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1.
Disorders of Iron Metabolism: New Diagnostic and Treatment Approaches to Iron Deficiency.
Powers, JM, Buchanan, GR
Hematology/oncology clinics of North America. 2019;(3):393-408
Abstract
Iron deficiency anemia is the leading cause of anemia worldwide and affects many young children and adolescent girls in the United States. Its signs and symptoms are subtle despite significant clinical effects. Iron deficiency anemia is diagnosed clinically by the presence of risk factors and microcytic anemia. Improvement following a trial of oral iron therapy is confirmative. An array of iron laboratory tests is available with variable indications. Clinical trial and iron absorption data support a shift to lower-dose oral iron therapy. Intravenous iron should be considered in children who fail oral iron or who have more complex disorders.
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Hepcidin as a Prospective Individualized Biomarker for Individuals at Risk of Low Energy Availability.
Badenhorst, CE, Black, KE, O'Brien, WJ
International journal of sport nutrition and exercise metabolism. 2019;(6):671-681
Abstract
Hepcidin, a peptide hormone with an acknowledged evolutionary function in iron homeostasis, was discovered at the turn of the 21st century. Since then, the implications of increased hepcidin activity have been investigated as a potential advocate for the increased risk of iron deficiency in various health settings. Such implications are particularly relevant in the sporting community where peaks in hepcidin postexercise (∼3-6 hr) are suggested to reduce iron absorption and recycling, and contribute to the development of exercise-induced iron deficiency in athletes. Over the last decade, hepcidin research in sport has focused on acute and chronic hepcidin activity following single and repeated training blocks. This research has led to investigations examining possible methods to attenuate postexercise hepcidin expression through dietary interventions. The majority of macronutrient dietary interventions have focused on manipulating the carbohydrate content of the diet in an attempt to determine the health of athletes adopting the low-carbohydrate or ketogenic diets, a practice that is a growing trend among endurance athletes. During the process of these macronutrient dietary intervention studies, an observable coincidence of increased cumulative hepcidin activity to low energy availability has emerged. Therefore, this review aims to summarize the existing literature on nutritional interventions on hepcidin activity, thus, highlighting the link of hepcidin to energy availability, while also making a case for the use of hepcidin as an individualized biomarker for low energy availability in males and females.
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3.
Therapeutic Opportunities for Hepcidin in Acute Care Medicine.
Chawla, LS, Beers-Mulroy, B, Tidmarsh, GF
Critical care clinics. 2019;(2):357-374
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Abstract
Iron homeostasis is often disrupted in acute disease with an increase in catalytic free iron leading to the formation of reactive oxygen species and subsequent tissue-specific oxidative damage. This article highlights the potential therapeutic benefit of exogenous hepcidin to prevent and treat iron-induced injury, specifically in the management of infection from enteric gram-negative bacilli or fungi, malaria, sepsis, acute kidney injury, trauma, transfusion, cardiopulmonary bypass surgery, and liver disease.
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Improving Erythropoiesis Stimulating Agent Hyporesponsiveness in Hemodialysis Patients: The Role of Hepcidin and Hemodiafiltration Online.
Rosati, A, Ravaglia, F, Panichi, V
Blood purification. 2018;(1-3):139-146
Abstract
Hyporesponsiveness to erythropoietin stimulating agents (ESAs) is a condition associated with increased mortality. Even after identifying the condition, the causes are difficult to treat and only partially reversible in end-stage renal disease patients. Thus, the role of more recent hemodialysis (HD) techniques in improving such conditions is an emerging issue. However, major randomized clinical trials have not confirmed the results of smaller observational studies in which online hemodiafiltration has shown some efficacy in improving patients' response to ESAs. In our interpretation, these findings are not in contrast, but they can be explained by a better understanding of the interactions between HD and ESAs on iron mobilization, first of all through the role of hepcidin. The kinetics of hepcidin removal through HD combined with the action of selected ESAs may help the clinician in prescribing the best association between HD treatment and ESAs to overcome hyporesponsiveness.
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Inflammation, Hemolysis, and Erythropoiesis Lead to Competitive Regulation of Hepcidin and Possibly Systemic Iron Status in Sickle Cell Disease.
Ginzburg, YZ, Glassberg, J
EBioMedicine. 2018;:8-9
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6.
Hepcidin: a real-time biomarker of iron need.
Hare, DJ
Metallomics : integrated biometal science. 2017;(6):606-618
Abstract
There are numerous blood-based biomarkers for assessing iron stores, but all come with certain limitations. Hepcidin is a hormone primarily produced in the liver that has been proposed as the 'master regulator' of dietary uptake and iron metabolism, and has enormous potential to provide a 'real time' indicator of body iron levels. In this Minireview, the biochemical function of hepcidin in regulating iron levels will be discussed, with a specific focus on how hepcidin can aid in the assessment of iron stores and clinical diagnosis of iron deficiency, iron deficiency anaemia and other iron-related disorders. The role hepcidin itself plays in diseases of iron metabolism will be examined, and current efforts to translate hepcidin assays into the clinic will be critically appraised. Potential limitations of hepcidin as a marker of iron need will also be addressed, as well as the development of new therapies that directly target the hormone that sits atop the hierarchy of systemic iron metabolism.
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7.
Iron metabolism and the role of the iron-regulating hormone hepcidin in health and disease.
Daher, R, Manceau, H, Karim, Z
Presse medicale (Paris, France : 1983). 2017;(12 Pt 2):e272-e278
Abstract
Although iron is vital, its free form is likely to be involved in oxidation-reduction reactions, leading to the formation of free radicals and oxidative stress. Living organisms have developed protein systems to transport free iron through the cell membranes and biological fluids and store it in a non-toxic and readily mobilizable form to avoid iron toxicity. Hepcidin plays a crucial role in maintaining iron homeostasis. Hepcidin expression is directly regulated by variations in iron intake and its repression leads to an increase in bioavailable serum iron level. However, in pathological situations, prolonged repression often leads to pathological iron overload. In this review, we describe the different molecular mechanisms responsible for the maintenance of iron metabolism and the consequences of iron overload. Indeed, genetic hemochromatosis and post-transfusional siderosis are the two main conditions responsible for iron overload. Long-term iron overload is deleterious, and treatment relies on venesection therapy for genetic hemochromatosis and chelation therapy for iron overload resulting from multiple transfusions.
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8.
Role of hepcidin-ferroportin axis in the pathophysiology, diagnosis, and treatment of anemia of chronic inflammation.
Langer, AL, Ginzburg, YZ
Hemodialysis international. International Symposium on Home Hemodialysis. 2017;(Suppl 1):S37-S46
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Abstract
Anemia of chronic inflammation (ACI) is a frequently diagnosed anemia and portends an independently increased morbidity and poor outcome associated with multiple underlying diseases. The pathophysiology of ACI is multifactorial, resulting from the effects of inflammatory cytokines which both directly and indirectly suppress erythropoiesis. Recent advances in molecular understanding of iron metabolism provide strong evidence that immune mediators, such as IL-6, lead to hepcidin-induced hypoferremia, iron sequestration, and decreased iron availability for erythropoiesis. The role of hepcidin-ferroportin axis in the pathophysiology of ACI is stimulating the development of new diagnostics and targeted therapies. In this review, we present an overview of and rationale for inflammation-, iron-, and erythropoiesis-related strategies currently in development.
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Current status of iron metabolism: Clinical and therapeutic implications.
Conde Diez, S, de Las Cuevas Allende, R, Conde García, E
Medicina clinica. 2017;(5):218-224
Abstract
Hepcidin is the main regulator of iron metabolism and a pathogenic factor in iron disorders. Hepcidin deficiency causes iron overload, whereas hepcidin excess causes or contributes to the development of iron-restricted anaemia in chronic inflammatory diseases. We know the mechanisms involved in the synthesis of hepcidin and, under physiological conditions, there is a balance between activating signals and inhibitory signals that regulate its synthesis. The former include those related to plasmatic iron level and also those related to chronic inflammatory diseases. The most important inhibitory signals are related to active erythropoiesis and to matriptase-2. Knowing how hepcidin is synthesised has helped design new pharmacological treatments whose main target is the hepcidin. In the near future, there will be effective treatments aimed at correcting the defect of many of these iron metabolism disorders.
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[Anemic syndrome in rheumatoid arthritis: Diagnostic approaches and treatment opportunities].
Grinshtein, YI, Shabalin, VV, Kusaev, VV
Terapevticheskii arkhiv. 2016;(5):107-112
Abstract
Anemia of chronic disease (ACD) is a leading cause of anemic syndrome in patients with rheumatoid arthritis (RA). Enhanced hepcidin production mainly stimulated by excess interleukin-6 levels is a key pathodgentic component of ACD (frequently known as anemia of inflammation) by causing the degradation of the transmembrane protein ferroportin, hepcidin impairs iron metabolism. On the basis of the material of recent publications the review gives present-day views on the pathodgenesis of ACD in RA, approaches to the diagnosis and differential diagnosis of ACD, especially in its concomitance with iron-deficiency anemia, as well as approaches to therapy for the type of anemic syndrome with the complex mechanism for its development.