Prognosis, Diagnosis, and Treatment of Iron Deficiency Anemia Essay

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Iron Deficiency Anemia

Iron (Fe) is an essential element used in the manufacture of hemoglobin (Hb), a necessary constituent of red blood cells (RBCs). Iron deficiency anemia (IDA) results from the body’s iron stores, dramatically reducing RBCs’ normal production. Women with regular menorrhagia are more prevalent to IDA because of excessive blood loss under this condition. According to Muriuki et al. (2020), the disease affects many Africans, especially children, but the WHO guidelines have underestimated it. Barton et al. (2020) showed that IDA was more prevalent in black and Hispanic women than in white and Asian women. Identifying IDA’s prognostic factors, laboratory diagnostic methods, and treatment is crucial in its management.

Prognosis of Iron Deficiency Anemia

IDA has a good prognosis, especially in children without other underlying health diseases. The recovery from IDA is excellent if the patient begins an iron supplement intervention diet early enough (Bouri & Martin, 2018). The serum iron levels start improving after two months of iron therapy treatment; thus, more iron is available for the hematopoietic function. The prognosis of the condition will vary based on the etiology of the IDA. IDA resulting from chronic bleeding, if practitioners replace blood within time, will have a better prognosis. A delayed blood transfusion will quickly worsen the prognosis of IDA or even result in death. Other factors such as age, chronic disease, and speed of onset play a role in IDA prognosis.

Children will have a better IDA prognosis than the elderly because of the difference in the rate of hematopoiesis. The hematopoietic stem cell (HSC) pool in young people is higher than in the elderly (Pang et al., 2017). During aging, the HSC pool undergoes degenerative changes resulting in mutations and decreases in their number. There is a diminished renewal capacity of the HSC, which reduces the RBC synthesis in the elderly (Daugirdas, 2019). In most old-aged adults, there is a decreased renal function, and the kidney plays an essential role in the production of erythropoietin hormone that stimulates RBC production. Hepatic failure is mainly experienced in the elderly, and the liver plays a significant role in heme synthesis (Nakao et al., 2017). Heme forms an integral part of the hemoglobin molecule, and thus, a decreased hepatic function means a decreased heme synthesis that ultimately affects the RBC production rate. Even if iron deficiency is administered and the adult has these deficiencies, IDA will have a poor prognosis because of the depressed RBC synthesis.

The existence of an underlying chronic health condition worsens the prognosis of IDA. Many older adults have underlying health conditions because of the immunocompromised state or age-associated degenerative processes (Singh et al., 2018). A healthy individual will quickly recover from IDA under iron therapeutic management compared to a person with chronic conditions like congestive heart failure (CHF), peptic ulcer disorder (PUD), hypertension, and diabetes mellitus (DM). Some of these conditions, such as PUD, hypertension, and DM, can cause internal hemorrhage, worsening the condition’s prognosis. Some of the underlying diseases, such as ileal cancer, can lead to ileal resection, leading to a decreased iron absorption rate. Decreased Fe absorption leads to decreased hepatic Fe availability, which causes a reduced heme synthesis in the liver.

Diagnosis of Iron Deficiency Anemia

Complete blood count (CBC) tests and other serum tests are determined to diagnose IDA in the laboratory. Blood pictures and RBC indices play a considerable role in IDA diagnosis (Mohan & Damjanov, 2019). In CBC of IDA due to bleeding, the RBCs are normochromic and normocytic, have a decreased hematocrit, and an increased number of reticulocytes is observed in the blood smear. The increased reticulocyte count is because of an increased erythropoietin hormone by the kidneys to produce new RBCs. In IDA, because of a different etiology, the RBCs are observed to be hypochromic and microcytic. The RBCs of these patients may also exhibit anisocytosis and poikilocytosis. In these patients, there is a normal platelet count unless the patient has had recent bleeding. The reticulocyte count is usually normal but may be slightly increased in these IDA individuals.

Biochemical serum measurements can also be used as a diagnostic marker for IDA. Serum measurement of hemoglobin (Hb) and hematocrit (Hct) reveals decreased values (Mohan & Damjanov, 2019). The mean cellular volume (MCV), mean corpuscular hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC) also reduces in IDA except for IDA of chronic hemorrhagic etiology. The serum iron (Fe) level and serum ferritin are all decreased in IDA. The serum total iron-binding capacity (TIBC) increases, while the serum iron saturation dramatically reduces in IDA. If IDA is diagnosed, other tests such as fecal occult blood test, gynecologic evaluation, and testing urine for blood or hemoglobin are done. The fecal occult test helps determine if the cause of IDA is of gastric origin. These tests are essential in helping the practitioner identify the cause of anemia to offer the correct therapeutic management.

Treatment of Iron Deficiency Anemia

The first mode of IDA treatment involves treating the underlying condition causing the disease. The practitioner may refer the patient to a specialist who can handle the underlying cause appropriately. The treatment of the condition also involves the correction of blood loss and correction of iron deficiency. There are multiple ways through which a medical practitioner can replace the Fe deficiency defect. The patient should consume a diet rich in Fe and foods that help in Fe absorption, such as vitamin C (He et al., 2018). These foods include red meat, seafood, beans, iron-fortified cereals and bread, and dried fruits such as apricots. These sources provide heme that is easily absorbable by the body and incorporated into RBC synthesis.

The other method of IDA treatment involves the correction of Fe deficiency through oral or parenteral iron therapy. The dosage of elemental iron required to treat IDA in adults is about 120mg for at least three months (Sales et al., 2021). A Hb increase of 1mg/dL shows the patient’s response to treatment. Medical personnel should continue the therapy for three months after IDA correction to encourage the buildup of Fe stores. Parenteral Fe therapy is used for patients that can not tolerate or absorb the oral Fe administration (Resál et al., 2021). These patients include those who have undergone gastrojejunostomy, gastrectomy, and other minor bowel surgeries. Iron sucrose and sodium ferric gluconate have a higher preference because of their increased bioavailability and decreased risk of life-threatening anaphylactic reactions (Basavareddy, 2020). Ferumoxytol and ferric-carboxy maltose are also preferred because it allows significant Fe amounts in fewer infusions than iron sucrose (Auerbach et al., 2018). Practitioners have observed severe side effects in the patients receiving the parenteral iron dextran solution in IDA management.

Blood transfusions play a crucial role in the treatment of IDA. In chronic blood loss, compatible blood transfusion can help quickly restore the normal iron levels in the body (Mishra et al., 2018). It provides the temporal improvement of the patient’s condition and does not entirely correct the IDA defect. A change of diet and therapeutic intervention is vital when a blood transfusion has been done to control IDA. Blood transfusion is given to replace the deficient RBCs in the body. If blood matching is not appropriately done, severe hemolytic complications may worsen the status of the patient.

References

Auerbach, M., Chertow, G. M., & Rosner, M. (2018). . Expert Review of Hematology, 11(10), 829–834.

Barton, J. C., Wiener, H. H., Acton, R. T., Adams, P. C., Eckfeldt, J. H., Gordeuk, V. R., Harris, E. L., McLaren, C. E., Harrison, H., McLaren, G. D., & Reboussin, D. M. (2020). . PLOS ONE, 15(4), e0232125.

Basavareddy, A. (2020). . Indian Journal of Pharmacology, 52(1), 53.

Bouri, S., & Martin, J. (2018). . Clinical Medicine, 18(3), 242–244.

Daugirdas, J. T. (2019). Handbook of chronic kidney disease management. Wolters Kluwer.

He, H., Qiao, Y., Zhang, Z., Wu, Z., Liu, D., Liao, Z., Yin, D., & He, M. (2018). . Food & Function, 9(10), 5390–5401.

Mishra, V., Verneker, R., Gandhi, K., Choudhary, S., & Lamba, S. (2018). Journal of Mid-Life Health, 9(2), 92.

Mohan, H., & Damjanov, I. (2019). Textbook of pathology. Jaypee Brothers Medical Publishers.

Muriuki, J. M., Mentzer, A. J., Webb, E. L., Morovat, A., Kimita, W., Ndungu, F. M., Macharia, A. W., Crane, R. J., Berkley, J. A., Lule, S. A., Cutland, C., Sirima, S. B., Diarra, A., Tiono, A. B., Bejon, P., Madhi, S. A., Hill, A. V. S., Prentice, A. M., Suchdev, P. S., & Elliott, A. M. (2020). . BMC Medicine, 18(1).

Nakao, M., Nakayama, N., Uchida, Y., Tomiya, T., Ido, A., Sakaida, I., Yokosuka, O., Takikawa, Y., Inoue, K., Genda, T., Shimizu, M., Terai, S., Tsubouchi, H., Takikawa, H., & Mochida, S. (2017). . Journal of Gastroenterology, 53(6), 752–769.

Pang, W. W., Schrier, S. L., & Weissman, I. L. (2017). . Seminars in Hematology, 54(1), 39–42.

Resál, T., Farkas, K., & Molnár, T. (2021). Frontiers in Medicine, 8.

Sales, C. H., Rogero, M. M., Sarti, F. M., & Fisberg, R. M. (2021). Nutrients, 13(6), 1888.

Singh, N., Bhatt, S., Muthu, V., Prasad, K. T., Behera, D., & Sharma, P. (2018). . Journal of Clinical Oncology, 36(15_suppl), e21169–e21169.

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