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Trace Mineral Deficiencies – Diagnosis and Treatment
Published in Jennifer Doley, Mary J. Marian, Adult Malnutrition, 2023
Kavitha Krishnan, Julianne Werner
Iron deficiency may present as fatigue, sleepiness, headache, loss of appetite, and nausea.18 Additional physical characteristics may include pallor, glossitis, koilonychia, pale conjunctivae, and pale gum color.2,19 Patients can also exhibit extreme sensitivity to cold temperatures, increased susceptibility to infections and even an increase in lead absorption.2,18 Iron deficiency can also cause restless leg syndrome.20
Haematological Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
The underlying cause of iron deficiency must be found. In a woman of reproductive age, iron deficiency is nearly always caused by imbalance between dietary intake and iron losses (menstrual and pregnancy related blood loss).In all males and postmenopausal women, the development of iron deficiency must be assumed to be caused by a gastrointestinal malignancy until proven otherwise by full gastrointestinal investigation, including endoscopy.
Dental Disease, Inflammation, Cardiovascular Disease, Nutrition and Nutritional Supplements
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
Douglas G. Thompson, Gregori M. Kurtzman, Chelsea Q. Watkins
Iron is required for the synthesis of proteins, including hemoglobin and enzymes. Foods such as red meat, spinach, fish (tuna and salmon), and beans are rich sources of iron. Iron deficiency leads to anemia, which is associated with many oral manifestations including recurrent ulceration, pale mucosa and oral burning sensation. Iron-deficiency anemia leads to a reduction in antioxidant enzymes, leading to an increased oxidative stress and a worsening of periodontal diseases.237 Iron supplements should be considered in those patients who have iron anemia and conditions such as Crohn’s disease as this deficiency can complicate periodontal disease due to an increase in inflammation.238
Schisandrin B promotes senescence of activated hepatic stellate cell via NCOA4-mediated ferritinophagy
Published in Pharmaceutical Biology, 2023
Mingyue Ma, Na Wei, Jieren Yang, Tingting Ding, Anping Song, Lerong Chen, Shuguo Zheng, Huanhuan Jin
Iron, an element necessary for various physiological activities, is involved in the formation of hemoglobin and some vital enzymatic groups. Iron homeostasis plays a key role in cellular and organism viability, and iron overload increases the risk of various diseases including liver disease (Haase et al. 2010). Growing evidence revealed that pathological iron overload could induce cellular senescence (Yang et al. 2017; Mangan 2021; Chen et al. 2022). Iron has a strong catalytic effect and generates reactive oxygen species (ROS) through the Fenton reaction, resulting in cellular oxidative damage and senescence (Dixon and Stockwell 2014; Nakamura et al. 2019; Qi et al. 2021; Yuan et al. 2021). Ferritinophagy, a cell-selective autophagy mediated by nuclear receptor coactivator 4 (NCOA4), is responsible for iron overload. NCOA4 can interact with ferritin heavy chain 1 (FTH1) in autophagosomes, leading to ferritin degradation and ferritin-bound iron release (Dowdle et al. 2014; Mancias et al. 2015). Increased intracellular free iron can then promote ROS accumulation and consequent cellular senescence (Qi et al. 2021).
SARS-CoV-2 Infection Dysregulates Host Iron (Fe)-Redox Homeostasis (Fe-R-H): Role of Fe-Redox Regulators, Ferroptosis Inhibitors, Anticoagulants, and Iron-Chelators in COVID-19 Control
Published in Journal of Dietary Supplements, 2023
Sreus A.G. Naidu, Roger A. Clemens, A. Satyanarayan Naidu
In human physiology, the dietary iron absorption is regulated in the GI tract via hepcidin from macrophages and eventually contributes to the surge in serum ferritin levels (24). Free iron compounds such as ‘non-transferable bound iron’ and ‘labile plasma iron’ accumulate in plasma and cells via saturated iron-storage proteins (ISPs) (25). Iron is potentially toxic due to its redox activity. Insufficient iron supply to erythroid cells, the major iron consumer in the body, leads to various forms of anemia. On the other hand, iron overload (hemochromatosis) may lead to tissue damage and diseases of liver, pancreas, and heart. Therefore, Fe-R-H is tightly regulated at the cellular and systemic level by iron regulatory proteins (IRP1, IRP2) and hepcidin (26). The nuclear factor (erythroid-derived 2)-like 2 (Nrf2) transcription factor responds to oxidative/electrophilic stress and regulates several genes involved in iron metabolism, heme synthesis, Hb catabolism, iron storage, and iron export (27).
α- and β-Globin Gene Mutations in Individuals with Hemoglobinopathies in the Chattogram and Sylhet Regions of Bangladesh
Published in Hemoglobin, 2023
Tamanna Kabir, Saeed Anwar, Jarin Taslem Mourosi, Shanjida Akter, Mohammad Jakir Hosen
All the index subjects in this study were on iron chelation therapy, yet they had very high SF levels, indicating inadequate chelation and vulnerability to developing iron overload-related complications in these patients (see Figure 1). It has been reported that ineffective erythropoiesis, increased gastrointestinal iron absorption, and multiple blood transfusions may lead to iron overload in patients with thalassemia [28–31]. Iron overload can result in serious health complications, e.g. cardiac and hepatic dysfunction and an impaired immune system. To avoid the complications of iron overload, patients with thalassemia are often recommended iron chelation therapies. The SF levels we observed were comparable with similar studies reported from India; however, they were much higher than those reported from other regions, e.g. North America [31–33]. To ensure efficient management of the individuals with thalassemic conditions, developing a national policy with a thorough delineation of how individuals undergoing iron chelation treatment should be handled pre- and post-therapy is required.