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Signs of folate deficiency anemia most of the time are subtle. [4] Anemia (macrocytic, megaloblastic anemia) can be a sign of advanced folate deficiency in adults. [1] Folate deficiency anemia may result in feeling tired, weakness, changes to the color of the skin or hair, open sores on the mouth, shortness of breath, palpitations, lightheadedness, cold hands and feet, headaches, easy bleeding ...
Macrocytic anemias have several causes but with the implementation of folic acid fortification in North America, folate deficiency has become a rare cause of megaloblastic macrocytic anemia in that part of the world. [1] In this region, Vitamin B 12 deficiency is a far more common cause of megaloblastic macrocytic anemia. [1]
For example, methotrexate is used as cancer chemotherapy because it can prevent neoplastic cells from dividing. [1] [2] Bacteria also need DHFR to grow and multiply and hence inhibitors selective for bacterial vs. host DHFR have found application as antibacterial agents. [3] Tetrahydrofolate synthesis pathway
Folate in the form of folic acid is used to treat anemia caused by folate deficiency. [3] Folic acid is also used as a supplement by women during pregnancy to reduce the risk of neural tube defects (NTDs) in the baby. [3] [10] NTDs include anencephaly and spina bifida, among other defects.
However, because they are analogues and therefore slightly different from regular nucleotides, causing the cell's growth to be halted and the cell to die. antifolates – chemicals that block the actions of folic acid (vitamin B9) which is needed to build DNA and allow cells to grow.
For determination of cause, further patient history, testing, and empirical therapy may be clinically indicated. A measurement of methylmalonic acid (methylmalonate) can provide an indirect method for partially differentiating Vitamin B 12 and folate deficiencies. The level of methylmalonic acid is not elevated in folic acid deficiency.
Other causes appear to be Kearns–Sayre syndrome [5] and autoantibodies to the folate receptor. [6] [7] [8] For people with the FOLR1 mutation, even when the systemic deficiency is corrected by folate, the cerebral deficiency remains and must be treated with folinic acid. Success depends on early initiation of treatment and treatment for a ...
Tetrahydrofolate and its derivatives are essential for purine and thymidylate synthesis, which are important for cell proliferation and cell growth. [11] DHFR plays a central role in the synthesis of nucleic acid precursors, and it has been shown that mutant cells that completely lack DHFR require glycine, a purine, and thymidine to grow. [ 12 ]