Author: Kalyani Jana & Dr. Abha Kumar
DOI Link: https://doi.org/10.70798/Bijmrd/03120013
Abstract: Iron Deficiency Anemia (IDA) is the most common micronutrient deficiency globally, affecting over two billion individuals and representing a major public health concern. It disproportionately impacts children, adolescents, and women of reproductive age, contributing to increased morbidity, impaired cognitive and physical development, and adverse maternal and perinatal outcomes. IDA arises from a multifactorial etiology, including inadequate dietary intake, increased physiological iron requirements, chronic blood loss, malabsorption syndromes, and genetic predispositions. At the cellular and molecular levels, iron deficiency impairs hemoglobin synthesis, resulting in microcytic, hypochromic erythrocytes, and triggers compensatory erythropoietic and systemic responses. The hepcidin-ferroportin axis serves as a central regulatory pathway controlling iron absorption and mobilization, while iron regulatory proteins (IRPs) modulate intracellular iron homeostasis. Clinical manifestations include fatigue, pallor, cognitive dysfunction, restless leg syndrome, and impaired immune function. Diagnosis relies on a combination of hematologic indices, serum ferritin, transferrin saturation, soluble transferrin receptor levels, and emerging molecular biomarkers. Management strategies encompass dietary and lifestyle interventions, oral and intravenous iron supplementation, and novel therapies targeting hepcidin modulation, iron absorption, and gut microbiome interactions. Understanding the pathophysiology, molecular mechanisms, and systemic consequences of IDA is essential for designing personalized interventions, optimizing therapeutic efficacy, and guiding future research in nutritional anemia.
Keywords: Iron Deficiency Anemia, Hemoglobin, Hepcidin, Ferroportin, Erythropoiesis, Iron Metabolism, Nutritional Deficiency, Molecular Mechanisms, Gut Microbiome.
Page No: 123-130