Iron Deficiency Anemia, Anemia of Chronic Disease, Iron Overload: Use of Hepcidin as a Laboratory Marker in the Diagnosis Along With its Therapeutic Implications and Management of Iron Homeostasis (original) (raw)

Iron deficiency is mostly affecting nutritional deficiency in low and middle-income countries. Infants, young children, adolescent females, young females with heavy bleeding during menstrual periods, women of childbearing age, and old people are at a significant risk of iron deficiency. Doctors usually prescribe iron therapy in treating iron deficiency. Along with iron deficiency, iron overload is a serious complication when there is an excess of iron storage in the human body. Hemochromatosis, a hereditary genetic defect where an excess of iron absorption happens, caused primary iron overload. Iron overload also develops secondary to multiple transfusions in transfusion-dependent anemic patients (thalassemia, Myelodysplastic syndromes, etc.). Iron overload can damage organs, including the heart and liver, leading to serious complications if it is inadequate or lacks iron chelation therapy. Cytokines and acute phase proteins play a significant role in the etiology of anemia of chronic disease, which is also known as anaemia of inflammation. Hepcidin a peptide hormone regulates iron efflux from plasma-absorbing enterocytes, iron-recycling macrophages, and iron-storing hepatocytes. Hepcidin binds to its receptor ferroportin, a cellular iron exporter, and regulates the membrane content of ferroportin and ferroportin-mediated iron transfer to blood plasma. In iron deficiency, hepcidin reduces iron efflux into the plasma and promotes iron-dependent erythropoiesis. Inflammatory stimuli promote the production of hepcidin, which reduces iron intake in inflammatory anaemia. Hepcidin deficiency results in iron overload in hereditary hemochromatosis, whereas excess hepcidin is associated with inflammatory anaemia, chronic renal disease and iron-refractory anaemia, leading to iron deficiency anemia. The mechanism of hemochromatosis is because of impaired synthesis of hepcidin or impaired hepcidin binding to ferroportin. Hematology parameters and iron studies have limits in diagnosing iron deficiency anaemia , anaemia caused by chronic disorders, according to several studies, as both conditions can produce similar laboratory results. This paper reviews the importance of hepcidin in making a thorough diagnosis of anemia, before starting the treatment, along with serum hepcidin as a prognostic tool for the early detection of early response to oral iron therapy and iron overload (hemochromatosis). Current therapeutic options are limited to control iron levels by regulating the hepcidin/ferroportin axis. This literature review includes reviewing a summary of some of the research in advanced clinical studies on various aspects of hepcidin tuning, understanding the mechanism of hepcidin and its pathological components which may lead to advanced therapies, and alternative therapies, along with the importance of new treatment options, including modulation and inhibition of hepcidin activity and its future use in clinical trials and implementing the latest treatment options. Methodology: The information was collected from secondary sources published in various scholarly journals selected from google scholar. The research articles systematically reviewed and identified hepcidin's role in iron homeostasis, therapeutic and diagnostic advances, and research gaps in the research field. Results/Findings: Based on a systematic review, the current status of the management of iron homeostasis and its limitations are identified. Hepcidin's role in the diagnostic and therapeutic field is explained. Future advances and research gaps in the management of iron homeostasis are explained in the literature review.