Folate deficiency

Hereditary folate malabsorption—a rare disorder caused by impairment of the folate transporter—can develop into severe folate deficiency manifesting as megaloblastic anemia and occasionally thrombocytopenia. Reportedly, megaloblastic anemia can manifest with hemorrhagic episodes, possibly due to ineffective platelet production and platelet dysfunction.

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Nutritional deficiencies, renal impairment and chronic inflammation are commonly mentioned determinants of anaemia. The aim of this study was to investigate the effects of these determinants, singly and in combination, on anaemia in the very old.

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In developing countries, prevalence of helminthiasis and anaemia has been one of the major public health problems where they cause micronutrient deficiencies of iron, folate, vitamin B12 and infectious diseases among children. Faecal samples and blood samples were obtained from 258 children. Faecal samples were examined using standard parasitological techniques, and anaemia was defined as blood haemoglobin

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Rice (Oryza sativa L.) is a major staple food crop for most of world’s population but unfortunately with low folate content when compared to other plant based foods. Folate is an essential micronutrient in human diet and its deficiency causes neural tube defects, coronary heart disease and certain forms of cancer, impaired cognitive functions.

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Anaemia is one of the most common nutritional problems affecting women in developing countries, where iron deficiency usually combines with other micronutrient deficiencies such as folate and vitamin B. In addition, the diet of the poorest populations is often monotonous and mainly based on staple foods, which are low in iron and contain absorption inhibitors. Other important factors involved in the occurrence of anaemia include malaria and hookworm infestations, chronic infections such as HIV, and congenital conditions like sickle cell disease, among others.

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Specific micronutrient deficiencies may affect maternal and foetal health. Iodine deficiency during pregnancy may cause foetal brain damage and mental retardation in infants. Vitamin A deficiency increases the risk in pregnant women of infection and anaemia, may cause blindness during pregnancy and early lactation, and has been associated to an elevated risk of HIV mother-to-child transmission. Folate deficiency may cause severe foetal neural tube defects like anencephaly and spina bifida.

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The megaloblastic anemias are a group of disorders characterized by the presence of distinctive morphologic appearances of the developing red cells in the bone marrow. The cause is usually deficiency of either cobalamin (vitamin B12) or folate, but megaloblastic anemia may arise because of genetic or acquired abnormalities affecting the metabolism of these vitamins or because of defects in DNA synthesis not related to cobalamin or folate (Table 100-1).

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Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài:Predicting iron and folate deficiency anaemias from standard blood testing: the mechanism and implications for clinical medicine and public health in developing countries

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Anemia occurs in ~80% of myeloma patients. It is usually normocytic and normochromic and related both to the replacement of normal marrow by expanding tumor cells and to the inhibition of hematopoiesis by factors made by the tumor. In addition, mild hemolysis may contribute to the anemia. A larger than expected fraction of patients may have megaloblastic anemia due to either folate or vitamin B12 deficiency. Granulocytopenia and thrombocytopenia are very rare.

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Nutritional Dietary folate deficiency is common. Indeed, in most patients with folate deficiency a nutritional element is present. Certain individuals are particularly prone to have diets containing inadequate amounts of folate (Table 100-5). In the United States and other countries where fortification of the diet with folic acid has been adopted, the prevalence of folate deficiency has dropped dramatically and is now almost restricted to high-risk groups with increased folate needs.

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Antifolate Drugs A large number of epileptics, who are receiving long-term therapy with phenytoin or primidone, with or without barbiturates, develop low serum and red cell folate levels. The exact mechanism is unclear. Alcohol may also be a folate antagonist, as patients who are drinking spirits may develop megaloblastic anemia that will respond to normal quantities of dietary folate or to physiologic doses of folic acid only if alcohol is withdrawn. Macrocytosis of red cells is associated with chronic alcohol intake even when folate levels are normal.

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Serum Folate This is also measured by an ELISA technique. In most laboratories, the normal range is from 11 nmol/L (2.0 µg/L) to ~82 nmol/L (15 µg/L). The serum folate level is low in all folate-deficient patients. It also reflects recent diet. Because of this, serum folate may be low before there is hematologic or biochemical evidence of deficiency.

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Acquired Abnormality of Cobalamin Metabolism: Nitrous Oxide Inhalation Nitrous oxide irreversibly oxidizes methylcobalamin to an inactive precursor; this inactivates methionine synthase. Megaloblastic anemia has occurred in patients undergoing prolonged N2O anesthesia (e.g., in intensive care units). A neuropathy resembling cobalamin neuropathy has also been described in dentists and anesthetists who are repeatedly exposed to N 2O. Methylmalonic aciduria does not occur as adocobalamin is not inactivated by N2O.

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Table 100-4 Malabsorption of Cobalamin May Occur in the Following Conditions But Is Not Usually Sufficiently Severe and Prolonged to Cause Megaloblastic Anemia Gastric causes Simple atrophic gastritis (food cobalamin malabsorption) Zollinger–Ellison syndrome Gastric bypass surgery Use of proton pump inhibitors Intestinal causes Gluten-induced enteropathy Severe pancreatitis HIV infection Radiotherapy Graft-versus-host disease Deficiencies of cobalamin, folate, protein, ?riboflavin, ?nicotinic acid Therapy with colchicine, para-aminosalicylate, neomycin, slow-release potassi...

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Most foods contain some folate. The highest concentrations are found in liver, yeast, spinach, other greens, and nuts (100 µg/100 g). The total folate content of an average Western diet is ~250 µg daily, but the amount varies widely according to the type of food eaten and the method of cooking. Folate is easily destroyed by heating, particularly in large volumes of water. Total-body folate in the adult is ~10 mg, the liver containing the largest store. Daily adult requirements are ~100 µg, so stores are only sufficient for 3–4 months in normal adults and severe folate deficiency may...

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Biochemical Basis of Megaloblastic Anemia The common feature of all megaloblastic anemias is a defect in DNA synthesis that affects rapidly dividing cells in the bone marrow. All conditions that give rise to megaloblastic changes share in common a disparity in the rate of synthesis or availability of the four immediate precursors of DNA: the deoxyribonucleoside triphosphates (dNTPs): dA(adenine)TP and dG(guanine)TP (purines), dT(thymine)TP and dC(cytosine)TP (pyrimidines).

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Psychiatric disturbance is common in both folate and cobalamin deficiencies. This, like the neuropathy, has been attributed to a failure of the synthesis of SAM, which is needed in methylation of biogenic amines (e.g., dopamine) as well as of proteins, phospholipids, and neurotransmitters in the brain (Fig. 100-1). Associations between lower serum folate or cobalamin levels and higher homocysteine levels and the development of Alzheimer's disease have been reported.

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Harrison's Internal Medicine Chapter 100. Megaloblastic Anemias Megaloblastic Anemias: Introduction The megaloblastic anemias are a group of disorders characterized by the presence of distinctive morphologic appearances of the developing red cells in the bone marrow. The cause is usually deficiency of either cobalamin (vitamin B 12) or folate, but megaloblastic anemia may arise because of genetic or acquired abnormalities affecting the metabolism of these vitamins or because of defects in DNA synthesis not related to cobalamin or folate (Table 100-1).

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Protein Starvation Decreased dietary intake of protein may lead to mild to moderate hypoproliferative anemia; this form of anemia may be prevalent in the elderly. The anemia can be more severe in patients with a greater degree of starvation. In marasmus, where patients are both protein- and calorie-deficient, the release of EPO is impaired in proportion to the reduction in metabolic rate; however, the degree of anemia may be masked by volume depletion and becomes apparent after refeeding.

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Toxicity The safe upper limit for vitamin B6 has been set at 100 mg/d, although no adverse effects have been associated with high intakes of vitamin B 6 from food sources only. When toxicity occurs, it causes a severe sensory neuropathy, leaving patients unable to walk. Some cases of photosensitivity and dermatitis have also been reported. Folate, Vitamin B12 See Chap. 90. Vitamin C Both ascorbic acid and its oxidized product dehydroascorbic acid are biologically active.

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