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Results for “FOLIC ACID DEFICIENCY”

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PubMed1999

Laboratory diagnosis of vitamin B12 and folate deficiency: a guide for the primary care physician.

At one time, the diagnosis of a deficiency of vitamin B12 or folate was considered to be relatively straightforward. As knowledge has accumulated, the limitations of such tests as serum vitamin level measurements and the Schilling test have become apparent. With the development of newer tests, atypical and subclinical deficiency states have been recognized. In this review, available tests used in the diagnosis of vitamin B12 and folate deficiency are discussed, and a rational approach to the diagnosis of these deficiency states is presented.

Antibodies↗
PubMed2000

Microbially produced acetaldehyde from ethanol may increase the risk of colon cancer via folate deficiency.

High alcohol and low folate intake are independent risk factors for colorectal cancer. Acetaldehyde has been postulated to be a factor responsible for ethanol-associated carcinogenesis. High levels of acetaldehyde accumulate in the large intestine via the microbial oxidation of alcohol. Acetaldehyde degrades folate in vitro. Thus, it is possible that high intracolonic acetaldehyde levels break down folate in the colon. Our aim was to test the effect of high alcohol and acetaldehyde concentrations in the gut on systemic and local intestinal folate levels in rats. Twenty rats received 3 g/kg of ethanol twice a day for 2 weeks with or without concomitant ciprofloxacin administration. Twenty control rats received saline with or without ciprofloxacin. All rats were fed a diet with normal folate content. Alcohol treatment led to very high intracolonic acetaldehyde levels (387 +/- 185 microM), which were markedly decreased by concomitant ciprofloxacin treatment (21 +/- 4 microM). Erythrocyte, serum and small intestinal folate levels were unaffected by alcohol treatment. Alcohol administration decreased significantly colonic mucosal folate levels by 48%, and this effect was prevented by ciprofloxacin. We conclude that alcohol administration for 2 weeks leads to local folate deficiency of colonic mucosa in rats, most probably via the degradation of folate by the high levels of acetaldehyde microbially produced from ethanol. Our findings offer a unique explanation for the increased risk of colonic cancer associated with alcohol intake and folate deficiency.

Acetaldehyde↗
PubMed1989

Cobalamin-folate interrelations.

Cobalamin deficiency leads to impaired folate function as demonstrated by markedly impaired single-carbon unit transfer into purine, thymidine and methionine. This occurs in the total absence of 'methylH4folate trapping'. In cobalamin deficiency there is impaired synthesis of formylH4folate and raised levels of endogenous formate in blood and liver. FormylH4folate and methionine reverse the effects of cobalamin deficiency. Methionine provides formate via its metabolism to methylthioribose. Recently it has been suggested that the neuropathy of cobalamin deficiency is due to impaired methylation but this was not confirmed. It is likely that defects demonstrated in marrow and liver are also the explanation for the effects of cobalamin deficiency in the CNS.

Anemia, Megaloblastic↗
PubMed2006

Kazakhstan: a folate-deficient area?

OBJECTIVE: In the Republic of Kazakhstan, located in central Asia, the traditional diet consists mainly of meat, and vegetable intake tends to be deficient. This eating lifestyle may contribute to folate deficiency, which is closely linked to abnormal homocysteine (HCY) metabolism. SUBJECTS AND METHODS: In order to evaluate current folate status in the healthy Kazakh population, we screened serum folate and plasma HCY in 50 healthy Kazakh adults aged 20-65 years (KZH) and 60 healthy Japanese control subjects aged 27-65 years (JPN). RESULTS: Serum levels of folate were significantly lower in KZH than in JPN (3.1 vs 10.0 ng/ml, P<0.01). Fifty of 61 (82.0%) subjects in KZH but none in JPN showed low concentrations of folate (<3.6 ng/ml). Plasma levels of HCY were significantly higher in KZH than in JPN (13.2 vs 7.8 nmol/ml, P<0.01). CONCLUSIONS: Our findings strongly suggest that owing to the insufficient intake of vegetables, folate deficiency exists in Kazakhstan. Furthermore, hyperhomocysteinemia was observed in this group, probably owing to the secondary effects of folate deficiency.

Adult↗
PubMed1994

Elevated serum homocysteine as a predictor for vitamin B12 or folate deficiency.

Tissue deficiency of vitamin B12 and folate results in an increase in serum homocysteine (sHcy). We have measured sHcy in patients with reduced serum vitamin B12 and/or red cell folate (RCF) to determine its usefulness as a discriminant for the diagnostic interpretation of reduced vitamin levels. Of 3846 patients who had serum vitamin B12 and RCF assayed, 335 (9%) had reduced vitamin levels. Multivariate analysis showed a significant association between sHcy and serum creatinine (p = 0.0001), positive intrinsic factor (IF) antibody or neutrophil hypersegmentation (NHS) (p = 0.001), increased MCV (p = 0.014) and low RCF (p = 0.025) but no relationship with the level of serum vitamin B12 or haemoglobin. After censoring the patients with renal impairment (n = 54), the distribution of the remaining 72 patients with elevated sHcy was 37/151 (25%) with low serum vitamin B12 with or without low RCF and 35/130 (27%) with low RCF alone. sHcy correctly identified response to vitamin therapy in 33/35 (94%) patients who had adequate parameters to assess response. The positive predictive values of IF antibody/NHS, macrocytosis and/or low RCF for elevated sHcy were 100% and 34% respectively. Twenty-four percent of patients with a low serum vitamin B12 and elevated sHcy had no abnormal haematologic parameters as determined by the routine laboratory staff. These data suggest that the usefulness of measuring sHcy in a routine diagnostic setting is limited and a careful review of the peripheral blood for macrocytosis and NHS plus determination of RCF may be a more cost-effective process than sHcy assay in most instances to determine the presence of tissue deficiency.

Adult↗
PubMed1979

[Investigations of iron and folate levels in serum after implantation of heart valve prostheses (author's transl)].

In 90 patients with prosthetic heart valves, the presence of iron and folate deficiencies was assessed in a double-blind study. Anemia was found in 18 cases. Average serum iron levels were below the normal range and could be incremented significantly through the administration of 193 mg Fe++ daily during a 4-week period. No evidence of folate deficiency was found.

Anemia, Hypochromic↗
PubMed1978

[Biochemical and hematological measures for determination of folate status in humans. 2. Comparative determination of folate in blood and in erythrocytes].

Criteria to judge the folate supply have been evaluated in previous studies. The present study is examining parameters to estimate the degree of folate deficiency. Serum folate levels and erythrocyte folate concentrations were measured in 116 volunteers (patients). The erythrocyte folate is to a large extend independent of exterior supply and is lowered only in severe chronic deficiency. Low levels of erythrocyte folate indicate longstanding undersupply. Our experiments show that folate concentration of greater than 250 ng per ml erythrocytes indicate adequate supply. Concentrations below this limit are characteristic for chronic folate deficiency. To confirm this statement further studies will take into account the urine concentration of formiminoglutamic acid.

Adult↗
PubMed1977

Effect of folate deficiency of the intestinal mucosa on jejunal transport in the rat.

The role of folate deficiency in the pathogenesis of the abnormalities of structure and transport of the small intestine that are often present in certain disorders such as alcoholism is unclear. One reason for this is that the folate status of the intestinal mucosa has never been ascertained in humans. Previous investigations have shown that a deficient diet supplemented with sulfa does produce folate deficiency of the intestinal mucosa in weanling rats and that this is associated with diarrhea and structural abnormalities of the jejunum. In the present study, we used then in vivo marker perfusion technique to examine the jejunal transport of water, sodium, xylose, glucose, and L-leucine in such folate-deficient rats. Supplementation of the normal diet with sulfa did not produce folate deficiency of the intestinal mucosa, but it was associated with a moderate reduction in water absorption; this was attributed to cecal enlargement in these rats. Rats placed on a folate-deficient diet plus sulfa developed markedly depressed serum and jejunal folate concentrations, net secretion of water and sodium, and persistent diarrhea; absorption of xylose, glucose, and L-leucine remained normal, however. Folate repletion of these rats by water and sodium transport to absorption ano cessation of diarrhea. These observations indicate that folate deficiency of the intestinal mucosa alters the transport of water and electrolytes but not that of such solutes as xylose, glucose, and L-leucine. They suggest that when transport abnormalities of these solutes occur in folate-deficient alcoholics, this in not due to the folate deficiency but rather to other pathogenic factors such as ethanol.

Animals↗
PubMedDate not supplied

[Folate and the nervous system (author's transl)].

The responsibility of the folate deficiency in some neuropsychiatric disorders is recent knowledge. The role of the folate on the nervous system is not yet well definite, but the action on the metabolism of the amino-acids, on the purine and the pyrimidine synthesis and on the metabolism of the catecholamins are certainly essential. The neuropsychiatric diseases secondary to the folate deficiency are numerous: dementia, schizophrenia like syndromes, insomnia, irritability, forgetfulness, endogenous depression, organic psychosis, pueperal psychosis, peripheral neuropathy, myelopathy (spinal cord syndrome and/or pyramidal tract damage), restless legs syndrome. Clinically the diagnosis may be difficult with sub acute combined degenration secondary to the pernicious anaemia, and the dosage of the folate (in serum, in red-cells and in cerebrospinal fluid) is necessary. The congenital defects in the uptake or utilization of the folate are associated with neuropsychiatric disturbances. The treatment is easy and safe if the vitamin B12 deficiency is eliminated and if employed with caution in epileptic patients because folate can induced seizures.

Anticonvulsants↗