcidin was noted in both groups post-infection.ConclusionOur study provides clinical pediatric data on the role of hepcidin in the face of an acute infection. In our sample of children, hepcidin was found to rise during the acute infection and fall post-infection.

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Section: Methodsmentioning

confidence: 99%

Serum hepcidin: indication of its role as an “acute phase” marker in febrile children

Kossiva

Soldatou

Gourgiotis³

et al. 2013

Ital J Pediatr

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“…Laboratory findings that distinguish iron deficiency anemia, anemia of chronic disease (also known as iron-restricted erythropoiesis and functional iron deficiency), and anemia of mixed origin are presented in Table 3. Hepcidin-25 assays that can better distinguish between iron deficiency anemia and anemia of chronic disease are currently being investigated 22,23…”

Section: Diagnosis Of Iron Deficiency Anemiamentioning

confidence: 99%

Iron deficiency anemia in patients with inflammatory bowel disease

Goldberg

2013

CEG

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Iron deficiency anemia is the most common form of anemia worldwide, caused by poor iron intake, chronic blood loss, or impaired absorption. Patients with inflammatory bowel disease (IBD) are increasingly likely to have iron deficiency anemia, with an estimated prevalence of 36%–76%. Detection of iron deficiency is problematic as outward signs and symptoms are not always present. Iron deficiency can have a significant impact on a patient’s quality of life, necessitating prompt management and treatment. Effective treatment includes identifying and treating the underlying cause and initiating iron replacement therapy with either oral or intravenous iron. Numerous formulations for oral iron are available, with ferrous fumarate, sulfate, and gluconate being the most commonly prescribed. Available intravenous formulations include iron dextran, iron sucrose, ferric gluconate, and ferumoxytol. Low-molecular weight iron dextran and iron sucrose have been shown to be safe, efficacious, and effective in a host of gastrointestinal disorders. Ferumoxytol is the newest US Food and Drug Administration-approved intravenous iron therapy, indicated for iron deficiency anemia in adults with chronic kidney disease. Ferumoxytol is also being investigated in Phase 3 studies for the treatment of iron deficiency anemia in patients without chronic kidney disease, including subgroups with IBD. A review of the efficacy and safety of iron replacement in IBD, therapeutic considerations, and recommendations for the practicing gastroenterologist are presented.

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“…First, anemias caused purely by iron deficiency manifest with red cells that are small and poorly hemoglobinized, while the red cells in ACDI typically display normal size and hemoglobinization (8). Second, patients with ACDI have not consistently demonstrated increased serum or urinary hepcidin levels (14). Third, anemias caused directly by hepcidin overproduction due to hepatic adenomas or germline mutations in TMPRSS6 resemble iron deficiency anemia with hypochromic microcytic red cells (15,16).…”

Section: Introductionmentioning

confidence: 99%

Isocitrate ameliorates anemia by suppressing the erythroid iron restriction response

Richardson¹,

Delehanty²,

Bullock³

et al. 2013

J. Clin. Invest.

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The unique sensitivity of early red cell progenitors to iron deprivation, known as the erythroid iron restriction response, serves as a basis for human anemias globally. This response impairs erythropoietin-driven erythropoiesis and underlies erythropoietic repression in iron deficiency anemia. Mechanistically, the erythroid iron restriction response results from inactivation of aconitase enzymes and can be suppressed by providing the aconitase product isocitrate. Recent studies have implicated the erythroid iron restriction response in anemia of chronic disease and inflammation (ACDI), offering new therapeutic avenues for a major clinical problem; however, inflammatory signals may also directly repress erythropoiesis in ACDI. Here, we show that suppression of the erythroid iron restriction response by isocitrate administration corrected anemia and erythropoietic defects in rats with ACDI. In vitro studies demonstrated that erythroid repression by inflammatory signaling is potently modulated by the erythroid iron restriction response in a kinase-dependent pathway involving induction of the erythroid-inhibitory transcription factor PU.1. These results reveal the integration of iron and inflammatory inputs in a therapeutically tractable erythropoietic regulatory circuit.

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Evaluation of the First Commercial Hepcidin ELISA for the Differential Diagnosis of Anemia of Chronic Disease and Iron Deficiency Anemia in Hospitalized Geriatric Patients

Cited by 29 publications

References 10 publications

Serum hepcidin: indication of its role as an “acute phase” marker in febrile children

Serum hepcidin: indication of its role as an “acute phase” marker in febrile children

Iron deficiency anemia in patients with inflammatory bowel disease

Isocitrate ameliorates anemia by suppressing the erythroid iron restriction response

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