Megaloblastic anemia is either caused by deficiencies in either vitamin B12 or folic acid which results in identical bone marrow and peripheral blood changes that occur with both vitamin deficiencies that are essential for the normal synthesis of DNA. In either form of megaloblastic anemia, the red blood cells that are produced are abnormally large hence the term megaloblastic is coined referring to outsized erythrocytes. Other cells derived from the myeloid stem cells such as lymphocytes and platelets are also abnormal in size. Upon a bone marrow analysis would reveal an abnormal increase in the number of cells produced which are abnormal in appearance because of immaturity of the myeloid cells resulting in the inability for mature erythrocytes to fully develop capable of efficient oxygen transport.
Megaloblastic anemia resulting from folic acid deficiency
Megaloblastic anemia as a result if insufficient folic acid in the body is a result of the inadequacy of folic acid stores in the body. The folic acid stores are usually depleted very quickly when dietary intake of folate is insufficient (usually within four months). Folate is basically found in green leafy vegetables and liver. Folate deficiency occurs in people who rarely eat uncooked vegetables. Moreover, alcohol consumption aggravates the deficiency and the folic acid requirements also increases in people with chronic hemolytic anemia and in women who are in their pregnant state due to the need for RBC production is significantly increased in the aforementioned condition. Furthermore, some patients with malabsorptive diseases of the small bowel also affect folic acid absorption.
Megaloblastic anemia resulting from vitamin B12 deficiency
In cases of megaloblastic anemia that is caused by a deficiency in vitamin B12, it basically occurs when there is an inadequate dietary intake such as those individuals strictly adhering to vegetarianism as their primary diet of choice. Moreover, faulty absorption in the G.I. tract is also a common cause as well as resections in some portions of the small bowel and gastrectomy of the stomach. Another cause of this type of anemia is the absence of the intrinsic factor that are normally secreted by the cells lining the gastric mucosa. Without this intrinsic factor, orally consumed vitamin B12 rich food cannot be absorbed and erythrocyte production is impaired and diminished. Usually, the body normally stores large amounts of vitamin B12 in the body, hence it would take several years before the body will consume its vitamin B12 stores before the deficiency results in anemia. Since the body fairly compensates so well the anemia can only be severe before the individual becomes actually symptomatic.
Medical management of megaloblastic anemia
Folate deficiency resulting in megaloblastic anemia is treated by increasing the amount of folic acid in the diet and administering 1 mg of supplemental folic acid daily. Folic acid is only administered intramuscularly to people with malabsorption problems with the single exception of vitamins administered during pregnancy. After hemoglobin levels return to normal, the folic acid supplementation may be stopped and resume intake through their diet. Vitamin B12 deficiency, treatment is focused by replacement and supplementation. Vegetarians can prevent or treat deficiency with oral supplements with vitamins or fortified soymilk. When the result is absent in intrinsic factor, replacement of the vitamin insufficiency can be done through monthly IM injections of vitamin B12 to prevent megaloblastic anemia from occurring as a complication.
The manifestations of megaloblastic anemia are all similar with the two related vitamin deficiency problem. These types of anemia are generally attributed to being a complication brought about by the insufficiency of certain precursors of the myeloid cells to produce healthy and functional erythrocytes capable of efficient oxygen transport. Treatment for megaloblastic anemia is primarily preventive, supportive and not at all invasive.