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Pathology of Vitamin Abnormality

Three main types of folate deficiency may affect man. The deficiency most frequently arises because of inadequate intake of the vitamin, and this is likely to occur when a diet deficient in fresh greens, fruit, nuts and liver is taken; particularly if demands for the vitamin are also increased, as in pregnancy, prematurity, chronic dialysis or in conditions of increased cell proliferation, e.g. hemolytic anemia, myelosclerosis, inflammatory diseases or malignancy. Malabsorption, e.g. in cceliac disease or tropical sprue, and anticonvulsant drug therapy, may also cause a general body deficiency of folate. A second type of folate deficiency, a metabolic defect, may be produced by treatment with a drug inhibiting folate metabolism, most commonly an inhibitor of the enzyme dihydrofolate reductase, e.g. methotrexate or pyrimethamine. These drugs deprive the body of the fully reduced (tetrahydro-) folates which form the active folate coenzymes needed for a variety of different biochemical reactions. The third type of deficiency is the metabolic defect of folate metabolism caused by lack of vitamin B12, as in pernicious anmmia. Vitamin B 2 deficiency, when severe, causes a secondary reduction in all the intracellular folate coenzymes. Although there is still discussion of the exact mechanism, it seems most probable that vitamin B12 deficiency causes 'trapping' of folate in its plasma form, methyltetrahydrofolate. This is thought to occur because vitamin B12 is needed as a cofactor in the homocysteine-methionine reaction by which methyltetrahydrofolate entering cells from plasma is 'demethylated' to release tetrahydrofolate, from which all the intracellular folate coenzymes are subsequently made (Lavoie et al. 1974). A wide variety of tissues may be affected by all three types of folate deficiency (Table 1), so that a number of clinical lesions may occur. Folate is required in three reactions in DNA synthesis, one in pyrimidine synthesis (thymidylate synthesis) and two in purine synthesis. Thymidylate synthesis is a rate-limiting reaction in DNA synthesis and the most rapidly dividing tissues of the body suffer the main effects of the deficiency. The organs most affected are the bone marrow, the epithelial cell surfaces and the gonads. The defects produced in the bone marrow include a fall in red cell, white cell and platelet counts, due partly to death of their precursors in the marrow (ineffective hemopoiesis) and partly to shortened survival of the cells that do reach the peripheral blood. The circulating