Anaemia folic acid deficiency

Deficiency symptoms The characteristic feature of folic acid deficiency is megaloblastic anaemia. Deficiency also leads to glossitis, enteritis, diarrhoea, general debility, weight loss and sterility. 

It is indicated in folic acid deficiency states e.g. megaloblastic anaemia, tropical... 

Deficiency of folic acid leads to a megaloblastic anaemia because it is necessary for the production of purines and pyrimidines, which are essential precursors of deoxyribonucleic acid (DNA). The megaloblastic marrow of cobalamin deficiency is due to interference with folic acid utilisation and the morphological changes of cobalamin deficiency can be reversed by folic acid. It is vital to realise that folic acid does not provide adequate treatment for pernicious anaemia. Nor does vitamin 3 2 provide adequate treatment for the megaloblastic anaemia of folic acid deficiency, although a partial response may occur because vitamin plays a role in folate metabolism. 

RIO. Ryser, J. E., Farquet, J. T., and Petite, )., Megaloblastic anaemia due to folic acid deficiency in a young woman on oral contraceptives. Acta Haematol. 45,319-324 (1971). 

Folic acid deficiency leading to a megaloblastic anaemia, which requires oral folic acid (bottom right), may occur in pregnancy (folate requirement is increased) and in malabsorption syndromes (e.g. sieai-orriioea and sprue). 

The body stores of folates tire relatively low (5-20 mg) and. as daily reijuircmcnis are high, folic acid deficiency and megaloblastic anaemia can quickly develop (1-6 months) if the intake of folic acid stops. Folic acid itself is completely absorbed in the proximal jejunum, but dietary folates are mainly polygluiamaie forms of folate. All but one... 

Folic acid deficiency, when it occurs, results more commonly from a failure of utilization than from an inadequate dietary intake. It is manifested by macrocytic anaemia and leucopenia. As the name suggests, green leaves are good sources so is yeast. 

The other clinical feature of vitamin B deficiency, which is very rarely seen in folic acid deficiency, is degeneration of the spinal cord - hence the name pernicious for the anaemia of vitamin B deficiency. The spinal cord degeneration is due to a failure of the methylation of one arginine residue on myelin basic protein and occurs in about one-third of patients with megaloblastic anaemia due to vitamin B deficiency and in about one-third of patients who do not show signs of anaemia. 

Dietary deficiency of folic acid is not uncommon, and, as noted above, deficiency of vitamin Iso leads to functional folic acid deficiency. In either case, it is cells which are dividing rapidly, and which therefore have a large requirement for thymidine for DNA synthesis, which are most severely affected. These are the cells of the bone marrow which form red blood cells, the cells of the intestinal mucosa and the hair follicles. Clinically, folic acid deficiency leads to megaloblastic anaemia, the release into the circulation of immature precursors of red blood cells. 

Anaemia often becomes a characteristic feature of several chronic diseases, such as rheumatoid arthritis. In most instances this can be linked to lower than normal endogenous serum EPO levels (although in some cases a deficiency of iron or folic acid can also represent a contributory factor). Several small clinical trials have confirmed that administration of EPO increases haematocrit and serum haemoglobin levels in patients suffering from rheumatoid arthritis. A satisfactory response in some patients, however, required a high-dose therapy that could render this therapeutic approach unattractive from a cost benefit perspective. 

Folic acid (vitamin Bg) is a conjugate of a pteridine unit, p-aminobenzoic acid, and glutamic acid. Deficiency of folic acid leads to anaemia, and it is also standard practice to provide supplementation during pregnancy to reduce the incidence of spina bifida. 

Dietary deficiency anaemia, which is due to deficient supply of various factors e.g. iron, folic acid, vitamin vitamin C and pyridoxine which are essential for normal blood formation. 

Studies on growth factors required by certain microorganisms, for example Streptococcus faecalis and Lactobacillus casei, and of their relevance in animal nutrition, led to the isolation and characterization of folic acid, pteroylglutamic acid (104), the structure of which was determined in 1946. It is an essential vitamin for man and together with vitamin B12 it is involved in the development of blood cells. Deficiency causes macrocytic anaemia. Many microorganisms do not use exogenous folic acid, but synthesize their own, and some... 

Folacin (folic acid) is involved in metabolism and in the biosynthesis of purines and pyrimidines. It is a very stable vitamin but does not occur naturally in feedstuffs. Instead it occurs in reduced forms as polyglutamates, which are readily oxidized. These forms are converted to folic acid in the body. Diets commonly contain sufficient folacin but this is not assured. Folacin is therefore usually included in the vitamin supplement added to poultry diets to ensure adequacy. A deficiency in young chicks or poults results in retarded growth, poor feathering and perosis. Coloured plumage may lack normal pigmentation, and a characteristic anaemia is also present. Cervical paralysis is an additional symptom in deficient turkeys. 

Anaemia occurs when there is a decrease in haemoglobin below the appropriate level for the age and sex of the individual. The anaemia maybe due to several factors as lack of iron, vitamin Bi2 and folic acid all affect red cell production, resulting in anaemia. Bi2 deficiency may also cause neurological problems, such as numbness and weakness. Patients with Bi2 deficiency may also report mood swings and seem to suffer more infection and mild gastrointestinal problems than normal, so Maria s moodiness, stomach upsets and colds may be significant. 

Normocytic, normochromic anaemia (normal size, normal haemoglobin content) can be caused by damage to the bone marrow or by blood loss. Macrocytic (or megaloblastic), normochromic anaemia (large cells, normal amount of haemoglobin) is due to deficiency of folic acid or B12, or both. Microcytic, hypochromic anaemia (small cells, small amount of haemoglobin) is the most common type and is due to iron deficiency. 

Deficiency of Bi2 or folic acid, or both, causes a macrocytic, normochromic anaemia. Maria s red cells are larger than normal, so it is probable that she has this form of anaemia. Folate deficiency is more common that B12 deficiency because there is usually a good store of Bi2 in the liver. When Bi2... 

Folic acid is itself inactive it is converted into the biologically active coenzyme, tetrahydrofolic acid, which is important in the biosynthesis of amino acids and DNA and therefore in cell division. The formyl derivative of tetrahydrofolic acid is folinic acid and this is used to bypass the block when the body fails to effect the conversion of folic acid (see Folic acid antagonists, p. 606). Ascorbic acid protects the active tetrahydrofolic acid from oxidation the anaemia of scurvy, although usually normoblastic, may be megaloblastic due to deficiency of tetrahydrofolic acid. 

Imprecisely diagnosed megaloblastic anaemia is the principal contraindication. Tumour cell proliferation in some cancers may be folate dependent and folic acid should be used in malignant disease only where there is confirmed folate deficiency anaemia. 

Folic acid, or its various equivalents, is used to treat megaloblastic anaemia due to deficiency, which may be due to poor diet, malabsorption syndrome or to the use of certain drugs (e.g. methotrexate or antiepileptics). It is given prophylactically to pregnant women, neonates and in chronic haemolytic anaemia, including sickle-cell anaemia. 

A8. Arakawa, T., Tamura, T., Higashi, O., Ohara, K., Tanno, K., Honda, Y., Narisawa, K., Konno, T., Wada, Y., Sato, Y., and Mizuno, T., Formiminotransferase deficiency syndrome associated with megaloblastic anaemia responsive to pyridoxine or folic acid. Tohoku J. Exp. Med. 94, 3-16 (1968). 

Anaemia is treated according to its cause iron replacement therapy for iron deficiency vitamin B12 and folic acid for decreased production of erythrocytes and to alleviate the effects of increased destruction. 

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