Higher Plasma Homocysteine Levels Research Articles

PLASMA HOMOCYSTEINE LEVEL AND APATHY IN ALZHEIMER'S DISEASE

PLASMA HOMOCYSTEINE LEVEL AND APATHY IN ALZHEIMER'S DISEASE

P2-90 High levels of plasma homocysteine predicts development of hypertension in a general population. The Tanushimaru Study

IntroductionHomocysteine has been implicated in promoting atherosclerotic vascular disease. We have already demonstrated that high level of plasma homocysteine is an independent correlates for increased carotid artery wall thickness in...

Testing homocysteine-induced neurotransmitter deficiency, and depression of mood hypothesis in clinical practice

high total plasma homocysteine (tHcy) levels may cause neurotransmitter deficiency, and consequently depression of mood. We have recently shown that mixed oral nutritional supplements containing B-group vitamins led to a statistically significant benefit on depressive symptoms. The aim of this report was to examine the association between elevated plasma tHcy and symptoms of depression in older patients. two-hundred and thirty-six hospitalised acutely ill older patients, who were part of a randomised double-blind placebo-controlled trial, were assigned to receive daily mixed oral nutritional supplements containing B-group vitamins or a placebo for 6 weeks. Outcome measures included symptoms of depression measured using Geriatric Depression score and plasma tHcy levels. the mean tHcy concentration fell by 22% among patients given the supplements compared with the placebo group (mean difference 4.1 µmol/l (95% CI: 0.14-8.03), P = 0.043). tHcy concentrations was divided into four quartiles and analysed against depression scores. tHcy concentrations in the first relative to the fourth quartile of the distribution were associated with a lower depression symptoms at the end of the supplement period (Geriatric depression score r = -0.20, P = 0.042). lower plasma tHcy concentrations were associated with reduced depression symptoms in older patients recovering from acute illness.

Brain Biochemical Correlates of the Plasma Homocysteine Level: A Proton Magnetic Resonance Spectroscopy Study in the Elderly Subjects

An elevated plasma homocysteine level has been reported to be associated with various neuropsychiatric diseases. However, little is known about the brain biochemical changes associated with the higher plasma homocysteine level. The main goal of this study was to examine the sex difference in brain biochemical concentrations using brain proton magnetic resonance spectroscopy (H MRS), and to elucidate the biochemical changes associated with plasma homocysteine levels by sex in healthy elderly subjects. Seventy elderly subjects without any clinical psychiatric and neurological disease underwent 3-T brain H MRS. MRS spectra were acquired from voxels placed on the left side of the basal ganglia, frontal lobe, and hippocampus. Brain biochemical concentrations were compared between the elderly male and female participants. Correlations between these biochemical concentrations and plasma homocysteine levels by sex were analyzed. Female participants had significantly higher levels of choline in the left frontal lobe and hippocampus, and lower creatine and myo-inositol, in the left basal ganglia than did males. A higher homocysteine level was correlated with a lower N-acetylaspartate (NAA) concentration in the left hippocampus in elderly women (r = -0.44; p = 0.03) but not in elderly men. This study found that there was a sex difference in brain biochemical concentrations in the elderly participants. A higher plasma homocysteine level was associated with a lower NAA in the hippocampus of elderly women. The sex difference in association between brain biochemical concentrations and plasma homocysteine levels needs further investigation. We speculate that after menopause, women lose protection of estrogen from the neurotoxic effects of homocysteine in the hippocampus. Future studies are required to examine this speculation.

131 Aetiological role of folate deficiency in congenital heart disease: evidence from Mendelian randomisation and meta-analysis

<h3>Background</h3> The existence of a causal relationship between lower levels of plasma folate and congenital heart disease (CHD) remains contentious. Randomised trials of this question are not possible, in view of the known protective effect of folate against neural tube defects (NTDs). Folate fortification of flour is known to reduce the incidence of NTDs, but it is not known whether there is any effect on CHD. Clarity regarding the relationship between folate and CHD could potentially inform the practice of folate fortification. We present a genetic approach using “Mendelian randomisation” to determining the causality of folate in CHD risk. <h3>Methods</h3> We compared genotype frequencies at the methylene tetrahydrofolate reductase (MTHFR) C677T single nucleotide polymorphism (SNP) in 1186 CHD cases and 4168 controls. The TT genotype at MTHFR C677T is known to be associated with lower activity of MTHFR and plasma folate, and higher levels of plasma homocysteine. The effect of TT genotype on plasma folate levels is greater in conditions of folate deficiency. Thus, if lower plasma folate had a causal effect on CHD risk, a higher frequency of TT genotype among CHD cases than among healthy controls would be anticipated, and this would be expected to be more marked in conditions of folate deficiency. We placed our results in the context of a meta-analysis of all previously published studies of this question (to September 2010), which together included 1883 cases and 3069 controls in 25 studies. Thus, the combined analyses included 3069 CHD cases and 7271 controls. We used random-effects models to combine the data. We conducted sensitivity analyses to examine folate fortification of flour as a potential source of heterogeneity. <h3>Results</h3> The primary genotyping data in 1186 cases and 4168 controls revealed a trend towards increased risk with the TT genotype, but this did not reach statistical significance (OR 1.15 (95% CI 0.94 to 1.40)). Combination of our primary data with previous studies, however, revealed association in the larger dataset (OR 1.45 (95% CI 1.12 to 1.89); p=0.005). The population attributable fraction for the TT genotype was 3% of CHD. There was no evidence of publication bias among the contributing studies. We discovered folate fortification status to be a significant source of heterogeneity. Studies conducted in countries with mandatory folate fortification showed no effect of C677T genotype on CHD risk (OR 0.96 (95% CI 0.64 to 1.44)), whereas studies conducted in countries without mandatory fortification showed a significant effect of genotype (OR 1.63 (95% CI 1.19 to 2.25)). These ORs were significantly different from each other (p=0.032). <h3>Conclusions</h3> We demonstrate genetic evidence in favour of a causal relationship between plasma folate and CHD. The absence of a genetic association in countries practicing folate fortification suggests that fortification largely abrogates the risk of CHD attributable to folate deficiency.

An evaluation of plasma homocysteine levels and the hematological toxicity of pemetrexed even with folate supplementation.

2594 Background:Systemic folic acid and vitamin B12 supplementation is necessary for pemetrexed treatment, because severe toxicities of pemetrexed treatment without folate supplementation were observed in patients who had high levels of plasma homocysteine (Hcy) in early clinical trials. However, it was not examined whether the plasma Hcy levels would still associated with the hematological toxicity of pemetrexed in patients receiving folate supplementation. The purpose of this study was to examine the relationship between the pretreatment plasma Hcy levels after folate supplementation and the hematological toxicity of pemetrexed monotherapy in advanced non-small cell lung cancer (NSCLC). Methods: From June 2009 to September 2010, 52 NSCLC patients received pemetrexed monotherapy (500mg/m2, every 3 weeks) and also received oral folic acid (0.5mg) daily and a vitamin B12 injection (1.0mg) every 9 weeks, beginning 1 to 2 weeks before the first dose and continuing until 3 weeks after the last dose of the study treatment. The plasma Hcy levels before the first dose of pemetrexed were measured. Complete blood cell counts were measured at least once a week during first cycle of pemetrexed monotherapy. The relationship between the plasma Hcy levels and hematological toxicities during the first cycle of pemetrexed monotherapy were evaluated. Results: The patient characteristics were as follows: male/female: 22/30; median age: 65 years (39-79); histology, adeno/large: 51/1; PS, 0/1/2/3: 25/24/2/1. The mean pretreatment plasma Hcy was 9.01μmol/ml (3.8-34.6μmol/ml). The pretreatment plasma Hcy significantly correlated with the nadir of the absolute leukocyte counts (r=-0.315 p=0.023) and the nadir of the absolute thrombocyte counts (r=-0.302 p=0.032). In addition, the pretreatment plasma Hcy significantly correlated with the decline rates of leukocytes (r=+0.351 p=0.012), hemoglobin (r=+0.414 p=0.002) and thrombocytes (r=+0.417 p=0.002). Conclusions: The Plasma Hcy levels are thus considered to be associated with the hematological toxicity of pemetrexed monotherapy even with folate supplementation.

Early reduction of circulating homocysteine levels in Goto–Kakizaki rat, a spontaneous nonobese model of type 2 diabetes

Diabetes mellitus is associated with increased risk for cardiovascular disorders, which are major causes of mortality in this disease. Hyperhomocysteinemia, defined by high plasma homocysteine levels, is an independent risk factor for the development of cardiovascular diseases. Type 2 diabetic patients have higher circulating homocysteine levels than healthy subjects and these levels are even higher in plasma of obese than nonobese diabetic patients. Homocysteine metabolism that has been studied in 2 animal models of type 2 diabetes with obesity led to conflicting data. The aim of the present study was to analyze homocysteine metabolism in a spontaneous nonobese model of type 2 diabetes, the Goto–Kakizaki rats at various successive and well characterized stages of the disease: during early postnatal normoglycemia, at the onset of hyperglycemia (around weaning), and during chronic mild hyperglycemia with progressive insulin resistance. Compared to age-matched Wistar controls, Goto–Kakizaki rats showed lower plasma levels of homocysteine and a falling trend in its major byproduct antioxidant, glutathione, from the prediabetic stage onwards. Concomitantly, Goto–Kakizaki rats exhibited increased liver activity of cystathionine beta synthase, which catalyzes the condensation of homocysteine with serine in the first step of the transsulfuration pathway. These results emphasize a strong association between homocysteine metabolism and insulin via the first step of the hepatic transsulfuration pathway in Goto–Kakizaki rats.

Relationship Between Plasma Homocysteine Levels and Congestive Heart Failure in Patients With Acute Myocardial Infarction Homocysteine and Congestive Heart Failure

Heart failure after acute myocardial infarction (AMI) is an important factor in determining clinical outcome. We examined whether the plasma homocysteine level was a predictor of heart failure in patients with AMI. A series of 96 patients without renal failure who were admitted to our hospital because of AMI between January 2003 and December 2005 were assigned to two groups; a group with a high homocysteine level (group H: n = 48) and a group with a low homocysteine level (group L: n = 48) based on a median homocysteine level. Congestive heart failure was defined as Killip Class II or higher at the time of admission or the development of congestive heart failure after hospitalization. The mean brain natriuretic peptide (BNP) level at the time of admission in group H was higher than that of group L (175.3 pg/mL versus 89.9 pg/mL; P = 0.068). The incidence of heart failure in group H was significantly higher than that in group L (43.7% versus 12.5%; P < 0.001, log-rank test; hazard ratio: 2.92). Multivariate Cox regression analysis indicated that a high plasma homocysteine level of 10.8 µmol/L or higher was a risk factor for the development of heart failure (HR: 7.175, P < 0.01). The plasma homocysteine level in patients with AMI may be related to the development of heart failure.

Relationship between L-arginine/asymmetric dimethylarginine, homocysteine, folic acid, vitamin B levels, and coronary artery ectasia

Coronary artery ectasia (CAE) is characterized by an abnormal dilatation of the coronary arteries. The ratio of L-arginine/asymmetric dimethylarginine (ADMA) and homocysteine are important factors for endothelial function. In this study, we investigate the ratio of L-arginine/ADMA, homocysteine, and folic acid/vitamin B levels in patients with CAE. Forty patients diagnosed with CAE using coronary angiography were included in the study (24 male; mean age, 56 ± 11 years). The control group consisted of 30 patients who had normal coronary arteries as determined by coronary angiography (11 male; mean age, 54 ± 8 years). The ratio of L-arginine/ADMA and plasma homocysteine was measured using high-performance liquid chromatography. The L-arginine/ADMA ratio and L-arginine levels were significantly lower in the CAE group compared with the control group (110 ± 27 vs. 149 ± 77, P=0.02 and 157 ± 32 μmol/l vs. 187 ± 59 μmol/l, P=0.02, respectively). Plasma ADMA levels were similar in the two groups. Patients with CAE had higher plasma homocysteine levels (P=0.01). Plasma folic acid, vitamin B6, and vitamin B12 levels were similar between the two groups. This study shows that patients with CAE have a lower L-arginine/ADMA ratio and higher plasma homocysteine levels. These results show a potential relationship between endothelial dysfunction and CAE.

Plasma Homocysteine Levels and Major Depressive Disorders in Alzheimer Disease

The main aim of this study was to examine the symptomatology of major depression in Alzheimer disease (AD) and its relationship with plasma homocysteine level. Eighty-three patients with AD were enrolled for clinical assessments and examination of fasting plasma homocysteine. Diagnosis of major depression was made, and the severity of the depression was assessed. The moderate dementia patients presented with more common behavioral disturbances related to major depression than mild dementia patients. Major depression in patients with moderate AD was associated with higher plasma homocysteine levels. Furthermore, a high plasma homocysteine level was positively associated with behavioral disturbance among study participants with major depression. More behavioral disturbance associated with major depression occurred as the dementia progressed. Patients with a higher level of plasma homocysteine presented with a higher behavioral disturbance symptomatology. This finding may account for the relationship between elevated homocysteine levels and depression only in patients with moderate AD.

Relation of homocysteine levels with patency and flow rate of infarct related artery in patients receiving fibrinolytic therapy

Elevated homocysteine levels induce a hypercoagulable state and make the clot more resistant to fibrinolysis. In this prospective observational study, we investigated the influence of homocysteine levels on infarct-related artery (IRA) patency and flow as determined with regard to thrombolysis in myocardial infraction (TIMI) flow grade and corrected TIMI frame count (CTFC). Sixty-one patients who received fibrinolytic therapy for a first ST elevation myocardial infarction (STEMI) within 12 hours of chest pain were included. Coronary angiography was performed according to the Judkins technique within 72 hours after fibrinolytic therapy. Total plasma homocysteine level was determined by the high-performance liquid chromatography method with fluorescence detection. Statistical analysis was performed using Chi-square, Student's t and Pearson correlation tests. Logistic regression analysis was used to determine the predictors of IRA occlusion. Of the 61 patients, 22 (36.1%) had an occluded IRA (group 1), 39 (63.9%) had a patent IRA (group 2). Mean plasma homocysteine levels were found to be significantly higher in the group 1 compared to the group 2 (18.5±9.6 µmol/L vs 14.3±5 µmol/L, p=0.04). In addition, we found a significant positive correlation between CTFC and plasma homocysteine levels (r=0.415; p=0.01). In multiple logistic regression analysis, high levels of plasma homocysteine (OR=1.2; 95% CI 1.1-1.25; p=0.03) and being a non-smoker (OR=5.9; 95% CI 1.1-31.6; p=0.03) were found to be significant independent predictors of having an occluded IRA. There is an inverse relation between plasma homocysteine levels and IRA patency and flow in patients receiving fibrinolytic therapy for STEMI.

Frequency of Prothrombotic Risk Factors in Patients with Deep Venous Thrombosis and Controls: Their Implications for Thrombophilia Screening in Chilean Subjects

In this work, we evaluated the frequency of prothrombotic defects associated with deep venous thrombosis (DVT) in southern Chilean subjects. A total of 261 individuals, 87 patients with DVT confirmed by Doppler ultrasonography and 174 controls, were included in this study. Factor V and factor VIII levels, activated protein C (APC) resistance, and lupus anticoagulant detection were assayed by clotting methods. Basal homocysteine was quantified by immunoassay, and the polymorphisms in factor V (F5), methylenetetrahydrofolate reductase (MTHFR), and cystathionine β-synthase (CBS) genes were genotyped by molecular methods. The most frequent defects were APC resistance, hyperhomocysteinemia, and increased levels of factor VIII. We observed a complete absence of the F5 G1691A variant in the studied population, and the frequency of MTHFR C677T polymorphism was significantly different between patients and controls (odds ratio = 3.2; 95% confidence interval, 1.513-6.735; p = 0.016). In addition, subjects carrying the homozygous MTHFR 677TT genotype exhibited higher levels of plasma homocysteine. Our data suggest that the APC resistance is the most important defect in Chilean patients with DVT. However, this phenotype is not associated with the presence of the F5 G1691A variant. In addition, only MTHFR C677T polymorphism constituted a molecular biomarker of DVT in Chilean population.

Study on correlation of high plasma homocysteine with cerebral infarction and the formation of carotid plaque

Objective To study the correlation of high plasma homocysteine with cerebral infarction and the formation of carotid plaque, and to research and analysis. Methods 71 examples with cerebral infarction patients from March 2007 to December 2008 in my courtyard treatment was observation group and the formation of carotid plaque was tested at the same time ,50 examples normal healthy people were selected as the control group. The high plasma homocysteine level of the two groups were tested and compared. The high plasma homocysteine level of cerebral infarction with and without formation of carotid plaque were compared. Results The high plasma homocysteine level of observation group was compared with that of control group , P ＜ 0.05, the difference had statistical significance. The high plasma homocysteine level of cerebral infarction with formation of carotid plaque were compared with that of cerebral infarction without formation of carotid plaque , P ＜ 0.01, the difference had statistical significance. Conclusion The level of cerebral infarction with formation of carotid plaque has high value in the diagnostic value of cerebral infarction, and it can reflect the formation of carotid plaque, and is worth further studying. Key words: Cerebral infarction; High plasma homocysteine; Formation of carotid plaque; Correlation

Homocysteine Potentiates Seizures and Cell Loss Induced by Pilocarpine Treatment

Patients affected by recurrent seizures frequently present increased homocysteine plasma levels in consequence of treatment with antiepileptic drugs. Homocysteine is proconvulsant and can affect the response to antiepileptic drugs. In addition, high homocysteine plasma levels represent a risk factor for cardiovascular and neurodegenerative diseases. To better define the role of increased homocysteine in epilepsy, we analyzed the effects of homocysteine pretreatment in the pilocarpine model of status epilepticus (SE), which is used to mimic temporal lobe epilepsy (TLE) in rodents. Precisely, we investigated whether a moderate hyperhomocysteinemia, unable to cause seizures, could sensitize rats to pilocarpine and cooperate in inducing brain lesions. We found that a subthreshold dose of pilocarpine (200 mg/kg) is sufficient to induce SE in the majority (approximately 90%) of rats pretreated with homocysteine for 2 weeks, whereas only 40% of saline-treated controls developed SE following the same pilocarpine dose. Furthermore, homocysteine pretreatment led to a significant increase in neuronal cell loss evaluated by counting toluidine blue-stained or Fluoro-Jade-positive cells in hippocampal and parahippocampal regions. Pilocarpine augmented amyloid beta expression in both animal groups. However, pretreatment with homocysteine favored the intraneuronal fibrillar conformation of amyloid beta, thus promoting neurodegeneration. These findings indicate that increased homocysteine levels enhance seizure activity and neurodegeneration in pilocarpine-treated rats and suggest that similar detrimental effects may occur in patients affected by TLE.

MTHFR Gene Polymorphism and Its Relationship with Plasma Homocysteine and Folate in a North Indian Population

There is a paucity of data on the prevalence of elevated homocysteine and its relation with plasma folate and the methylenetetrahydrofolate reductase (MTHFR) gene in the population of North India. This study evaluates MTHFR gene polymorphism and its relationship with plasma homocysteine and folate levels in a healthy North Indian population. The age of the 200 subjects included in this study was in the range 18-73 (mean 39.4) years. The plasma homocysteine level was elevated in 56.5%, and the plasma folate level was low in 49.5% of the subjects. Heterozygous MTHFR gene polymorphism (CT) was present in 15.5%, and homozygous (TT) in 3.5% of the subjects. Age, diet, and MTHFR gene polymorphisms were related to homocysteine level. All the subjects with the TT and 79% with the CT genotype had a high level of plasma homocysteine, whereas 51% with the CC genotype had a high homocysteine level. After adjustment for the effect of covariates, however, homocysteine was not related to MTHFR gene polymorphism.

High plasma homocysteine levels contribute to the risk of stroke recurrence and all-cause mortality in a large prospective stroke population

Plasma homocysteine concentrations have been associated with the risk of stroke, but its relevance to secondary vascular events and mortality after stroke remains unclear because of inconsistent results from clinical trials. The aim of the present study was to investigate whether plasma homocysteine levels and the MTHFR (methylenetetrahydrofolate reductase) variant C677T contributed to the risk of stroke recurrence and all-cause mortality in a large prospective cohort of stroke patients in a Chinese population. A total of 1823 stroke patients (age, 35-74 years) were recruited during 2000-2001 and prospectively followed-up for a median of 4.5 years. During the follow-up, 347 recurrent strokes and 323 deaths from all-causes were documented. After adjustment for age, gender and other cardiovascular risk factors, a high homocysteine concentration was associated with an increased risk of 1.74-fold for stroke recurrence {RR (relative risk), 1.74 [95% CI (confidence interval), 1.3-2.3]; P<0.0001} and 1.75-fold for all-cause mortality [RR, 1.75 (95% CI, 1.3-2.4); P<0.0001] when highest and lowest categories were compared. Spline regression analyses revealed a threshold level of homocysteine for stroke recurrence. By dichotomizing homocysteine concentrations, the RRs were 1.31 (95% CI, 1.10-1.61; P=0.016) for stroke recurrence and 1.47 (95% CI, 1.15-1.88; P<0.0001) for all-cause mortality in patients with homocysteine levels > or =16 micromol/l relative to those with levels <16 micromol/l. The association of elevated plasma homocysteine concentrations with all-cause mortality was mainly due to an increased risk of cardiovascular deaths. No significant association was found between MTHFR C677T and stroke recurrence or mortality. In conclusion, our findings suggest that elevated homocysteine concentrations can predict the risk of stroke recurrence and mortality in patients with stroke.

Genotype of the CYBA promoter −930A/G, polymorphism C677T of the MTHFR and APOE genotype in patients with hypertensive disorders of pregnancy: An observational study

Background and objective Hypertensive disorders of pregnancy could be favoured by polymorphisms in genes affecting vascular physiology. The aim of our work was to study several variants in the genes regulating oxidative stress, plasma lipids metabolism and endothelial function (observational study). Material and methods We studied the −930A/G polymorphism of the CYBA gene promoter, the apolipoprotein E (APOE) genotype and the methylene-tetrahydrofolate reductase (MTHFR) gene C677T polymorphism in 134 healthy pregnant women, 266 pregnant with non-proteinuric hypertension (NPH) and 184 patients with preeclampsia (PE). Results The GG genotype of the CYBA gene promoter was present in 32.1% of the control population, 38.7% of patients with NPH ( P=0.19) and 21.2% of the women with PE ( P=0.03). A higher frequency of ∈3/∈4 and ∈4/∈4 genotypes of APOE was observed in patients with PE or NPH compared with controls ( P<0.01). There were no significant differences detected in genotype or allele distribution of the MTHFR, C677T polymorphism. APOE ∈3/∈4 and ∈4/∈4 genotypes had a worse lipoprotein profile characterized by higher plasma values of total cholesterol ( P<0.05) and triglycerides ( P<0.005). Despite no differences in MTHFR C677T polymorphism distribution, higher levels of plasma homocysteine were observed in patients with PE than in patients with NPH or controls. Conclusions CYBA and APOE polymorphism showed a different distribution in the groups studied, while no differences were observed in MTHFR C677T polymorphism. APOE genotype was associated with changes in lipid and lipoprotein profiles in pregnant women.

The association between high plasma homocysteine levels and lower bone mineral density in Slovak women: the impact of vegetarian diet

A long-term vegetarian diet is generally poor in vitamin B group. The lack of vitamin B(12) together with vitamin B(6) and folate deficiency is closely related to homocysteine metabolism. Hyperhomocysteinemia was found to be associated with increased bone turnover markers and increased fracture risk. Thus, hyperhomocysteinemia, vitamin B(12) and folate deficiency may be regarded as novel risk factors for micronutrient deficiency-related osteoporosis. To assess the possible impact of a vegetarian diet on bone mineral density in cohort of Slovak vegetarian women. Fasting serum glucose, albumin, calcium, phosphorous and creatinine as well as bone markers, serum vitamin B(12), folate and plasma levels of total homocysteine were assessed in two nutritional groups (vegetarians vs. nonvegetarians) of apparently healthy women (age range 20-70 years). Bone mineral density of the femoral neck, trochanter, total femur and lumbar spine was measured in all subjects. Vegetarians had a significantly lower weight (p < 0.05), higher PTH (p < 0.01) and homocysteine (p < 0.001). Vitamin B(12) was significantly higher in nonvegetarians (p < 0.001). No differences were observed in folate levels. Univariate analysis showed significant association between homocysteine and B(12) (p < 0.01), folate (p < 0.001), creatinine (p < 0.001), total proteins (p < 0.049), age (p < 0.001) and vegetarian food intake (p < 0.001). Vegetarians had a significantly lower TrFBMD (p < 0.05) and ToFBMD (p < 0.05). Age and CTx were significant predictors in all sites of measured BMD and PTH. A strong correlation between homocysteine and FNBMD (r = -0.2009, p < 0.002), TrFBMD (r = -0.1810, p < 0.004) and ToFBMD (r = -0.2225, p < 0.001) was found in all subjects. Homocysteine is one of the predictors of bone mineral density, and hyperhomocysteinemia is associated with lower bone mineral density. In healthy adults, homocysteine levels are dependent on age as well as on nutritional habits. Thus, elderly women on a vegetarian diet seem to be at higher risk of osteoporosis development than nonvegetarian women.

A Novel Mutation of Cystathionine β-synthase Gene in a Thai Boy With Homocystinuria

The authors reported a 14-year-old boy who presented with multiple organs thrombosis and subluxation of lens. His diagnosis of homocystinuria was delayed owing to the unrecognition of the disease resulting in significant morbidity. The mutation analysis showed one novel mutation that can explain the high level of plasma homocysteine.

Folic acid influences plasma homocysteine levels and arterial endothelial function in patients with unstable angina

Objective High plasma homocysteine (Hcy) levels are associated with coronary artery disease, but the precise level associated with an increased risk is yet controversial. Whether the beneficial effects of folic acid on arterial endothelial function persist over longer periods is not known. This study aimed to assess whether folic acid supplementation could produce improvements in Hcy levels and arterial endothelial function in the patients with unstable angina (UA) and hyperhomocysteinemia. Design and method The plasma Hcy levels of 52 cases with UA and 30 age and sex-matched control subjects were measured by using high-performance liquid chromatography (HPLC) with fluorescence detection, plasma folic acid and VitB12 levels were measured with immunoassay. The patients with hyperhomocysteinemia were treated with 5 mg of folic acid for 8 weeks, and then rechecked the plasma levels of Hcy, folic acid and VitB12 at the end of the 4th and 8th weeks. Arterial endothelial function was measured as flow-mediated dilation of the brachial artery using high-resolution B-mode ultrasound in 22 cases with UA and hyperhomocysteinemia. Conclusions Hcy level is elevated in patients with UA. Folic acid can reduce the plasma Hcy levels and improve arterial endothelial function in the UA patients with hyperhomocysteinemia. Objective High plasma homocysteine (Hcy) levels are associated with coronary artery disease, but the precise level associated with an increased risk is yet controversial. Whether the beneficial effects of folic acid on arterial endothelial function persist over longer periods is not known. This study aimed to assess whether folic acid supplementation could produce improvements in Hcy levels and arterial endothelial function in the patients with unstable angina (UA) and hyperhomocysteinemia. Design and method The plasma Hcy levels of 52 cases with UA and 30 age and sex-matched control subjects were measured by using high-performance liquid chromatography (HPLC) with fluorescence detection, plasma folic acid and VitB12 levels were measured with immunoassay. The patients with hyperhomocysteinemia were treated with 5 mg of folic acid for 8 weeks, and then rechecked the plasma levels of Hcy, folic acid and VitB12 at the end of the 4th and 8th weeks. Arterial endothelial function was measured as flow-mediated dilation of the brachial artery using high-resolution B-mode ultrasound in 22 cases with UA and hyperhomocysteinemia. Conclusions Hcy level is elevated in patients with UA. Folic acid can reduce the plasma Hcy levels and improve arterial endothelial function in the UA patients with hyperhomocysteinemia.