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BACKGROUND: Because reference values for vitamin B(12) concentrations and vitamin B(12)-binding capacities for pregnant women have not been established, the reference values for nonpregnant women are often applied to assess vitamin B(12) status. The aim of the present study was to describe ranges of biochemical indices of vitamin B(12) status, including red blood cell (RBC) vitamin B(12), saturated and unsaturated cobalamin-binding proteins, and binding capacities in all trimesters of uncomplicated pregnancy. METHODS: A total of 39 healthy pregnant women with long-term daily intake of vitamin B(12) >2.6 microg/day and uncomplicated pregnancies participated in the study throughout their pregnancies. RBCs and serum vitamin B(12), holo-haptocorrin, unsaturated cobalamin-binding proteins, unsaturated and total vitamin B(12)-binding capacities, total homocysteine (tHcy), and RBC count were assessed in weeks 9-12, 20-22, and 36-38 of gestation. RESULTS: Significant changes in vitamin B(12) status occurred in the course of pregnancy. Serum vitamin B(12) concentrations and percentage of saturation of vitamin B(12)-binding proteins decreased steadily throughout pregnancy. In the third trimester, 35% of the participants had serum vitamin B(12) concentrations <150 pmol/L and 68.6% had <15% saturation of total vitamin B(12)-binding capacities, but no women had RBC vitamin B(12) concentrations <148 pmol/L. However, the decrease in these indices was not associated with reduced hemoglobin concentrations or RBC count or with increased tHcy concentrations. CONCLUSIONS: Our findings suggest that the reference values for vitamin B(12) status in nonpregnant women may not be applicable to pregnant women.
Using homocysteine as a functional marker, we determined optimal folic acid, vitamin B(12), and vitamin B(6) dosages in 21 pediatric sickle cell disease (SCD) patients (11 HbSS, 10 HbSC; 7-16 years). Daily supplements of folic acid (400, 700, or 1,000 microg), vitamin B(12) (1, 3, or 5 U.S. 1989 RDA), and vitamin B(6) (1 or 3 U.S. 1989 RDA) were gradually increased in an 82-week dose-escalation study. Blood was taken at 9 occasions for measurements of erythrocyte (RBC) and serum folate, plasma vitamin B(12), whole-blood vitamin B(6), and plasma homocysteine. Augmentation of folic acid from 700 to 1,000 microg and vitamin B(12) from 3 to 5 RDA did not further decrease homocysteine. Percentages of patients exhibiting significant individual homocysteine decreases amounted to 43% (folic acid from 0 to 400 microg, vitamins B(12) and B(6) from 0 to 1 RDA), 14% (folic acid from 400 to 700 microg), 24% (vitamin B(12) from 1 to 3 RDA), and 18% (vitamin B(6) from 1 to 3 RDA ). The lowest plasma homocysteine at 82 weeks was 5.9 +/- 2.2 micromol/L. Patients with HbSS had higher RBC folate than HbSC. The entire group exhibited an inverse relation between RBC folate and hemoglobin. We conclude that RBC folate is less valuable for folate status assessment in SCD patients. Optimal dosages are as follows: 700 microg folic acid (3.5-7 U.S. 1989 RDA), 3 U.S. 1989 RDA vitamin B(12) (4.2-6.0 microg), and 3 U.S. 1989 RDA vitamin B(6) (4.2-6.0 mg). A practical daily combination is 1 mg folic acid (4.3-8.5 U.S. 1998 RDA when taken with meals), 6 microg vitamin B(12) (2.5-5 U.S. 1998 RDA), and 6 mg vitamin B(6) (4.6-10 U.S. 1998 RDA). This combination may by simple and relatively inexpensive means reduce these patients' inherently high risk of endothelial damage.
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BACKGROUND: In the elderly, deficiencies of folate, cobalamin (vitamin B(12)) and pyridoxal phosphate (vitamin B(6)) are common. The metabolites homocysteine, methylmalonic acid, 2-methylcitric acid and cystathionine have been reported to be sensitive markers of these vitamin deficiencies. OBJECTIVE: The long-term (269 days) effect of an intramuscular vitamin supplement containing 1 mg vitamin B(12), 1.1 mg folate, and 5 mg vitamin B(6) on serum concentrations of homocysteine (tHcy), methylmalonic acid (MMA), 2-methylcitric acid (2-MCA), and cystathionine (Cysta) was studied in 49 elderly subjects with normal levels of vitamin B(12). METHODS: Vitamin supplement was administered 8 times over a 21-day period, metabolite concentrations were measured until day 269 (e.g. 248 days after the end of vitamin supplementation). RESULTS: From day 0 to 21, the serum levels of the 3 vitamins increased significantly, after cessation of supplementation the levels returned to baseline within the follow-up period. The MMA, 2-MCA and tHcy levels decreased during the treatment period significantly and did not reach baseline values within the 248-day period. Cysta levels did not differ significantly from baseline, either during or after treatment. CONCLUSION: MMA and 2-MCA levels rather reflect the availability of vitamins, especially cobalamin, than the actual serum levels. Since deficiencies of folate, cobalamin and pyridoxal phosphate in the elderly may cause hyerhomocysteinemia and hence may have unfavorable effects on mental performance, determination of MMA and 2-MCA levels in elderly patients with mental disturbances may be a cost-effective measure to improve or maintain mental performance.
The concentrations of CoA in the livers of severely vitamin B(12)-deficient ewes were about 2.6 times those in pair-fed animals treated with vitamin B(12). When the feeding rates of the pair-fed animals were closely similar, the concentrations of methylmalonic acid in deficient livers were about twice those in vitamin B(12)-sufficient livers. The molar concentrations of CoA present were more than three times those of methylmalonic acid in both deficient and treated animals, and it is concluded that the elevated concentrations of CoA in the deficient livers were not primarily due to accumulation of methylmalonyl-CoA.
Low serum vitamin B12 levels and vitamin B12 deficiencies are frequently found in the elderly. The full syndrome of a vitamin B12 deficiency is rather simple to diagnose. The large applicability of the vitamin B12 assay also gives rise to many probably incomplete features. Low/low-normal vitamin B12 levels in screening procedures raise uncertainty whether this finding represents deficiency and should be followed by supplementation. In this paper the occurrence of low serum levels of vitamin B12 are discussed. To assess the clinical relevance of low/low-normal outcomes supplementary diagnostic procedures will be needed. Within this scope we illustrate the d.o.s.-test and the MMA-assay. Especially the latter will probably provide more answers to the treatment question. Systematic research is needed to clarify this issue. Meanwhile supplementation of all low and low-normal outcomes of the B12-assay seems the best answer.
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The vitamin B(12) level and the capacity of serum to bind B(12) are higher in the West Indian population living in Great Britain than in Europeans. The B(12) level fell during pregnancy in both groups but remained higher in the West Indians. West Indians had higher levels of IgG.
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A third vitamin B(12) binding protein present in normal serum has been shown to participate in transport of labelled vitamin B(12) absorbed from the gut. All three vitamin B(12) binding proteins in serum were labelled at the same time after oral administration of vitamin B(12), implying that "free" vitamin B(12) reached the portal blood from the gut mucosa.
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The effect of partial pancreatectomy (80-90%) on vitamin B(12) absorption was studied in the rat. The absorption of 5 ng of (57)Co-labeled vitamin B(12) was significantly reduced from 70 +/-2.5% (mean +/-SE) in control and sham-operated rats to 32 +/-2.6% in partially pancreatectomized rats. Hog pancreatic extract (0.17 g/kg) improved vitamin B(12) absorption from 30.0 to 61.0% in partially pancreatectomized rats but did not alter vitamin B(12) absorption in control rats. Chloramphenicol did not enhance vitamin B(12) absorption in partially pancreatectomized rats with pancreatic extract-improved vitamin B(12) malabsorption. The partially pancreatectomized rats with pancreatic extract-improved vitamin B(12) malabsorption were sacrificed and the stomach and small bowel studied in vitro to further define the pathogenesis of the vitamin B(12) malabsorption. Rat gastric intrinsic factor stimulated vitamin B(12) uptake by intestinal sacs prepared from partially pancreatectomized rats 3.1-fold. Gastric intrinsic factor prepared from partially pancreatectomized rats was as effective in promoting vitamin B(12) uptake by rat intestinal sacs as intrinsic factor prepared from control rats. These data indicate that partially pancreatectomized rats develop an abnormality in the absorption of labeled vitamin B(12) which can be corrected by pancreatic extract. The vitamin B(12) malabsorption is due to neither an alteration in gastric intrinsic factor activity nor an impairment of the intrinsic factor-vitamin B(12) receptor in the intestine. It is suggested that in the partially pancreatectomized rats the intrinsic factor-vitamin B(12) complex exists in a form which is not available for absorption.