Red blood cells folate levels

Folate deficiency results in a megaloblastic anemia that is microscopically indistinguishable from the anemia caused by vitamin B12 deficiency (see above). However, folate deficiency does not cause the characteristic neurologic syndrome seen in vitamin B12 deficiency. In patients with megaloblastic anemia, folate status is assessed with assays for serum folate or for red blood cell folate. Red blood cell folate levels are often of greater diagnostic value than serum levels, since serum folate levels tend to be quite labile and do not necessarily reflect tissue levels. 

Folate status can be assessed by the measurement of serum or red blood cell folate levels, by the histidine load test, and by hematological methods. 

A vegetarian diet would be expected to supply folate in ample amoimts. B12 deficiency can provoke decreases in tissue folate levek, even with a normal intake of folate. What was the effect of the B12 injections on red blood cell folate levels (Figure 9.22) ... 

Red blood cell folate levels which are reduced in vitamin Bj 2 deficient patients increase upon initiation of vitamin therapy (Herbert and Zalusky, 1962). The reduction in total RBC folate is due primarily to decreased folyl polyglutamates with little change in monoglutamates (Jeejeebhoy et al., 1965 Chanarin et al, 1974). Stokstad and co-workers have demonstrated decreased pteroylpolygluta-mates (Thenen and Stokstad, 1973) and an increase in the ratio of methylated to non-methylated folates in the livers of vitamin B 2 deficient rats (Vidal and Stokstad, 1974). Reduction of Me THF uptake was seen in bone marrow cells (Tisman and Herbert, 1973) and PHA-stimulated lymphocytes (Lavoie et al., 1974) from vitamin patients. Lavoie et al. also found a reduction in transfer of methyl groups from C-Me THF to non-folate compounds. 

Herbert, V. and Colman, N. (1978) Selective nutrient deficiency in one cell line and not another Subnormal white cell and normal red blood cell folate levels correlate with state of DNA synthesis in these cells, Clin. Res., 26 487A. 

With investigations of phytochemicals and functional foods, the outcome measure is generally going to be a biomarker of disease, such as serum cholesterol level as a marker of heart disease risk, or indicators of bone turnover as markers of osteoporosis risk. Alternatively, markers of exposure may also indicate the benefit from a functional food by demonstrating bioavailability, such as increased serum levels of vitamins or carotenoids. Some components will be measurable in both ways. For instance, effects of a folic acid-fortified food could be measured via decrease in plasma homocysteine levels, or increase in red blood cell folate. 

As was mentioned earlier, reports by Shojania et al. (Sll, S12) of decreased plasma and red blood cell folate concentrations in users of OCAs first drew attention to this subject. Luhby et al. (LIO) also found evidence of folate deficiency in some women taking OCAs, and Wertalik et al. (W6) found lower plasma folate levels in women on the pill than in controls. It was felt (S12) that a large number of subjects given these agents for long periods of time needed to be studied in order to demonstrate a statistically significant difference, because folate concentrations were seldom profoundly depressed in such women. 

Folate can be measured in plasma or serum by microbiological assay using L. casei as the test organism, but this test can be confounded if the subject is on antibiotic treatment. Serum folate values reflect recent dietary intake and a vitamin deficiency is ascribed only where serum folate remains low over a period of time. Plasma folate levels are thought to reflect the day-to-day variations in dietary folate levels while red blood cell folate is a better indicator of long-term tissue storage levels. 

John Scott and co-workers (Daly ct ai, 1995) coilecled about 56,000 blood samples from women attending prenatal clinics in Ireland, and measured the level of folate in red blood cells. Of these women, 81 produced an MTD infant. The results indicated a dramatic association between an NTD birth and low maternal red cell folate (under 0,15 pg folate/ml cells). 

Folate, bound to protein, is transported in the blood to the liver. There it is methylated and carried to the bone marrow cells, the maturing red blood cells, and perhaps to other cells. Methyl-folate seems to be the chief form of the vitamin in body tissues. Serum levels of folacin range from 7 to 16 nanograms per milliliter of serum. The total body stores of folate normally range between 5 and 12 mg, about half of which is in the liver. The measurement of folacin levels in both blood serum and red blood cells is the procedure used to evaluate folacin nutriture in human beings. 

DEFICIENCY SYMPTOMS. Folacin deficiency in man may result in megaloblastic anemia (of infancy), also called macrocytic anemia (of pregnancy), in which the red blood cells are larger and fewer than normal, and also immature. The anemia is due to inadequate formation of nucleoproteins, causing failure of the megaloblast (young red blood cells) in the bone marrow to mature. The hemoglobin level is low because of the reduced number of red blood cells. Also, the white blood cell, blood platelet, and semm folate levels are low. 

Folate deficiency can occur in alcoholics, pregnancy and dietary insufficiency. Deficiency results in changes in the red and white blood cells. Changes in the red blood cells lead to the same symptoms as pernicious anaemia which are observed in vitamin B12 deficiency. Increased levels of folate are required during pregnancy, lactation and rapid growth. 

Most patients who require dialysis have a normocytic normochronic anemia and a hypoproliferative bone marrow. As erythropoiesis decreases with advancing renal disease, iron shifts from circulating red cells to the reticuloendothelial system, leading to high serum ferritin levels. Repeated blood transfusion is also a common cause of iron overload and hyperferritinemia. Clearly the most important cause of the anemia of chronic renal failure is decreased erythropoietin production by the kidneys uremic patients have much lower plasma erythropoietin levels than comparably anemic patients with normal renal function (E8). Less important causes are shortened red cell survival, iron or folate deficiency, aluminum intoxication, and osteitis fibrosa cystica (E8). Uremic retention products such as methylguanidine (G10) and spermidine (R2) may also have an adverse effect on erythropoiesis. 

---