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Anemia is a condition in which there is a deficiency of red cells or of hemoglobin in the blood (Peate & Jones, 2014). It is the most common disorder of the blood (2014). When a person has anemia, they have fewer red blood cells than normal, or they have less hemoglobin than normal in each red blood cell and this will result in a reduction in the amount of oxygen being transported throughout the body (2014).Iron deficiency anemia (IDA) is the most common type of anemia throughout the world and occurs in 2-5% of adult men and postmenopausal women in the developed world (2014). IDA is the result of low iron stores in the body due to decreased red blood cell (RBC) production(Cadet, 2018). IDA may be caused by decreased production of RBC related to poor diet (deficient iron, folate, or B12) (2018). It can also occur secondary to increased iron requirements such as during pregnancy, lactation, or infancy (2018). Blood loss is another potential etiology of IDA (2018). Iron is an essential component of haemoglobin in red blood cells and of myoglobin in muscles, which contain around 60% of total body iron (Lopez et al, 2016). The main source of iron in humans comes from the destruction of erythrocytes by macrophages of thereticuloendothelial system including the spleen or in other words, a recycled internal iron supply (Alhossain, Khalafallah & Dennis, 2012). It is also necessary for the functioning of various cellular mechanisms, including enzymatic processes, DNA synthesis, and mitochondrial energy generation (2016). The amount of iron absorbed depends largely on the presence or absence of pathology of the gastrointestinal tract or a comorbidity (such as chronic inflammatory diseases) that may result in expression of the iron regulatory proteins and a peptide called hepcidin, which ultimately blocks iron absorption (2012). Outside the liver, other cell types and organs, such as macrophages, adipocytes, the heart, and the kidneys, can produce hepcidin (2012). In plasma, hepcidin is bound to α2-macroglobulin and albumin, and can be cleared via the kidney (2012).
The main role of hepcidin is to control surface expression of FPN1 by binding to the protein, which is then internalised and degraded by lysosomes (2012). FPN1 is the only known iron-exporting protein, so after its degradation enterocytes, macrophages, and hepatocytes can no longer export iron, which is sequestrated in these cells (2012).Pernicious anemia is the hematologic manifestation of chronic atrophic gastritis affecting the corpus of the stomach that denudes the gastric mucosa of gastric parietal cells (Toh, 2017b). It is the most common type of macrocytic anemia, is caused by vitamin B12deficiency, which is often associated with end stage type A chronic atrophic (autoimmune) gastritis (2017a). This type of anemia develops over 20-30 years (Huether & McCance , 2017a). The underlying alteration in pernicious anemia is the absence of intrinsic factor (IF), a transporter required for gastric absorption of dietary B12(2017a). Vitamin B12is essential for nuclear maturation and DNA synthesis in red blood cells (2017a). Pernicious anemia resulting from autoimmune