Iron-deficiency Anemia

Iron deficiency anemia (IDA) is a common type of anemia that refers to a lack of adequate amounts of healthy red blood cells in the blood. Iron deficiency anemia is caused by an iron deficiency. IDA is the final stage of iron deficiency (including ID, IDE, and IDA), which manifests as microcytic hypochromic anemia and other abnormalities caused by iron deficiency. Iron deficiency anemia can be divided into 3 stages: storage iron deficiency, iron deficiency erythropoiesis, and iron deficiency anemia.

Iron Metabolism Abnormalities in Iron Deficiency Anemia

Iron deficiency anemia can be divided into 3 stages. Storage iron deficiency, iron deficiency erythropoiesis and iron deficiency anemia. Initially, during blood loss, body iron reserves are preferentially used to accelerate erythropoiesis. After depletion of the body's iron reserves, erythropoiesis and production of other iron-containing proteins are limited, leading to marked iron deficiency anemia. The anemia is exacerbated by the shortened survival time of iron-deficient erythrocytes due to their fragility, which accelerates the destruction of reticuloendothelial cells. The observed morphological changes in erythrocytes with underlying iron deficiency reflect a severe impairment of hemoglobin synthesis, characterized by hypopigmentation and microcytosis.

Iron Deficiency Anemia Diagnosis

The diagnostic approach to iron deficiency anemia includes a thorough history, physical examination, and diagnostic evaluation to determine the underlying disease or causative agent.

Iron-refractory Iron Deficiency Anemia

The vast majority of IDAs are acquired. With the intensive study of systemic iron homeostasis, a rare autosomal recessive disorder, IRIDA, has been newly identified. IRIDA is the result of mutations in TMPRSS6, which encodes a type 2 transmembrane serine protease that acts to inhibit the signaling pathway that activates ferroregulin. Loss-of-function mutations in TMPRSS6 result in high expression of ferromodulin, which impedes iron absorption from the intestine. Typical clinical manifestations include normal or low ferritin levels, high ferritin levels, and very low transferrin saturation.

Working model of matriptase-2 (TMPRSS6) regulation of iron homeostasis ^[1].

Iron Metabolism Disorders in IDA

IDA is anemia caused by insufficient intake or loss of iron resulting in a decrease in total body iron insufficient to meet the requirements for erythropoietic activity. In IDA, iron-sensing proteins (BMP6, TFR2, HFE, etc.) in hepatocytes downregulate BMP/SMAD or TFR2-dependent signaling pathways, resulting in decreased hepcidin expression and delivery of more iron to the circulation via FPN. Clinical manifestations include decreased serum iron, ferritin, and transferrin saturation.

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With the in-depth study of systemic iron homeostasis, the physiological mechanisms and causes of the formation of iron deficiency anemia have been further understood. Protheragen, with its research experience in the field of physiological metabolism, helps clients to conduct in-depth research on the physiological mechanisms of iron deficiency anemia, providing new therapeutic ideas for the prevention and treatment of the disease. If you are interested in the services we offer, please contact us for more information.