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Results for “Serum Folate Level”

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PubMed1987

[Treatable dementia syndromes].

Dementia--a syndrome of acquired intellectual deterioration--is an etiologically non-specific condition which is permanent, progressive, or reversible. In the evaluation of demented patients, a careful exposure history will determine the possible role of drugs, metals, or toxins. The physical examination may reveal focal deficits in cases of intracranial mass lesions and spasticity or ataxia of the lower limbs if hydrocephalus is present. Coexistance of dementia and peripheral neuropathy usually indicates a toxic or metabolic disorder. Asterixis, myoclonus, and postural tremor are common in toxic-metabolic dementias, while resting tremor, choreoathetosis, and rigidity occur in progressive extrapyramidal disorders. EEG is focally abnormal in cases of cerebral mass lesions and exhibits generalized slowing in toxic-metabolic encephalopathies. CT will aid in the identification of hydrocephalus, subdural hematomas, and intracranial mass lesions. A thorough laboratory evaluation including complete blood count, erythrocyte sedimentation rate, electrolytes, blood urea nitrogen and blood sugar, liver and thyroid tests, calcium and phosphorus levels, B12 and folate levels, serum copper and ceruloplasmin, VDRL, chest X-ray, electrocardiogram, and lumbar puncture may demonstrate treatable disorders that are adversely affecting intellectual function. Elderly individuals are particularly susceptible to the effects of toxic or metabolic disorders, and a mild dementia might be exaggerated by relatively minor fluctuations in metabolic status. Treatable causes of dementia should be considered in all demented patients.

Aged↗

PubMed1985

Oral candidiasis--its pleomorphic clinical manifestations, diagnosis and treatment.

Up to 60% of the population carry Candida albicans as part of the oral flora without having evidence of candidiasis. The pleomorphic clinical manifestations of oral candidiasis viz. thrush, denture stomatitis, angular cheilitis, median rhomboid glossitis, speckled leukoplakia, and chronic mucocutaneous candidiasis and its variants are briefly discussed. Current diagnostic techniques of oral candidiasis (OC) are reviewed. A simple and quick method of helping the clinician in the diagnosis of OC by taking a direct smear of the lesion is emphasized. OC is a 'disease of the diseased'. As a routine a full blood picture, serum iron and serum folate levels should be looked at. Several predisposing causes of OC need to be investigated. An up-date on the treatment of OC with nystatin, amphotericin B lozenges, clotrimazole and miconazole is made.

Candidiasis, Oral↗

PubMed1985

Acanthosis nigricans-like hyperpigmentation secondary to triazinate therapy.

Cutaneous hyperpigmentation resembling acanthosis nigricans developed in two patients with malignant brain tumors following chemotherapy with triazinate (Baker's Antifol), a folic acid antagonist. In both cases, the eruption resolved after the cessation of drug administration and reappeared after the reinstitution of triazinate therapy. A skin biopsy specimen from one patient showed microscopic changes consistent with those found in acanthosis nigricans. The other patient had a decreased serum folate level that returned to normal as the hyperpigmentation resolved. Folate may have a role in triazinate-induced acanthosislike hyperpigmentation.

Acanthosis Nigricans↗

PubMed1985

Alteration of bone marrow cell cycle kinetics by diphenylhydantoin: relationship to folate utilization and immune function.

Female B6C3F1 mice were administered the anticonvulsant drug diphenylhydantoin (DPH) for 1 to 4 weeks by gavage at doses of 25 to 200 mg/kg. None of the dosing regimens caused toxicological manifestations other than hepatomegaly. Evaluation of the immune status of the drug-treated mice revealed no alteration of cellular immunity, measured by delayed hypersensitivity response and lymphocyte responsiveness to mitogens or allogeneic leukocytes. Humoral immunity, as measured by serum immunoglobulin quantitation and plaque-forming cell response to sheep erythrocytes, was depressed by DPH at 100 mg/kg after 2 weeks, as was host resistance to infection with the parasite Plasmodium yoelii. The bone marrow was the most sensitive target organ with loss of the multipotent stem cell colony-forming unit-spleen occurring within 1 week at a dose of 50 mg/kg. The colony-forming unit-spleen suppression was the result of a selective loss of stem cells in S phase. Committed granulocyte macrophage progenitor cells, colony-forming unit-granulocyte macrophage, were also inhibited by DPH in vivo, as well as in vitro at concentrations as low as 0.2 microM. Bone marrow cells from DPH-treated mice were folate deficient, as determined by the inability of these cells to convert deoxyuridine to thymidine. However, these mice had normal serum folate levels, even after 4 weeks of treatment. Folic acid protected bone marrow stem cells after both in vivo and in vitro treatment with DPH. It is suggested that DPH inhibits folate utilization or metabolism at the cellular level, selectively affecting bone marrow stem cells and resulting in altered stem cell kinetics. This lesion ultimately results in altered humoral immunity and impaired host resistance.

Animals↗

PubMed1985

Investigations into the effect of nitrous oxide anaesthesia on folate metabolism in patients receiving intensive care.

Anaesthesia with nitrous oxide inactivates vitamin B12 and impairs DNA synthesis in bone marrow cells. The secondary development of folate deficiency may prolong the recovery from these abnormalities in some seriously ill patients. This was investigated, using the deoxyuridine (dU) suppression test, in 48 patients admitted to an Intensive Care Unit (ICU). On admission to the ICU, following nitrous oxide anaesthesia, the pattern of correction of the abnormal dU-suppression tests was typical of that seen in vitamin B12 deficiency; 3 days later the pattern had changed to that usually seen in folate deficiency. During the same period the serum folate levels fell to subnormal values. Further evidence for the development of folate deficiency was provided by treatment with physiological amounts of folic acid which accelerated the recovery of the bone marrow abnormalities present after nitrous oxide anaesthesia. Urinary folate excretion was measured by radioassay, and increased following anaesthesia with nitrous oxide, however, this was insufficient by itself to explain the development of folate deficiency.

Adolescent↗

PubMed1984

Interactions between folate metabolism, phenytoin metabolism, and liver microsomal cytochrome P450.

The majority of epileptic patients treated with phenytoin (DPH) develop a drug-related decrease in serum folate levels. In the present study the hypothesis was investigated that increased folate utilization for DPH metabolism or for enzyme induction may contribute to the mechanism by which DPH induces folate deficiency. In addition, the effect of folate deficiency on microsomal enzyme induction was determined. Sprague-Dawley rats were fed AIN-76 diet which contained either no folate or 2 mg/kg folic acid. The DPH metabolism as well as the folate-dependent oxidation of formate and histidine and the metabolism of model substrates of microsomal cytochrome P450 (ethoxycourmarin and p-nitroanisole) were measured in hepatocytes isolated from these rats. Hepatocyte concentrations of cytochrome P450 were also determined. Cells from rats fed folate-deficient diet had reduced concentrations of folate, but the cytochrome P450 concentrations were unchanged. Phenobarbital increased cytochrome P450 concentration to an equal extent in both diet groups, but it had no effect on liver folate levels. Phenytoin, at the dose given, did not induce cytochrome P450, but a small increase in the metabolism of DPH, p-nitroanisole, and ethoxycoumarin was observed. The metabolism of formate and histidine to CO2 was decreased in folate-deficient cells but not altered by phenobarbital pretreatment. Ethoxycoumarin and p-nitroanisole metabolism were the same in control and folate-deficient hepatocytes, and the rates were increased in both diet groups by phenobarbital pretreatment. The rate of DPH metabolism was unaltered by folate deficiency and the rate was increased by phenobarbital pretreatment in both folate-deficient and control cells. The results of these experiments show that hepatic DPH metabolism is not dependent upon the cellular concentration of folates. Furthermore, folate deficiency does not alter the activity of the liver microsomal cytochrome P450 system or its inducibility. The results suggest that the folate deficiency induced by DPH is not due to utilization of folates in DPH metabolism.

Animals↗

PubMed1981

Intestinal absorption of [3H]folic acid in the chronic alcoholic monkey.

The intestinal absorption of labeled folic acid ([3H]pteroylmonoglutamate) was determined from urinary and fecal recoveries of tritium in pairs of monkeys fed control liquid diets or diets containing 50% of energy as ethanol for a 24-mo period. Weight gain, fecal fat excretion, nitrogen balance, D-xylose absorption, serum folate levels, jejunal histology, and intestinal enzyme activities were similar in each group. Liver biopsies obtained after 12 and 24 mo of feeding demonstrated steatosis and megamitochondria in the ethanol-fed group, with decreased hepatic levels of folate at 24 mo. Intestinal malabsorption of labeled folic acid in the ethanol-fed monkeys was indicated by decreased urinary recovery of tritium but increased fecal recovery of tritium after intragastric administration of [3H]pteroylmonoglutamate. These studies suggest that folic acid malabsorption follows the chronic administration of ethanol together with a nutritious diet.

Alcoholism↗

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↗

PubMed1976

The clinical value of the radioassay of serum folate.

Measurement of serum folate levels in humans using a radioassay has now been frequenly reported. However, very little data is available assessing the diagnostic value of this test in comparison with other laboratory and clinical information pertaining to folate status. A radioassay, using the folate binder in dried milk was used in parallel with the well established Lactobacillus casei microbiological assay. Three slightly different modifications of the radioassay were tested. At first, a partially purified milk binder was used, in the second the unpurified milk and, third, the unpurified milk with variation of the incubation periods during the assay, were utilized. A total of 159 sera were tested by one of the modifications of the radioassay as well as by the L. casei method. Duplicate estimations were done in all cases. Using the first method, the correlation between the radio- and microbiological assays was 0.89, with the second 0.52, and with the third 0.85. The final assay system gave the most reliable results when compared to the L. casei assay which was taken as the standard of reference. However, in a number of cases, normal levels by L. casei gave low levels by radioassay and vice versa. In 13 such instances, clinical and other laboratory data were assessed and it was concluded that the microbiological assay gave the more accurate indication of folate stores in humans. Some reasons for the discrepancies between the assay systems were discussed.

Biological Assay↗

PubMed1977

[Sideroblast content of the bone marrow at the end of pregnancy or 1st days of puerperium, respectively].

We examine in the last month of the pregnancy, resp. in the first week of their lactation period, the frequency of sideroblasts in the bone marrow of 265 pregnant women without iron or folate supplements. In 69,4% of the cases the frequency of sideroblasts was not more than 10% (in 34,7% of the cases sideroblasts were absent). After previously parenteral administered 0,6 to 0,9 g iron (10 to 15 Amp. Ferrlecit), iron was present in the marrow. In all examined megaloblastic anaemia of pregnancy cases and in 91% of praemegaloblastic cases, the marrow contained sideroblasts. If the number of sideroblasts proved increased (greater than 25%) the serum folate level was decreased (less than 4 ng/ml).

Bone Marrow↗

PubMed2002

The interaction of serum folate and estradiol levels in Alzheimer's disease.

OBJECTIVES: In vitro and in vivo animal studies suggest that sex steroids, such as estrogens and testosterone, could protect the brain. However, estrogen replacement therapy (ERT) for Alzheimer's disease (AD) in women has not been successful. We hypothesised that the lack of effect of ERT might be related to an interaction between estrogens and some other factor(s) associated with AD. DESIGN, SETTING AND METHODS: We analysed total estrogen (TE) and testosterone (TT) levels in women diagnosed with AD and controls of the Oxford Project To Investigate Memory and Ageing. Because estradiol (TE2) after the menopause is largely derived from estrone (TE1), we computed the ratio TE2/(TE1+TE2) and a total steroid index (TT+TE2+TE1). RESULTS: Women with AD (n=66) had significantly higher levels of TE2 (27+/-13 vs. 21+/-13) and a higher TE2/(TE1+TE2) ratio. Stepwise logistic regression analyses showed that the TE2/(TE1+TE2) ratio was the main sex steroid predictor for AD (O.R.=1.06, 95% C.I.=1.01-1.11, p<0.01). Multiple regression analyses revealed that dementia severity was associated with an interaction between the TE2/(TE1+TE2) ratio and serum folate (B=4.59 (SE=1.48), beta=1.22, 95% C.I.=1.62-7.56, p<0.005). None of the other potential mediators of this association (body mass index, sex hormone binding globulin, homocysteine levels, ApoE genotype, smoking, diabetes, blood pressure) was significant. MAIN FINDINGS: A high ratio of estradiol to total estrogens is associated with AD but, in subjects with a high ratio, the dementia severity was lower in those with high serum folate levels. CONCLUSIONS: If this association is causal, then supplementation with folic acid might be considered in future studies on ERT in AD.

Aged↗

PubMed2004

Coronary artery bypass grafting surgery is associated with a marked reduction in serum homocysteine and folate levels in the early postoperative period.

OBJECTIVE: It has been suggested that cardiac surgery-related ischemia-reperfusion injury to the myocardium is caused by the oxidative stress, derived from the formation of reactive oxygen species in the early phases of the reperfusion. The availability of cysteine, mostly deriving from homocysteine (Hcy) via the trans-sulfuration pathway, is determinant for the synthesis of glutathione (GSH), which in turn acts as a first line of defence against oxidative stress. Indeed, an increased consumption of Hcy in response to oxidative stress has been described. Previous research has shown that Hcy levels increase during the first weeks or months after coronary artery bypass grafting (CABG). This study was designed to evaluate the Hcy metabolism in CABG patients during the early postoperative period. METHODS: Serum Hcy and folate were measured by an automatic immunometric system on blood samples obtained from 48 (mean age 67+/-10 years) consecutive patients undergoing CABG, preoperatively and at 0, 12, 48, and 120 h after surgery. A subgroup of 22 of these patients was also studied 6 months postoperatively. RESULTS: A significant decrement of Hcy and folate was observed throughout the study (P<0.0001) from 17.3+/-9.3 to 8.5+/-5.6 micromol/l at 12 h postoperatively for Hcy, and from 5.1+/-2.8 to 2.5+/-1.5 ng/ml at 48 h for folate. The reduction of Hcy and folate levels remained significant after correction for haemodilution (as assessed by measurement of plasma proteins). Furthermore, the use of cardiopulmonary bypass significantly interacted with the time of sampling in affecting the Hcy levels. Hcy levels returned to near-baseline values 48 h postoperatively, and were similar to base-line at follow-up. CONCLUSION: Our study indicates that serum Hcy and folate levels are markedly reduced during the early postoperative period after CABG. This reduction is at least in part independent of haemodilution, and may be caused by an altered Hcy turnover, due to an increased consumption of GSH during and soon after CABG.

Aged↗

PubMed1998

Folate, vitamin B12, and serum total homocysteine levels in confirmed Alzheimer disease.

BACKGROUND: Recent studies suggest that vascular disease may contribute to the cause of Alzheimer disease (AD). Since elevated plasma total homocysteine (tHcy) level is a risk factor for vascular disease, it may also be relevant to AD. OBJECTIVE: To examine the association of AD with blood levels of tHcy, and its biological determinants folate and vitamin B12. DESIGN: Case-control study of 164 patients, aged 55 years or older, with a clinical diagnosis of dementia of Alzheimer type (DAT), including 76 patients with histologically confirmed AD and 108 control subjects. SETTING: Referral population to a hospital clinic between July 1988 and April 1996. MAIN OUTCOME MEASURES: Serum tHcy, folate, and vitamin B12 levels in patients and controls at entry; the odds ratio of DAT or confirmed AD with elevated tHcy or low vitamin levels; and the rate of disease progression in relation to tHcy levels at entry. RESULTS: Serum tHcy levels were significantly higher and serum folate and vitamin B12 levels were lower in patients with DAT and patients with histologically confirmed AD than in controls. The odds ratio of confirmed AD associated with a tHcy level in the top third (> or = 14 micromol/L) compared with the bottom third (< or = 11 micromol/L) of the control distribution was 4.5 (95% confidence interval, 2.2-9.2), after adjustment for age, sex, social class, cigarette smoking, and apolipoprotein E epsilon4. The corresponding odds ratio for the lower third compared with the upper third of serum folate distribution was 3.3 (95% confidence interval, 1.8-6.3) and of vitamin B12 distribution was 4.3 (95% confidence interval, 2.1-8.8). The mean tHcy levels were unaltered by duration of symptoms before enrollment and were stable for several years afterward. In a 3-year follow-up of patients with DAT, radiological evidence of disease progression was greater among those with higher tHcy levels at entry. CONCLUSIONS: Low blood levels of folate and vitamin B12, and elevated tHcy levels were associated with AD. The stability of tHcy levels over time and lack of relationship with duration of symptoms argue against these findings being a consequence of disease and warrant further studies to assess the clinical relevance of these associations for AD.

Aged↗

PubMedDate not supplied

Red blood cell folate and serum vitamin B12 status in children with sickle cell disease.

PURPOSE: To determine red blood cell (RBC) folate and serum vitamin B12 levels in children with sickle cell disease, SS-type, and to evaluate the associations of these nutrient levels with growth and hematologic parameters. PATIENTS AND METHODS: Subjects enrolled in this prospective, cross-sectional study were recruited from one tertiary care setting. Complete blood counts, measurement of red blood cell (RBC) folate and serum vitamin B12, anthropometric measures (height, weight, skinfold measurements), pubertal status, and 24-hour dietary recalls were obtained from 70 patients ages 1 to 19 years. RESULTS: Low RBC folate levels were found in 15% of the children. Fifty-seven percent of the sample had inadequate dietary folate intake. Three percent of the children had low serum vitamin B12 levels. All children and adolescents sampled had adequate dietary intake of vitamin B12. Both RBC folate (P = 0.01) and serum vitamin B12 levels (P < 0.01) decreased with increasing age. CONCLUSIONS: More than half of the subjects had inadequate intake of folate from food, and despite daily folate supplementation, 15% had low RBC folate levels. Low serum vitamin B12 levels were rare, and dietary vitamin B12 intake was adequate. Additional research is needed to explore the effects of improved folate status, the need for folate supplementation, and the relationship of folate, vitamin B12, and homocysteine levels and the risk for vascular damage and stroke in children with sickle cell disease.

Adolescent↗

PubMed2004

Serum total homocysteine levels, folate, and B-vitamins intake and coronary heart disease risk factors among tri-ethnic college students.

The main objective of our study was to determine and compare total serum homocysteine (tHcy) levels among tri-ethnic college students. The 180 tri-ethnic subjects completed Cardiovascular Risk Assessment questionnaires, and gave 15 mL fasting blood for serum tHcy and blood lipid analysis. The mean tHcy (+/- SD) of the all subjects was 6.33 +/- 3.15 micromol/L. Male subjects had significantly (P=.001) higher serum tHcy levels compared with female subjects. Black non-Hispanic females and Hispanic females showed significantly (P=.003) lower tHcy levels than White non-Hispanic females. Moderate elevations of tHcy levels were strongly related to cigarette smoking, physical inactivity, behavioral style, high blood pressure, and low intakes of folate, and vitamins B6 and B12. A positive association of tHcy levels with cardiovascular heart disease (CHD) risk point standards was observed in females (P=.001), Hispanic (P=.001), Hispanic males (P=.049), Hispanic females (P=.009), and Black non-Hispanic females (P=.005). We observed gender and ethnic differences in tHcy levels of this young population with normal tHcy levels. Abnormally high tHcy concentrations appear to be acquired later in life.

Adult↗

PubMed1983

Stomatitis and recurrent oral ulceration: is a full blood screen necessary?

A full haematology screen was carried out on 398 patients under investigation for recurrent oral ulceration or stomatitis. Thirty-three patients were found to have lowered serum folate and/or red cell folate levels without iron deficiency. Of these only six were found to have a mean corpuscular volume (MCV) outside normal limits or to have recognisable erythrocyte abnormalities. No correlation was found between serum or red cell folate levels and the MCV. Eighteen patients were found to have lowered serum B12 levels without iron deficiency, of these seven were found to have a MCV outside normal limits. A significant negative correlation was found between serum B12 levels and the MCV. It is concluded that haematological screening in these cases should include estimations of serum folate, red cell folate and serum B12 levels even in the face of an apparently normal peripheral blood film.

Erythrocyte Indices↗

PubMed2000

Low serum folate but normal homocysteine levels in patients with atherosclerotic vascular disease and matched healthy controls.

Mild hyperhomocysteinemia has been considered a cardiovascular risk factor. However, recent prospective studies have not demonstrated that hyperhomocysteinemia or the underlying genetic defect on methylentetrahydrofolate reductase is associated with a higher risk of coronary or peripheral artery disease. We compared serum homocysteine, folate, and vitamin B(12) levels of patients with coronary and peripheral vascular disease with those of age- and sex-matched healthy individuals. Subjects taking multivitamins, with diabetes mellitus, or serum creatinine levels over 1.5 mg/dL were excluded from the study. Homocysteine was measured by fluorimetric high-performance liquid chromatography. Serum folate and vitamin B(12) levels were measured by an ion-capture method. We studied 32 patients with peripheral vascular disease (10 female), aged 69.6 +/- 11 y, 24 age- and sex-matched control subjects, 52 patients with coronary artery disease (7 female), aged 59.5 +/- 10.4 y, and 42 age- and sex-matched control subjects. Serum homocysteine levels were 11.7 +/- 7.4 and 9.3 +/- 4.5 micromol/L in vascular patients and in the control counterparts, respectively (not significant). The levels for coronary patients and the control counterparts were 9.0 +/- 3.9 and 8.6 +/- 3.6 micromol/L, respectively (not significant). Folate levels were 4.48 +/- 2.42 and 7.14 +/- 4.04 ng/mL in vascular patients and control subjects, respectively (P < 0.02); the levels in coronary patients and control counterparts were 5.15 +/- 1.9 and 6.59 +/- 2.49 ng/mL, respectively (P < 0.01). No differences in vitamin B(12) or tocopherol levels were observed between patients and control subjects. There were no differences in homocysteine levels, but lower serum folate levels were observed when comparing patients with atherosclerotic vascular disease and healthy control subjects.

Aged↗

PubMed1988

Folate nutriture in pregnancy.

Folacin intakes from diet and supplements consumed during pregnancy were determined by interview in 566 women. Eight percent of this population (48 women) obtained folacin from diet only. Thirteen percent (76 women) received less than two-thirds of the RDA for folacin for pregnant women. Serum and erythrocyte folate levels in maternal and cord blood were correlated with dietary folacin intakes in subsamples of the group. Women who received their folate from diet alone showed marginal or deficient maternal serum folate levels. Of the group of women whose folacin intake was equal to or greater than the RDA for pregnant women, some had intakes as high as eight times the RDA from supplements. When, in a subsample, total folacin intake was correlated with maternal and cord folate levels, significant correlations were obtained. The high serum and erythrocyte folate levels resulting from self-medication with folate supplements are of concern because of possible deleterious interaction with other nutrients.

Adult↗