Implants seen as reversible contraceptives.
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Since physicians are routinely taught to review the peripheral blood smear results of all anemic patients, we analyzed the diagnostic value of the laboratory's blood smear reading and the incremental value of a physician's personal reading in anemic inpatients. Blood smear abnormalities, as reported by the laboratory and two hematologists, were poorly reproducible, with only five of the 11 types of abnormalities being more reproducible than could be expected by chance. The blood smear performed no better than RBC indices in detecting probable iron deficiency or low serum levels of folate or vitamin B12. In anemias not caused by deficiency states, the blood smear reading performed by the hospital laboratory provided unique information in 6% of the cases and helpful information in another 25%, but the additional reading performed by a hematologist never provided unique information and provided incremental helpful information in only 4% of the cases. The peripheral blood smears of all anemic inpatients should be read by the hospital laboratory, but in our hospital, a routine additional personal reading by a physician had limited incremental value and could be reserved for selected cases.
Explore the source record for details and available documents.
Thirty patients had mild cognitive impairment and increased homocysteine levels in serum. On average, they were supplemented orally with a high dose of a vitamin B12-B6-folate combination for 270 days. All patients had normal serum B12 and folate levels at baseline. Cerebrospinal fluid levels of the tau protein (CSF-tau) and the albumin ratio were measured before and after treatment. The serum homocysteine levels were normalised after treatment. The albumin ratio significantly correlated with vascular risk factors. At baseline, the ratio was higher in the patients in comparison with age-matched controls. After treatment, the ratio was significantly reduced, which may indicate a tightening of the blood-brain barrier. The CSF-tau levels did not change significantly although there was a numeric decline. None of the patients progressed into dementia during the treatment period. When treated with a vitamin B12-B6-folate combination, patients with mild cognitive impairment and hyperhomocysteinaemia appear to improve their blood-brain barrier function. They may also stabilise their cognitive status. Further investigations are warranted on the role of blood-brain barrier dysfunction in the pathogenesis of dementia.
The primary aim of this study was to assess the biochemical vitamin B12 and folate status of a representative group of elderly women (70-80 y) living in Dunedin, New Zealand. A second aim was to determine the prevalence of hyperhomocysteinaemia and to explore the determinants of homocysteine (hcy) concentration in this population. A cross-sectional study was carried out between June and August of 2000. Two hundred and fifty women were randomly selected from the 1998 electoral roll. Fasting blood samples were analysed for folate, vitamin B12, total hcy, creatinine, and haematological parameters. Of the women selected, 87 did not respond, 37 were not traceable, 23 were not eligible or had died, and 103 agreed to participate. The overall response rate was 46%. Based on a cut-off of 150 pmol/L for serum B12, 13% of participants would be classified as having sub-optimal vitamin B12 status. Of the women, 3 and 5%, respectively, had low serum (< 6.6 nmol/L) and erythrocyte folate (< 317 nmol/L) concentrations. No participant had megaloblastic anaemia. The prevalence of hyperhomocysteinaemia (> 15 mumol/L) in this population was 18%. Hyperhomocysteinaemia in this group may be partly explained by renal insufficiency because there was a significant association between serum creatinine and plasma hcy (P < 0.001). Blood folate levels but not serum B12 were significantly inversely associated with hcy. In conclusion, there was a moderately high prevalence of hyperhomocysteinaemia and suboptimal plasma vitamin B12 concentrations but not low blood folate concentrations in this elderly female population.
Dietary intakes were obtained by 24-h recall from 25 women in the first and third trimesters of pregnancy and 25 women in the first 3 months of lactation from eight towns in the Amazon valley. No consistent differences were found between the towns, so the results have been analysed together. Intakes of iron, free and total folate and zinc were nearly all very low compared with current recommendations. Despite their low intakes, the majority of the women had acceptable values of haemoglobin, haematocrit and MCHC. Serum folate concentrations were almost all extremely low (less than 2.5 ng/ml). The levels of RBC folate were also low, but in general not as severely so as those for serum folate. Serum zinc concentrations ranged from 0.2 to 0.7 microgram/ml, whereas the lower limit of acceptability has been put by various authors as 0.59-0.69 microgram/ml according to the stage of pregnancy. In breast milk, total folate in the majority of women ranged from 25 to 50 ng/ml, the greater part of it being in the free form. Zinc levels in breast milk were within the range 0-2 microgram/ml.
A study was performed on the breakfast habits of 200 schoolchildren between 9 and 13 years of age. The subjects were classified into two groups: group C, children who consumed fortified breakfast cereals (65 boys and 35 girls), and group NC, children who did not (64 boys and 36 girls). The different dietary habits and the nutritional status of the two groups were analyzed. Haematological, biochemical, anthropometric, and dietary data were collected, the latter involving a 5-day food record. The children of the C group were found not only to have a more complete and nutritive breakfast, but also showed better dietary patterns for the rest of the day. Their lipid intake (% kJ) was lower and the carbohydrate intake (g/d and % kJ) higher than in the NC children. The intakes of thiamine, pyridoxine, folates, and beta-carotenes were also higher in group C. Better dietary habits were reflected in higher blood levels of some important compounds. Group C children had higher retinol, serum folate, and riboflavin levels than NC children. The percentage of children with hypercholesterolaemia (serum cholesterol > 4.5 mmol/l) was higher amongst those of the NC group: 37% as compared with 18% of the C children.
Growing evidence indicates that elevated total homocysteine (tHcy) levels can elicit autoimmune response in vivo. Antibodies against Nepsilon-Hcy-proteins have been shown to be associated with stroke and premature myocardial infarction. The aim of the current study was to investigate the effect of treatment with folic acid on anti-Nepsilon-Hcy-albumin and -hemoglobin antibodies. We recruited 20 apparently healthy men and 12 male patients with documented coronary artery disease (CAD). All participants had plasma fasting tHcy levels >15 microM. At baseline, and after three and six months of treatment with folic acid 1 mg daily, we determined tHcy, serum folate and vitamin B12 levels, along with serum anti-Nepsilon-Hcy-albumin and -hemoglobin IgG antibodies using the home-made immunoenzymatic assays. Both groups did not differ with regard to age, tHcy, folate, lipid profile, and CRP. The only significant difference between healthy subjects and CAD patients was levels of antibodies against Nepsilon-Hcy-albumin. As expected, folic acid administration led to significant decreases in tHcy and increases in folate levels in both groups. Levels of both anti-Nepsilon-Hcy-albumin and -hemoglobin antibodies fell markedly following a three-month folic acid administration in healthy subjects, but not in CAD patients, without any changes at six months in either group. Folic acid administration resulted in a loss of significant correlations between tHcy and antibodies both following three and six months of the therapy in healthy subjects, in contrast to CAD patients. Carriers of the methylenetetrahydrofolate reductase (MTHFR) 677T allele with CAD had significantly higher levels of anti-Nepsilon-Hcy-albumin before and during folic acid administration as compared to healthy subjects. In conclusion, our findings suggest that Hcy-related autoimmune response is resistant to folic acid administration in CAD patients, while in healthy subjects reduced tHcy levels are associated with suppressed production of antibodies against Nepsilon-Hcyproteins. These observations might explain at least in part the failure of vitamin therapy to reduce the risk of cardiovascular events as recently reported.
There is concern that exposure of patients to folic acid may prevent the development of the macrocytosis of cobalamin deficiency and thus delay the detection of the neurological complications. We examined the relationship between low cobalamin levels and mean cell volume (MCV) at different serum folate concentrations in 63,472 blood samples tested in a community pathology laboratory over 2 years. We found no evidence that high serum folate levels masked the macrocytosis of cobalamin deficiency in this population with similar increases in MCV regardless of whether the serum folate was low, normal or high. Macrocytosis appears to retain its value as a marker of cobalamin deficiency in people with serum folate concentrations above the population average.
The nutritional status and dietary intake of children with sickle cell anemia were examined to confirm the presence of deficiencies. Nine children with sickle cell anemia and 19 controls were assessed. Resting energy expenditure was measured with open circuit indirect calorimetry and body composition was estimated from skinfold measurements. Three-day food records were analyzed for protein, zinc, vitamin A, folic acid, and iron content. Serum vitamin A, red blood cell zinc, red blood cell folate, serum folate, serum ferritin, hematocrit, total urine nitrogen, and 24-h urine creatinine levels were measured. The children with sickle cell anemia were leaner, weighed less, and had lower red blood cell zinc levels, lower serum vitamin A levels, lower urine nitrogen levels, and greater resting energy expenditure than controls. Serum and red blood cell folate levels were within normal ranges and similar to controls. The serum ferritin level was higher than controls and higher than normal for age. Dietary intake of energy and protein was more than that of controls, and dietary intake of zinc, vitamin A, folic acid, and iron was similar to that of controls and adequate compared to the Recommended Dietary Allowances. Further studies are needed to explain the physical and biochemical differences seen in children with sickle cell anemia despite dietary intakes that appear to be adequate and similar to those of controls.
BACKGROUND: Folate deficiency is a global nutritional problem associated with multiple adverse health outcomes, including impaired one-carbon metabolism and elevated homocysteine levels (hyperhomocysteinemia). Gut microbiota-mediated folate biosynthesis has emerged as a promising strategy for improving the host's folate status. This study aimed to isolate folate-producing probiotic strains, clarify their folate synthesis mechanisms, and evaluate their regulatory effects on folate metabolism and gut microbiota. METHODS: High-throughput cultivation and screening were performed to isolate folate-producing candidate probiotics. Whole-genome sequencing analysis, pathway reconstruction, and metabolite profiling in fermented milk were performed to explore folate biosynthesis pathways and microbial cross-feeding interactions. A folate-deficient mouse model was established to evaluate the effects of a candidate probiotic cocktail on serum folate, homocysteine (Hcy) levels, and gut microbiota composition using quantitative PCR (qPCR) and 16S rRNA gene sequencing. RESULTS: High-throughput screening identified 8 high-folate-producing candidate probiotic strains, including Lactiplantibacillus plantarum and Heyndrickxia coagulans, from over 1,000 isolates. Genomic analysis revealed that most commonly used probiotics lacked para-aminobenzoic acid (pABA) biosynthesis genes but retained downstream modules, suggesting a reliance on cross-feeding with pABA-producing gut commensals such as Bacteroides. Metabolite profiling of fermented milk demonstrated that selected strains significantly increased bioactive 5-methyltetrahydrofolate (5-MeTHF) and tetrahydrofolate levels. In vivo, only a high-dose candidate probiotic cocktail significantly elevated serum folate (p < 0.05) and reduced homocysteine levels (p < 0.05) in deficient mice. Fecal qPCR confirmed dose-dependent transient persistence of the administered bacterial species. Consistent with the qPCR data, 16S rRNA gene sequences demonstrated significant enrichment of these administered species observed in the high-dose group. Furthermore, beta-diversity analysis found that high-dose candidate probiotic supplementation promoted a shift in the gut microbiota composition toward a normal profile, partially mitigating the dysbiosis induced by the folate-deficient diet. This effect was accompanied by a significant enrichment of potential short-chain fatty acid producers (e.g., Lachnospiraceae and Oscillospiraceae) and the depletion of potential opportunistic pathogens. CONCLUSION: This study screened high-folate-producing candidate probiotic strains and demonstrated their ability to synthesize the active form of 5-MeTHF. Moreover, folate-producing candidate probiotic cocktail treatment significantly improved folate status and Hcy metabolism and modulated the gut microbiota by enriching potential beneficial bacterial taxa. These findings suggested that folate-producing probiotics may serve as a promising microbiota-based strategy to improve folate availability and homocysteine metabolism.
A prospective analysis of all cyclosporine treated renal transplants performed between 1987 and 1990 was performed to determine the incidence and etiologic factors of post transplant erythrocytosis (PTE) and its effect on short-term outcome. PTE developed in 25 (8.1%) recipients (mean age, 41 +/- 10 years). PTE occurred more frequently in men (12.8%) than women (1.6%) (p < 0.001), diabetic patients (22.9%) than nondiabetic patients (6.2%) (p < 0.001), and rejection-free recipients (11%) compared with those with early rejection (4%) (p < 0.05) but was independent of recipient race and donor source. Sixteen patients in whom PTE subsequently developed had pretransplant hematocrits above 30%. PTE occurred most frequently in the first year posttransplant (range, 2-29 months). Serum erythropoietin levels were inappropriately elevated in all patients (mean, 24 +/- 2.2 mU/ml), but serum iron, folate, and B12 levels were all normal. Mean serum creatinine and creatinine clearance were 1.7 +/- 0.5 mg/dl and 58 +/- 20 ml/min, respectively. Twenty-three patients underwent phlebotomy (mean, 3.5 +/- 0.5 units) and six had PTE-related complications. In 14 patients, PTE persisted with hematocrit of 53 +/- 1.5% (range, 51-56) compared with 57 +/- 2.6% (range, 54-64) at the time of PTE onset. In conclusion, PTE occurs primarily in the first year posttransplant and is characterized by inappropriate elevation of erythropoietin. Predictors for PTE include male gender, diabetes mellitus, pretransplant hematocrit above 30%, absence of rejection, and excellent renal allograft function.
BACKGROUND: Associations between low levels of folate and vitamin B12 and cognitive impairment in patients with dementia have been reported. Some studies revealed correlations between low levels of vitamin B12 and behavioural and psychological signs and symptoms of dementia (BPSD) in Alzheimer's disease (AD) patients. Given the lack of studies in frontotemporal dementia (FTD) and on folate and given the methodological shortcomings of former publications, we set up a prospective study. METHODS: At inclusion, AD (n=152) and FTD (n=28) patients underwent a neuropsychological examination. Behaviour was assessed using a battery of behavioural assessment scales. Determination of serum vitamin B12 and red cell folate levels were performed within a time frame of two weeks of inclusion. RESULTS: In both patient groups, significantly negative correlations between levels of serum vitamin B12 and red cell folate and the degree of cognitive deterioration were found. No correlations with BPSD were found in the AD patient group. In FTD patients, levels of vitamin B12 were negatively correlated with both hallucinations (p=0.022) and diurnal rhythm disturbances (p=0.036). CONCLUSIONS: The observed negative correlations between levels of vitamin B12 and folate and cognitive impairment in both AD and FTD patients, raise the possibility of a non-specific etiological role. Although levels of vitamin B12 and folate did not correlate with BPSD in AD patients, negative correlations between serum vitamin B12 levels and BPSD in FTD patients were revealed. Decreased serum vitamin B12 levels may predispose FTD patients to develop hallucinations and diurnal rhythm disturbances.