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Intrathoracic extramedullary hematopoiesis is an unusual condition, usually associated with congenital hemolytic anemias. We present a rare case due to vitamin B12 and folate deficiency diagnosed by CT-guided biopsy.
Chromosomal damage can be detected in bone marrow or peripheral red blood cells in the form of micronuclei. In mice, folate deficiency increased the frequency of micronuclei in erythrocytes. Intraperitoneal caffeine administration, in the setting of folate deficiency, increased the risk of cytogenetic damage in rodents.
A thin-layer chromatographic method for the simultaneous assessment of formimino-glutamic (Figlu) and urocanic acid excretion after loading with 15 g. histidine has been applied to 15 control subjects and to 49 selected patients. Upper limits of normal excretion were determined for urocanic acid and Figlu alone (15 mg. and 30 mg/8 hr. respectively), and for the combined metabolites (40 mg./8 hr.). Of the 49 patients studied, 27 excreted total metabolites above 40 mg./8 hr.; of these 19 would have been revealed by their abnormal excretion of Figlu and 22 by their abnormal excretion of urocanic acid. Of 74 tests in the 64 subjects, urocanic acid was present in all but 27% of the tests, and in 29.8% of the tests urocanic acid was in excess of the amount of Figlu excreted. In six normal and six abnormal tests urocanic acid was the sole metabolite present. These results re-emphasize the value of estimating both histidine metabolites in tests for folate deficiency in man, and underline the greater relative importance of urocanic acid.
It has been reported that patients with vascular disease seem to increase their concentration of plasma homocysteine after the acute episode, whereas reexamined control subjects do not change their concentration of plasma homocysteine over time. Since the main determinants of plasma homocysteine are serum cobalamin, blood folate and serum creatinine we measured these quantities in 20 control subjects and 49 stroke patients in the acute phase and at reexamination 1.5-2 years after acute stroke onset. There were no significant differences between the levels of blood folate, serum cobalamin and serum creatinine in the acute and convalescent phase of all 49 stroke patients. However, we noted a significant decrease of blood folate concentrations in a subgroup of patients (n = 25) who had increased plasma homocysteine concentrations. Thus the increase in plasma homocysteine concentrations in this group of patients may partly be caused by a marginal folate deficiency.
The efficacy of weekly low-dose methotrexate treatment of rheumatoid arthritis is well documented. Efficacy and adverse events are both dose dependent, and side effects rather than lack of response are the main reason for discontinuing therapy. Several adverse effects appear to be related to folate deficiencies, and are largely due to the antifolate properties of methotrexate. In order to diminish side effects without compromising drug efficacy, clinical trials have been performed using folic acid or folinic acid concomitantly with methotrexate. Important to this achievement are both the timing of folate supplementation and the weekly folate-to-methotrexate ratio. Considering these and other factors, an individually adjusted supply of folic acid is proposed. For several patients a properly balanced diet is sufficient; they do not need additional folate supplements when using methotrexate.
Vitamin B-12 (cobalamin) is a cofactor for only two enzymes, methionine synthase and L-methylmalonyl-CoA mutase. The serum vitamin B-12 concentration has been shown to have limitations in specificity and sensitivity in diagnosing vitamin B-12 deficiency and predicting response to therapy in subjects with clinical deficiency syndromes. Serum methylmalonic acid and/or total homocysteine concentrations have been shown to be elevated in almost every patient who has a clinical response to vitamin B-12. In elderly populations serum methylmalonic acid concentrations are elevated in the majority (60-66%) of subjects who have elevated total homocysteine concentrations, suggesting that vitamin B-12 deficiency (with or without associated folate deficiency) and/or chronic renal insufficiency may be the primary cause of most of the elevated total homocysteine concentrations in elderly populations. In such subjects vitamin B-12 and folate concentrations are both frequently in the low or low normal range, making differentiation of the clinical syndromes by use of serum vitamin concentrations problematic. Elevations of 2-methylcitric acid and cystathionine also result from vitamin B-12 deficiency. Serum N-methylglycine concentrations are normal in cobalamin deficiency but are increased in 40% of patients deficient in folate. In conclusion, elevations of methylmalonic acid and total homocysteine are very sensitive and specific in diagnosing vitamin B-12 deficiency and can be used to help differentiate vitamin B-12 deficiency from folate deficiency. Elevated total homocysteine concentrations that may have been attributed to folate deficiency in elderly subjects may in many instances be the result of vitamin B-12 deficiency even though serum vitamin B-12 concentrations are within normal limits.
Measurement of total homocysteine (tHcy) in healthy and diseased children has documented the utility of this marker in pediatric research and diagnostics. This article focuses on novel data obtained in infants, children and adolescents, with emphasis on cobalamin status in infants. In children, determinants of plasma tHcy are similar to those established in adults, and include age, gender, nutrition, B-vitamin status, and some drugs interfering with B-vitamin function. In infants (age < 1 year), tHcy is moderately elevated and related to serum cobalamin, whereas in older children and throughout childhood, plasma tHcy is low (about 60% of adult levels), and folate status becomes a strong tHcy determinant. As in adults, hyperhomocysteinemia in childhood is a risk factor for stroke, and folate-responsive hyperhomocysteinemia has been detected in children with renal failure. tHcy seems to be a sensitive indicator of folate deficiency in children on a poor diet, in HIV-infected children, and in children treated with anti-folate drugs. In children at increased risk of cobalamin deficiency, which includes children born to vegetarian mothers or children in developing countries on a poor diet, tHcy and methylmalonic acid are responsive indicators of a deficiency state. In newborns and infants born to mothers with an adequate nutrition, there are consistent observations of low cobalamin, elevated tHcy and methylmalonic acid, and reduction of both metabolites by cobalamin supplementation. These data have raised the question whether cobalamin deficiency may be widespread and undetected in babies born to non-vegetarian women on a Westernized diet.
Only two (2.5%) of 80 outpatients with histologically proven ulcerative colitis had folate deficiency associated with anaemia or macrocytosis. Mean folate absorption, measured using micrograms/kg body weight of a tritium-labelled physiological folate derivative, 5-methyltetrahydroteroylglutamic acid, in six newly diagnosed patients was 76.7% (normal greater than 95%) but fell to 69.4% after three months' treatment with sulphasalazine. Mean difference in individual patients was 7.5% +/- 5.2% (SD) (p less than 0.02). Mean folate absorption in four patients with megaloblastic anaemia or macrocytosis which developed during treatment with sulphasalazine was 66.3%. This rose to 82.4% after the drug was stopped. Mean difference in individual patients was 16.6 +/- 6.6% (SD) (p less than 0.001). All patients who developed anaemia or macrocytosis with sulphasalazine had additional reasons for folate deficiency. These included coeliac disease, severe nutritional deficiencies, and haemolysis. It was concluded that sulphasalazine impairs folate absorption but this only becomes significant if other reasons for folate deficiency are also present.
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The relationship of anemia as a risk factor for maternal mortality was analyzed by using cross-sectional, longitudinal and case-control studies because randomized trials were not available for analysis. The following six methods of estimation of mortality risk were adopted: 1) the correlation of maternal mortality rates with maternal anemia prevalence derived from national statistics; 2) the proportion of maternal deaths attributable to anemia; 3) the proportion of anemic women who die; 4) population-attributable risk of maternal mortality due to anemia; 5) adolescence as a risk factor for anemia-related mortality; and 6) causes of anemia associated with maternal mortality. The average estimates for all-cause anemia attributable mortality (both direct and indirect) were 6.37, 7.26 and 3.0% for Africa, Asia and Latin America, respectively. Case fatality rates, mainly for hospital studies, varied from <1% to >50%. The relative risk of mortality associated with moderate anemia (hemoglobin 40-80 g/L) was 1.35 [95% confidence interval (CI): 0.92-2.00] and for severe anemia (<47 g/L) was 3.51 (95% CI: 2.05-6.00). Population-attributable risk estimates can be defended on the basis of the strong association between severe anemia and maternal mortality but not for mild or moderate anemia. In holoendemic malarious areas with a 5% severe anemia prevalence (hemoglobin <70 g/L), it was estimated that in primigravidae, there would be 9 severe-malaria anemia-related deaths and 41 nonmalarial anemia-related deaths (mostly nutritional) per 100,000 live births. The iron deficiency component of these is unknown.
A 57-year-old woman developed dementia and peripheral neuropathy 16 years after a partial gastrectomy (Billroth II). Serum cobalamin was 198 pmol/l (reference interval 150-550), and the vitamin B12 absorption test (Schilling) showed decreased absorption (1.7% without and 2.2% with intrinsic factor). In spite of 20 months' therapy with vitamin B12, the neurological symptoms progressed. Folate deficiency was suggested by a very low erythrocyte folate and a slightly abnormal FIGLU test. There were no other signs of general malabsorption. A few months' treatment with folic acid significantly improved the massive neurological manifestations which were verified neurophysiologically as well as histologically. A common role of vitamin B12 and folate in the development of neuropathy is suggested.
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In order to determine the prevalence of micronutrient deficiencies (iron, zinc and folate) in Sri Lankan adolescent school children and the extent to which multiple micronutrient deficiencies exist in this population, a cross-sectional survey (2003) in the Galle district of the micronutrient and anthropometric status of 945 school children of ages 12-16 years was performed. The prevalence of anemia (Hb < 120.0 g/L) was 49.5% in males and 58.1% in females (overall 54.8%, gender difference, P = 0.004). In anemic children 30.2% of males and 47.8% of females were iron deficient (serum ferritin < 30.0 microg/L). Folate deficiency (<6.80 nmol/L) was found in 54.6% and 52.5% of boys and girls respectively whereas zinc deficiency (<9.95 micromol/L) occurred in 51.5% and 58.3%. Anemic boys had a 1.5 (95% confidence interval (CI) 0.9-2.6) and 1.6-fold (CI; 1.1-2.6) greater risk of being stunted and underweight, whereas the risk among anemic girls was 1.7 (CI; 1.1-2.7) and 1.0 (CI; 0.7-1.5) for being stunted and underweight. The relative risks of having at least two deficiencies in iron, zinc and folate among anemic children were 1.6 (CI; 0.6-4.2) among boys and 0.8 (CI; 0.5-1.5) among girls. Iron deficient subjects had a significantly increased risk of 1.8 (CI, 1.1-3.0) of being deficient in folate and 1.7 (CI, 1.2-2.6) of being deficient in zinc. Zinc deficient subjects had a risk of 1.3 (CI, 1.0-1.8) being iron deficient and 1.2 (CI, 0.9-1.7) of being folate deficient. Multiple micronutrient deficiencies are prevalent in Sri Lankan adolescents.