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The Patient with Anemia and Iron Deficiency
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
Haye H. van der Wal, Peter van der Meer
Novel markers, such as hepcidin and soluble transferrin receptor, are currently used in research and are not yet suitable for clinical practice. The hepatocyte-derived protein hepcidin is considered the main regulator of iron metabolism. By degrading the iron-exporting protein ferroportin 1 in duodenal enterocytes, hepcidin inhibits dietary iron uptake. Hepcidin also traps iron in the iron storage pool (e.g., liver, reticuloendothelial cells) by blocking ferroportin 1, which causes functional iron deficiency.36 Hepcidin levels are driven by several stimuli, including iron status, inflammation, infection, and renal dysfunction, making interpretation of circulating hepcidin levels in HF difficult (Figure 24.3).37 Soluble transferrin receptor (sTfR) is the shed fragment of transferrin receptor 1. Circulating sTfR levels are inversely related to the degree of cellular iron deficiency. Analysis of sTfR levels is not readily available and reference ranges are highly variable. Nevertheless, the prognostic value of both hepcidin and sTfR has been assessed in a small acute HF cohort. Patients with a combination of low hepcidin (i.e., depleted iron stores) and high sTfR levels (cellular iron deficiency) had the highest mortality after 12 months, with findings being comparable between anemic and non-anemic patients.38
Micronutrients
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Since iron is required for a number of diverse cellular functions, a constant balance between iron uptake, transport, storage, and utilization is required to maintain iron homeostasis in the body (3, 4, 18–19). The metabolism of iron differs from that of other minerals because the body lacks a defined mechanism for the active excretion of iron through kidneys and urine. Therefore, the maintenance of iron balance is mainly regulated at the point of absorption, namely the digestive tract (4, 18–19). Hepcidin is a circulating peptide hormone secreted by the liver that plays a central role in the regulation of iron homeostasis. It is the master regulator of systemic iron homeostasis, coordinating the use and storage of iron with iron acquisition (18). Thus, when the body needs more iron, absorption is increased, and when the quantity of iron in the body is sufficient, absorption is restricted. This control is not perfect, but is necessary for the prevention of Fe deficiency and excess (4). For maintaining iron balance and preventing iron deficiency and iron overload, the body has three main mechanisms: regulation of iron absorption, storage of iron as ferritin, and reutilization of iron liberated from the destruction of old red blood cells (erythrocytes) (4).
Micronutrients and Nutraceuticals: Effects on Exercise Performance
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Stella L. Volpe, Quentin Nichols
A major regulator of iron homeostasis is hepcidin, which is a hormone synthesized in the liver (77). Hepcidin plays a primary role in iron regulation by binding to the iron export protein ferroportin 1 (FPN1), thus inhibiting iron transport. Ferroportin 1 is located on the basolateral surface of the intestinal enterocytes and the plasma membrane of macrophages. By inhibiting ferroportin, hepcidin precludes iron from being exported, and thus, iron is sequestered in the cells. Hepcidin therefore decreases dietary iron absorption and decreases iron release from macrophages (5, 19, 54).
Biomarkers of erythropoiesis response to intravenous iron in a crossover pilot study in unexplained anemia of the elderly
Published in Hematology, 2023
Justin J. Yoo, Harvey J. Cohen, Andrew S. Artz, Elizabeth Price, Jeffrey A. Fill, Josef Prchal, Shelly Sapp, Huiman Barnhart
Several other markers beyond ferritin and serum iron may illuminate iron status in patients. Hepcidin is produced by hepatocytes and is the primary systemic negative regulator of iron absorption. Hepcidin levels are low in individuals with iron deficiency anemia, while hepcidin is induced in response to iron loading [23]. Hepcidin can also be induced in response to inflammation or infection inhibiting mobilization of iron stores [24]; in contrast, hepcidin is inhibited by hypoxia and augmented erythropoiesis through stimulation of the negative regulator; i.e. erythroferrone [25,26]. Plasma soluble transferrin receptor (STfR) is predominantly derived from the erythrons as a complex of transferrin, the primary carrier protein of iron, and transferrin receptor. STfR when elevated is a marker of iron deficiency but also may suggest effective iron accessibility, as IV iron correction of anemia reduces STfR in inflammatory anemias [27,28]. The STfR index, derived from STfR divided by ferritin, may help to identify a component of iron deficiency in the setting of concurrent inflammation although the clinical utility requires validation [11,29,30].
Molecular mechanisms of ferroptosis and their role in inflammation
Published in International Reviews of Immunology, 2023
Feng Wang, Jingya He, Ruxiao Xing, Tong Sha, Bin Sun
Furthermore, in COVID-19, in addition to the classic view of lung immune inflammation, the occurrence of hypoxic blood diseases with abnormal iron metabolism should also be considered [25]. Cell iron overload is tolerated up to a threshold, as with silent hypoxia during the first phase of COVID-19. The increase in multi-organ oxidative stress associated with ferroptosis exacerbates inflammation/immune overreaction (the so-called interleukin storm) in the most critical subsequent stage. Laboratory data showed that, compared with survivors, non-survivors have relatively low levels of hemoglobin and higher levels of ferritin [26–28]. In virus-infected lungs, excessive ferritin deposits lead to the onset of fibrin/coagulation disorders. Virus-induced abnormal iron metabolism, oxidative stress, and ferroptosis affect the host immune response [29]. The primary regulator of iron metabolism is hepcidin, which interacts with ferroportin to promote iron entry into cells. If certain viruses (such as SARS-COV-2) exert a hepcidin-like activity, significant abnormalities in iron metabolism with hyperferriproteinemia may occur, eventually leading to ferroptosis [30].
Levels of Serum Ferritin and Hepcidin in Patients with Uncomplicated Falciparum Malaria in Hodeidah, Yemen: Considerations for Assessing Iron Status
Published in Hemoglobin, 2022
Amal A. Al-Azazi, Rashad Abdul-Ghani, Mona H. El-Sayad, Nadia A. Sadek, Hend A. El-Taweel
Iron homeostasis can be assessed by measuring iron indices, including serum iron, total iron binding capacity (TIBC), and ferritin (FER). Measurement of serum iron indicates the iron level in the blood, whereas TIBC measures the blood capacity to bind iron with transferrin, an iron-binding glycoprotein produced by the liver and controls the level of free iron in biological fluids [10]. Ferritin is the predominant iron storage protein in the bone marrow and tissues [11,12]. The discovery of hepcidin (HEPC), a peptide hormone synthesized principally by hepatocytes, as a key regulator of iron homeostasis represents a major advance in the understating of iron metabolism [13–16]. Hepcidin regulates iron metabolism by interacting with the transmembrane receptor, ferroportin. Its synthesis increases as a result of iron overload and inflammation but decreases as a result of erythropoiesis [16].