Release into the circulation of immature precursors of red blood cells, due to deficiency of either folic acid or vitamin B12.
A prominent form of anemia, characterized by a diminished level of the oxygen-carrying pigment hemoglobin in the bloodstream, is megaloblastic anemia. This condition arises due to a deficiency of either vitamin B12 or another vitamin called folic acid. Insufficient levels of these vitamins significantly disrupt the production of red blood cells within the bone marrow. Consequently, an excess of abnormal and immature red cells known as megaloblasts appears in the marrow. These megaloblasts give rise to enlarged and distorted red blood cells referred to as macrocytes.
Vitamin B12 deficiency stems from the fact that this particular vitamin is exclusively found in animal-derived foods, such as meat and dairy products. Absorption of vitamin B12 occurs in the small intestine after it combines with a substance called intrinsic factor, which is produced by the lining of the stomach. The primary cause of vitamin B12 deficiency is pernicious anemia, a condition where the stomach lining fails to generate intrinsic factor, usually as a consequence of an autoimmune disorder characterized by the immune system attacking the body’s own tissues. Total gastrectomy, which involves the removal of the stomach, also hampers the production of intrinsic factor, while surgical resection of a portion of the small intestine or the presence of the intestinal disorder known as Crohn’s disease impedes B12 absorption. In a minority of cases, vitamin B12 deficiency occurs due to following a vegan diet, which excludes all animal-derived foods.
Folic acid, predominantly found in green vegetables and liver, constitutes an essential nutrient. Inadequate dietary intake stands as the typical cause of folic acid deficiency. However, factors that disrupt the absorption of folic acid from the small intestine, such as Crohn’s disease or coeliac disease, can also contribute to this deficiency. Folic acid is particularly crucial for rapidly dividing cells, including those in the developing fetus. As a preventive measure against neural tube defects in the fetus, women are advised to take folic acid supplements before conception and during early pregnancy. It should be noted that this recommendation primarily aims to reduce the risk of neural tube defects rather than to prevent anemia.
A considerable number of individuals with mild megaloblastic anemia may not exhibit any symptoms. However, others may encounter fatigue, discomfort in the mouth and tongue, weight loss, and mild jaundice. Prolonged deficiency of vitamin B12 can lead to further symptoms arising from nerve damage, which may include sensations of numbness and tingling in the feet.
The diagnosis of megaloblastic anemia is established through blood tests and can be confirmed if a bone marrow biopsy is performed, involving the extraction of a small sample of marrow for microscopic analysis. The presence of abundant megaloblasts within the sample serves as an indication of the condition.
Megaloblastic anemia resulting from a deficient diet can be effectively treated with a brief regimen of vitamin B12 injections or folic acid tablets, accompanied by the adoption of a regular, balanced diet. However, if the underlying cause of malabsorption is incurable, a lifelong course of vitamin B12 injections or folic acid tablets becomes necessary for management.