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BMJ Open Gastroenterology Jan 2022The WHO has recognised iron deficiency anaemia (IDA) as the most common nutritional deficiency in the world, with 30% of the population being affected with this... (Review)
Review
The WHO has recognised iron deficiency anaemia (IDA) as the most common nutritional deficiency in the world, with 30% of the population being affected with this condition. Although the most common causes of IDA are gastrointestinal bleeding and menstruation in women, decreased dietary iron and decreased iron absorption are also culpable causes. Patients with IDA should be treated with the aim of replenishing iron stores and returning the haemoglobin to a normal level. This has shown to improve quality of life, morbidity, prognosis in chronic disease and outcomes in pregnancy. Iron deficiency occurs in many chronic inflammatory conditions, including congestive cardiac failure, chronic kidney disease and inflammatory bowel disease. This article will provide an updated overview on diagnosis and management of IDA in patients with chronic conditions, preoperative and in pregnancy. We will discuss the benefits and limitations of oral versus intravenous iron replacement in each cohort, with an overview on cost analysis between the different iron formulations currently on the market.
Topics: Anemia, Iron-Deficiency; Chronic Disease; Female; Humans; Iron; Iron Deficiencies; Iron, Dietary; Pregnancy; Quality of Life
PubMed: 34996762
DOI: 10.1136/bmjgast-2021-000759 -
Nutrients Feb 2020A normal pregnancy consumes 500-800 mg of iron from the mother. Premenopausal women have a high incidence of marginal iron stores or iron deficiency (ID), with or... (Review)
Review
A normal pregnancy consumes 500-800 mg of iron from the mother. Premenopausal women have a high incidence of marginal iron stores or iron deficiency (ID), with or without anemia, particularly in the less developed world. Although pregnancy is associated with a "physiologic" anemia largely related to maternal volume expansion; it is paradoxically associated with an increase in erythrocyte production and erythrocyte mass/kg. ID is a limiting factor for this erythrocyte mass expansion and can contribute to adverse pregnancy outcomes. This review summarizes erythrocyte and iron balance observed in pregnancy; its implications and impact on mother and child; and provides an overview of approaches to the recognition of ID in pregnancy and its management, including clinically relevant questions for further investigation.
Topics: Adolescent; Adult; Anemia, Iron-Deficiency; Child; Child Development; Child, Preschool; Female; Fetal Development; Humans; Infant; Iron; Iron Deficiencies; Iron, Dietary; Male; Nutritional Physiological Phenomena; Nutritional Requirements; Pregnancy; Pregnancy Complications; Pregnancy Outcome; Premenopause; Young Adult
PubMed: 32053933
DOI: 10.3390/nu12020447 -
International Journal of Molecular... Apr 2021Iron is a critical metal for several vital biological processes. Most of the body's iron is bound to hemoglobin in erythrocytes. Iron from senescent red blood cells is... (Review)
Review
Iron is a critical metal for several vital biological processes. Most of the body's iron is bound to hemoglobin in erythrocytes. Iron from senescent red blood cells is recycled by macrophages in the spleen, liver and bone marrow. Dietary iron is taken up by the divalent metal transporter 1 (DMT1) in enterocytes and transported to portal blood via ferroportin (FPN), where it is bound to transferrin and taken up by hepatocytes, macrophages and bone marrow cells via transferrin receptor 1 (TfR1). While most of the physiologically active iron is bound hemoglobin, the major storage of most iron occurs in the liver in a ferritin-bound fashion. In response to an increased iron load, hepatocytes secrete the peptide hormone hepcidin, which binds to and induces internalization and degradation of the iron transporter FPN, thus controlling the amount of iron released from the cells into the blood. This review summarizes the key mechanisms and players involved in cellular and systemic iron regulation.
Topics: Animals; Cation Transport Proteins; Enterocytes; Ferritins; Hemoglobins; Hepatocytes; Humans; Iron; Iron, Dietary; Liver; Receptors, Transferrin; Spleen; Transferrin
PubMed: 33925597
DOI: 10.3390/ijms22094591 -
ACS Omega Jun 2022Iron is an essential element for human life since it participates in many functions in the human body, including oxygen transport, immunity, cell division and... (Review)
Review
Iron is an essential element for human life since it participates in many functions in the human body, including oxygen transport, immunity, cell division and differentiation, and energy metabolism. Iron homeostasis is mainly controlled by intestinal absorption because iron does not have active excretory mechanisms for humans. Thus, efficient intestinal iron bioavailability is essential to reduce the risk of iron deficiency anemia. There are two forms of iron, heme and nonheme, found in foods. The average daily dietary iron intake is 10 to 15 mg in humans since only 1 to 2 mg is absorbed through the intestinal system. Nutrient-nutrient interactions may play a role in dietary intestinal iron absorption. Dietary inhibitors such as calcium, phytates, polyphenols and enhancers such as ascorbic acid and proteins mainly influence iron bioavailability. Numerous studies have been carried out for years to enhance iron bioavailability and combat iron deficiency. In addition to traditional methods, innovative techniques are being developed day by day to enhance iron bioavailability. This review will provide information about iron bioavailability, factors affecting absorption, iron deficiency, and recent studies on improving iron bioavailability.
PubMed: 35755397
DOI: 10.1021/acsomega.2c01833 -
International Journal of Molecular... Jun 2021Despite its abundance in the environment, iron is poorly bioavailable and subject to strict conservation and internal recycling by most organisms. In vertebrates, the... (Review)
Review
Despite its abundance in the environment, iron is poorly bioavailable and subject to strict conservation and internal recycling by most organisms. In vertebrates, the stability of iron concentration in plasma and extracellular fluid, and the total body iron content are maintained by the interaction of the iron-regulatory peptide hormone hepcidin with its receptor and cellular iron exporter ferroportin (SLC40a1). Ferroportin exports iron from duodenal enterocytes that absorb dietary iron, from iron-recycling macrophages in the spleen and the liver, and from iron-storing hepatocytes. Hepcidin blocks iron export through ferroportin, causing hypoferremia. During iron deficiency or after hemorrhage, hepcidin decreases to allow iron delivery to plasma through ferroportin, thus promoting compensatory erythropoiesis. As a host defense mediator, hepcidin increases in response to infection and inflammation, blocking iron delivery through ferroportin to blood plasma, thus limiting iron availability to invading microbes. Genetic diseases that decrease hepcidin synthesis or disrupt hepcidin binding to ferroportin cause the iron overload disorder hereditary hemochromatosis. The opposite phenotype, iron restriction or iron deficiency, can result from genetic or inflammatory overproduction of hepcidin.
Topics: Animals; Autocrine Communication; Biological Transport; Cation Transport Proteins; Disease Susceptibility; Hepcidins; Homeostasis; Humans; Iron; Ligands; Metabolic Networks and Pathways; Paracrine Communication; Protein Binding; Signal Transduction; Tissue Distribution
PubMed: 34204327
DOI: 10.3390/ijms22126493 -
European Heart Journal Jan 2023Iron deficiency (ID) is common in patients with cardiovascular disease. Up to 60% of patients with coronary artery disease, and an even higher proportion of those with...
Iron deficiency (ID) is common in patients with cardiovascular disease. Up to 60% of patients with coronary artery disease, and an even higher proportion of those with heart failure (HF) or pulmonary hypertension have ID; the evidence for cerebrovascular disease, aortic stenosis and atrial fibrillation is less robust. The prevalence of ID increases with the severity of cardiac and renal dysfunction and is probably more common amongst women. Insufficient dietary iron, reduced iron absorption due to increases in hepcidin secondary to the low-grade inflammation associated with atherosclerosis and congestion or reduced gastric acidity, and increased blood loss due to anti-thrombotic therapy or gastro-intestinal or renal disease may all cause ID. For older people in the general population and patients with HF with reduced ejection fraction (HFrEF), both anaemia and ID are associated with a poor prognosis; each may confer independent risk. There is growing evidence that ID is an important therapeutic target for patients with HFrEF, even if they do not have anaemia. Whether this is also true for other HF phenotypes or patients with cardiovascular disease in general is currently unknown. Randomized trials showed that intravenous ferric carboxymaltose improved symptoms, health-related quality of life and exercise capacity and reduced hospitalizations for worsening HF in patients with HFrEF and mildly reduced ejection fraction (<50%). Since ID is easy to treat and is effective for patients with HFrEF, such patients should be investigated for possible ID. This recommendation may extend to other populations in the light of evidence from future trials.
Topics: Humans; Female; Anemia, Iron-Deficiency; Heart Failure; Cardiovascular Diseases; Quality of Life; Stroke Volume; Iron Deficiencies; Anemia
PubMed: 36282723
DOI: 10.1093/eurheartj/ehac569 -
Life (Basel, Switzerland) Sep 2021Recent years have brought about new understandings regarding the pathogenesis of anemia in sports. From hemodilution and redistribution considered to contribute to the... (Review)
Review
Recent years have brought about new understandings regarding the pathogenesis of anemia in sports. From hemodilution and redistribution considered to contribute to the so-called "sports anemia" to iron deficiency caused by increased demands, dietary restrictions, decreased absorption, increased losses, hemolysis, and sequestration, to genetic determinants of different types of anemia (some related to sport), the anemia in athletes deserves a careful and multifactorial approach. Dietary factors that reduce iron absorption (e.g., phytate, polyphenols) and that augment iron's bioavailability (e.g., ascorbic acid) should be considered. Celiac disease, more prevalent in female athletes, may underlie an unexplained iron deficiency anemia. Iron loss during exercise occurs in several ways: sweating, hematuria, gastrointestinal bleeding, inflammation, and intravascular and extravascular hemolysis. From a practical point of view, assessing iron status, especially in the athletes at risk for iron deficiency (females, adolescents, in sports with dietary restrictions, etc.), may improve the iron balance and possibly the performance. Hemoglobin and serum ferritin are measures that are easily employable for the evaluation of patients' iron status. Cutoff values should probably be further assessed with respect to the sex, age, and type of sport. A healthy gut microbiome influences the iron status. Athletes at risk of iron deficiency should perform non-weight-bearing, low-intensity sports to avoid inducing hemolysis.
PubMed: 34575136
DOI: 10.3390/life11090987 -
Blood Aug 2020Although the serum-abundant metal-binding protein transferrin (encoded by the Trf gene) is synthesized primarily in the liver, its function in the liver is largely...
Although the serum-abundant metal-binding protein transferrin (encoded by the Trf gene) is synthesized primarily in the liver, its function in the liver is largely unknown. Here, we generated hepatocyte-specific Trf knockout mice (Trf-LKO), which are viable and fertile but have impaired erythropoiesis and altered iron metabolism. Moreover, feeding Trf-LKO mice a high-iron diet increased their susceptibility to developing ferroptosis-induced liver fibrosis. Importantly, we found that treating Trf-LKO mice with the ferroptosis inhibitor ferrostatin-1 potently rescued liver fibrosis induced by either high dietary iron or carbon tetrachloride (CCl4) injections. In addition, deleting hepatic Slc39a14 expression in Trf-LKO mice significantly reduced hepatic iron accumulation, thereby reducing ferroptosis-mediated liver fibrosis induced by either a high-iron diet or CCl4 injections. Finally, we found that patients with liver cirrhosis have significantly lower levels of serum transferrin and hepatic transferrin, as well as higher levels of hepatic iron and lipid peroxidation, compared with healthy control subjects. Taken together, these data indicate that hepatic transferrin plays a protective role in maintaining liver function, providing a possible therapeutic target for preventing ferroptosis-induced liver fibrosis.
Topics: Animals; Carbon Tetrachloride Poisoning; Cation Transport Proteins; Cyclohexylamines; Cytokines; Erythropoiesis; Erythropoietin; Female; Ferroptosis; Hepatocytes; Homeostasis; Iron; Iron Overload; Iron, Dietary; Lipid Peroxidation; Liver; Liver Cirrhosis; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Muscle Proteins; Phenylenediamines; Transferrin
PubMed: 32374849
DOI: 10.1182/blood.2019002907 -
Nutrients Nov 2019Dietary trace minerals are pivotal and hold a key role in numerous metabolic processes. Trace mineral deficiencies (except for iodine, iron, and zinc) do not often...
Dietary trace minerals are pivotal and hold a key role in numerous metabolic processes. Trace mineral deficiencies (except for iodine, iron, and zinc) do not often develop spontaneously in adults on ordinary diets; infants are more vulnerable because their growth is rapid and intake varies. Trace mineral imbalances can result from hereditary disorders (e.g., hemochromatosis, Wilson disease), kidney dialysis, parenteral nutrition, restrictive diets prescribed for people with inborn errors of metabolism, or various popular diet plans. The Special Issue "Dietary Trace Minerals" comprised 13 peer-reviewed papers on the most recent evidence regarding the dietary intake of trace minerals, as well as their effect toward the prevention and treatment of non-communicable diseases. Original contributions and literature reviews further demonstrated the crucial and central part that dietary trace minerals play in human health and development. This editorial provides a brief and concise overview that addresses and summarizes the content of the Special Issue.
Topics: Deficiency Diseases; Diet, Healthy; Humans; Noncommunicable Diseases; Nutritional Status; Nutritive Value; Protective Factors; Recommended Dietary Allowances; Risk Factors; Risk Reduction Behavior; Trace Elements
PubMed: 31752257
DOI: 10.3390/nu11112823