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PubMed2004

A role for homocysteine increase in haemolysis of megaloblastic anaemias due to vitamin B(12) and folate deficiency: results from an in vitro experience.

Megaloblastic anaemias (MA) are frequently associated with haemolysis. The pathogenesis of these finding is not clear, but it is thought to depend on the greater destruction of abnormal and fragile megaloblastic erythrocytes. Vitamin B(12) and folate deficiencies are the commonest cause of MA; these deficiencies may simultaneously induce a significant alteration in homocysteine metabolism leading to hyperhomocysteinemia. Blood cells have enzymes involved in homocysteine metabolism. Considering the possible effects of hyperhomocysteinemia in erythrocyte toxicity (due to oxidative damage and/or to interaction with sulfhydryl residues of structural and enzymatic proteins), the aim of our study was to evaluate (1) the homocysteine blood cells production in patients with MA due to vitamin B(12) and folate deficiency and (2) the possible role and mechanism of hyperhomocysteinemia in MA haemolysis. After incubation at 37 degrees C, blood samples from MA patients showed higher and significant levels of Hcy, LDH, lipid peroxidation parameters (MDA), and ghost protein-bound Hcy than controls. Haemolysis (%) was higher in MA patients than controls and was significantly correlated with Hcy accumulation in the medium, lipid peroxidation indices and ghost protein-bound Hcy. No significant (or significantly lower) alterations through time in considered parameters were observed in the corresponding samples incubated at 4 degrees C or in samples incubated with methionine-free medium (lower Hcy production). Our data, deriving from an in vitro experience, suggest a possible role of Hcy accumulation due to vitamin B(12) and folate deficiencies in haemolysis associated to MA due to vitamin deficiency.

Adult↗
PubMed2005

Atrophic tongue associated with Candida.

BACKGROUND: Traditionally, total atrophic tongue has been due to nutritional deficiencies, such as vitamin B12, folic acid, or iron deficiencies, and partial atrophic tongue has been well known as median rhomboid glossitis or geographic tongue. The other cause of atrophic tongue is oral candidiasis. METHODS: Forty patients with atrophic change of the tongue were examined on a relation to candidiasis. All of them complained of tongue pain on spicy or hot diet. Laboratory examinations included blood examination for diabetes and anemia, culture test and direct cytologic examination. The intensity of tongue pain was evaluated pre- and post-treatment using visual analogue scale (VAS). RESULTS: Twenty-four of 40 (60%) had pre-disposing factors of candidiasis including diabetes mellitus, malignancy, systemic steroid therapy, long-term antibiotic therapy and others in their medical history. Blood examinations revealed mild anemia and/or Fe deficiency in 5 (12.5%), mild diabetes in 4 (10.0%), both in two, while residual 29 patients (72.5%) were within reference levels. In the culture examination, candidal species were isolated in 72.5%, and almost all of them were candida albicans. The direct cytologic examination performed in 17 of 40 patients, witch revealed pseudohyphae of fungi in 14 patients (82.4%). After the antifungal treatment, the tongue pain disappeared or improved markedly in 80%. Simultaneously, the regenerative tendency of filifolm papilla of the tongue dorsum was observed in these patients. CONCLUSION: Atrophic tongue associated with pain at eating, even though it is mild atrophic change, has a high probability of being a candida-induced lesion. Long disease duration and no benefit by topical steroids are suggestive and diagnostic factors of this disease.

Adult↗
PubMed1973

Neurological disease associated with folate deficiency.

In a general medical hospital population the neurological status of 24 patients with severe folate deficiency was compared with that of a control group of 21 patients with normal serum folate. A significant increase of organic brain syndrome and pyramidal tract damage was found in the folate-deficient group. These findings were independent of the degree of anaemia or the presence of alcoholism. These data are consistent with the view that severe folate deficiency may cause neurological deficits.

Alcoholism↗
PubMed2001

Deficiencies of folate and vitamin B(6) exert distinct effects on homocysteine, serine, and methionine kinetics.

Folate and vitamin B(6) act in generating methyl groups for homocysteine remethylation, but the kinetic effects of folate or vitamin B(6) deficiency are not known. We used an intravenous primed, constant infusion of stable isotope-labeled serine, methionine, and leucine to investigate one-carbon metabolism in healthy control (n = 5), folate-deficient (n = 4), and vitamin B(6)-deficient (n = 5) human subjects. The plasma homocysteine concentration in folate-deficient subjects [15.9 +/- 2.1 (SD) micromol/l] was approximately two times that of control (7.4 +/- 1.7 micromol/l) and vitamin B(6)-deficient (7.7 +/- 2.1 micromol/l) subjects. The rate of methionine synthesis by homocysteine remethylation was depressed (P = 0.027) in folate deficiency but not in vitamin B(6) deficiency. For all subjects, the homocysteine remethylation rate was not significantly associated with plasma homocysteine concentration (r = -0.44, P = 0.12). The fractional synthesis rate of homocysteine from methionine was positively correlated with plasma homocysteine concentration (r = 0.60, P = 0.031), and a model incorporating both homocysteine remethylation and synthesis rates closely predicted plasma homocysteine levels (r = 0.85, P = 0.0015). Rates of homocysteine remethylation and serine synthesis were inversely correlated (r = -0.89, P < 0.001). These studies demonstrate distinctly different metabolic consequences of vitamin B(6) and folate deficiencies.

Adult↗
PubMed2002

Interactions of ethanol and folate deficiency in development of alcoholic liver disease in the micropig.

Folate deficiency is present in most patients with alcoholic liver disease (ALD), whereas folate regulates and alcoholism perturbs intrahepatic methionine metabolism, and S-adenosyl-methionine prevents the development of experimental ALD. Our studies explored the hypothesis that abnormal methionine metabolism is exacerbated by folate deficiency and promotes the development of ALD in the setting of chronic ethanol exposure. Using the micropig animal model, dietary combinations of folate deficiency and a diet containing 40% of kcal as ethanol were followed by measurements of hepatic methionine metabolism and indices of ALD. Alcoholic liver injury, expressed as steatohepatitis in terminal 14 week liver specimens, was evident in micropigs fed the combined ethanol containing and folate deficient diet but not in micropigs fed each diet separately. Perturbations of methionine metabolism included decreased hepatic S-adenosylmethionine and glutathione with increased products of DNA and lipid oxidation. Thus, the development of ALD is linked to abnormal methionine metabolism and is accelerated in the presence of folate deficiency.

Animals↗
PubMed1983

Folate status in patients receiving maintenance doses of sulfasalazine.

Hematologic studies, including serum and RBC folate assays, were done on 45 outpatients with chronic colitis who either took sulfasalazine (n = 27) or did not use it (n = 18). Overall, sulfasalazine users and nonusers had similar mean hemoglobin, hematocrit, serum folate, and RBC folate levels. However, within the drug users, RBC folate was inversely correlated with drug dose; serum folate was not. Patients taking 2 g or more of sulfasalazine daily had lower mean RBC folate levels (221.2 +/- 27.3 ng/mL) than patients either taking less (371.7 +/- 35.0 ng/mL) or nonusers (330.3 +/- 30.3 ng/mL). Mean corpuscular volume was also related to drug dose but not to RBC folate. Although maintenance sulfasalazine use rarely causes clinically significant folate deficiency, subclinical tissue depletion occurs as a dose-related effect.

Colitis↗
PubMed1984

[Deficiency anemias in tropical countries].

Nutritional anaemias are common in tropical areas. The commonest cause is iron deficiency, which mainly arises from impaired absorption of iron from food. Substances which inhibit iron absorption in various diets play an important role in the pathogenesis of iron deficiency anaemia. Iron deficiency is further aggravated by blood loss in hook-worm infestation. Folic acid and vitamin B 12 deficiency are less important causes of nutritional anaemia. The efforts of the World Health Organization to supplement iron in food are described.

Anemia, Hypochromic↗
PubMed1972

Folate deficiency after anticonvulsant drugs: an effect of hepatic enzyme induction?

Serum and red cell folate levels were reduced in 59% and 58% respectively of 75 children with epilepsy attending a residential school. The degree of folate deficiency was significantly related to increased hepatic microsomal enzyme activity, assessed from increased urinary excretion of D-glucaric acid and also correlated with the daily dose of anticonvulsant taken. Anticonvulsant drugs are known to have inducing properties, and since folate is required as a cofactor in drug hydroxylations it is suggested that folate depletion results from increased demand for the cofactor after induction of drug-metabolizing enzymes. As folate deficiency may ultimately limit drug metabolism this hypothesis would explain why blood phenytoin levels decrease and fit control may worsen after correction of folate deficiency in epileptic patients.

Adipates↗
PubMed2002

Folate deficiency alters melatonin secretion in rats.

The final step of melatonin (MLT) synthesis is methylation of N-acetyl-serotonin, with S-adenosylmethionine as a methyl donor provided by a metabolic pathway involving sulfur-containing amino acids (homocysteine and methionine). Remethylation of homocysteine to methionine requires folate. The present study was undertaken to test the influence of folate deficiency on MLT secretion. Severe folate deficiency was induced in rats by feeding them a synthetic diet containing (per kg diet) 0 mg folate and 10 g succinylsulfathiazole. Control rats were fed the same diet containing 8 mg folate/kg. After 4 wk, erythrocyte folate concentrations were significantly lower and plasma homocysteine levels were greater in folate-deficient rats than in controls. Pineal MLT concentration and urinary excretions of MLT, 6 sulfatoxymelatonin (the main hepatic MLT metabolite) and methoxylated catechol compounds were lower in the folate-deficient group than in the controls, whereas plasma catecholamine concentrations did not differ. Decreases generally were more marked at wk 2 than at wk 4 for the urinary metabolite excretions. These findings indicate that folate deficiency dramatically alters MLT secretion in rats.

Animals↗
PubMed2003

[Lactation--a risk factor for elevated plasma homocysteine?].

INTRODUCTION: Women have an increased need of folate in the breastfeeding period and, as a consequence, may be in risk of having a negative folate balance. Elevated total homocysteine in plasma (P-tHcy) is a sensitive marker for deficiency of folate, B6, and B12 vitamins and a risk factor for developing cardiovascular disease. We examined whether there is a difference in P-tHcy among breastfeeding mothers depending on folic acid supplement and compared these results to women from the background population. MATERIAL AND METHODS: A total of 20 breastfeeding mothers had their plasma homocysteine content and their erythrocyte folate content measured through a standard blood sampling procedure in their homes. Half of the mothers took a folic acid supplement. The background population was age-matched, non-pregnant, and non-lactating women from a previous Danish study. RESULTS: The group of breastfeeding mothers who did not take folic acid supplements had a higher prevalence of elevated P-tHcy (70%) both than the group of breastfeeding mothers who took folic acid supplements (30%) and than the background population (33%). The difference between P-tHcy in the group of breastfeeding mothers who did not take folic acid supplements and the group of breastfeeding mothers who took folic acid supplements was non-significant (p = 0.12). However, we found a statistically significant difference between the group of breastfeeding mothers who did not take folic acid supplements and the background population (p = 0.02). DISCUSSION: Our study suggests that there is a significant fraction of Danish breastfeeding mothers in negative folate balance resulting in elevated P-tHcy compared to the background population.

Adult↗
PubMed1975

Serum and erythrocyte folates in combined iron and folate deficiency.

A high incidence of iron and folate deficiency was found in 80 female subjects living in a private institution. Iron therapy in individuals with low serum iron values resulted in a significant increase in hemoglobin levels. An improvement in serum and RBC folate levels was also found following iron therapy but this could not be attributed to treatment since a similar increase was observed in untreated control subjects, probably due to an increased dietary intake of folates during the study period. In subsequent studies small amounts of pteroylglutamic acid were given to all patients and their response to therapy was related to initial serum and RBC folate values. No correlation between serum folate levels and response to folate therapy could be demonstrated. Red cell folate levels on the other hand correlated well with response to therapy. A significant increase in hemoglobin was found following folate therapy in patients with low RBC folates, but not increase in subjects with normal RBC folates. Conversely, the increase in hemoglobin following iron therapy in subjects with normal RBC folates was three times as much as in patients with low RBC folates. Thus, unlike serum folate determinations, RBC folate measurements are a reliable index of tissue folate stores, and useful in the prediction of response to folate therapy in both the iron-deficient and iron-replete states.

Adult↗
PubMed1980

In vitro DNA synthesis by bone marrow cells and PHA-stimulated lymphocytes. Suppression by nonradioactive thymidine of the incorporation of 3H-deoxyuridine into DNA: enhancement of incorporation when inadequate vitamin B12 or folate is corrected.

Previous studies demonstrated that excess deoxyuridine (dU) added to short-term bone marrow and PHA-stimulated lymphocyte cultures, blocks the incorporation of radioactive thymidine into DNA via the salvage pathway. In the current study, we investigated the effects of added thymidine (TdR) in varying concentrations (10(-6) to 1 mumol) on the incorporation of 3H-dU into thymine-DNA, i.e. we executed 'thymidine suppression tests.' Increasing concentrations of exogenous TdR caused progressive inhibition of 3H-dU incorporation into DNA, and decreasing 3H-dU incorporation was parallelled by increasing incorporation of added 14C-TdR. These findings demonstrate reciprocity of the salvage and the de novo pathways of thymine-DNA synthesis, presumably mediated by thymidine-triphosphate (dTTP), the common end product of both pathways, via feedback inhibition. In patients with folate and/or vitamin B12 deficiency, the addition of appropriate vitamins to marrow and lymphocyte cultures enhanced the incorporation of 3H-dU into DNA. As predicted, this was not observed in normal subjects. The enhancing effect of these vitamins on in vitro incorporation of 3H-dU into DNA by deficient cell systems was similar to their correcting effect on abnormal dU suppression. These findings support the theoretical concept that the dU suppression test defines biochemical megaloblastosis due to deficiency of folate and vitamin B12.

Bone Marrow↗
PubMed2001

Nutrition: impact on oral and systemic health.

Good dietary practices and optimal nutritional status promote growth and tissue development, as well as feature prominently in the prevention of diseases. Malnutrition (particularly protein-energy malnutrition, which invariably involves concurrent deficiencies of the antioxidant micronutrients) promotes salivary gland hypofunction, impaired immunity, and an early shift in the oral microbial ecology toward a preponderance of anaerobic organisms. The immune suppression, which includes impaired cytokine function as well as diminished acute-phase response to infections, impacts negatively on the natural history of inflammatory periodontal diseases. The pathogenesis of oral cancer is influenced by deficiencies of antioxidant nutrients, and there is evidence for diminished DNA methylation, disruption of DNA integrity, and increased DNA damage in folate deficiency.

Acute-Phase Reaction↗