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Hyperhomocysteinemia clinical trials

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NCT ID: NCT01766310 Completed - Obesity Clinical Trials

Effect of Folic Acid Supplementation on Plasma Homocysteine Level in Obese Children

Start date: December 2012
Phase: Phase 4
Study type: Interventional

The purpose of the present study was to determine whether folic acid supplementation could reduce plasma homocysteine in obese children and to determine the association between dietary folate, serum folate and homocysteine level through the randomized double blinded placebo controlled trial.

NCT ID: NCT01661309 Completed - Clinical trials for Vitamin B12 Deficiency

Supplementary Vitamin B12 Effects on Elevated Homocysteine Levels of Vegetarians - Clinical Trial

Start date: March 2012
Phase: N/A
Study type: Interventional

Vegetarians are known to be deficient in vitamin B12, due to a lack or absence of dietary animal produce, which can elevate homocysteine. There is strong evidence indicating that elevated plasma total homocysteine (tHcy) is a contributor to chronic conditions, such as primary cardiovascular disease (CVD). The study hypothesis is: There will be a significant decrease in plasma tHcy of vegetarians following the intervention by supplementary vitamin B12 (of the methylcobalamin type) and this will lead to a reduction of the risk of CVD.

NCT ID: NCT01391416 Completed - Clinical trials for Cardiovascular Disease

Prevalence Of Hyperhomocysteinemia In Thai Chronic Kidney Disease (CKD) Patients

Start date: June 2010
Phase: N/A
Study type: Observational

It is well recognized that patients with chronic kidney disease (CKD) have an increased risk for cardiovascular disease (CVD) and hyperhomocysteinemia appears to be a predictor of future CVD events. Hyperhomocysteinemia has been reported to bo of high prevalence in patients with CKD. The investigators aim to study the prevalence of hyperhomocysteinemia in Thai CKD patients by using Thai Screening and Early Evaluation of Kidney Disease (SEEK) study database and their relationship to CVD.

NCT ID: NCT01371357 Completed - Clinical trials for Hyperhomocysteinemia

The Effects of 8-week Choline, Betaine, and Folic Acid Supplementation on Plasma Homocysteine Concentration During Guanidinoacetic Acid Loading in Young Healthy Volunteers

Start date: May 2011
Phase: Phase 3
Study type: Interventional

A methyl-group acceptor such as guanidinoacetic acid (GAA) could induce hyperhomocysteinemia with the effects of GAA expected to be dose-dependent. Due to the fact that hyperhomocysteinemia is thought to be an independent risk factor for cardiovascular and neurodegenerative diseases, different dietary agents were used in the past for the treatment of elevated total plasma homocysteine (T-HCy), e. g. betaine, choline (betaine precursor) or folic acid. In the context of GAA loading the question arises whether intake of betaine, choline (betaine precursor) or folic acid during GAA loading could affect plasma T-HCy in healthy humans. Forty healthy physically active men and women aged 20 to 30 years will take part in this GAA-controlled, double-blind and parallel-group intervention study. Subjects will be allocated to four randomly assigned trials, with treatment lasting for 8 weeks and washout period of 28 days. The 4 test treatment-groups will include TEST1 (GAA only), TEST2 (GAA, choline, B6, B12 and folic acid), TEST3 (GAA, betaine, B6, B12 and folic acid) and TEST4 (GAA, B6, B12 and folic acid). Plasma T-HCy will be the primary outcome measure assessed every second week throughout the study. Plasma B-vitamins and blood and urine metabolites (GAA, creatine, methionine, arginine) will be secondary outcome measures along with adverse-effects indicators assessed every second week throughout the study. Selected body composition indicators will be obtained at 0, 2, 8 and 12 weeks throughout the study to monitor the effects of experimental treatments on body hydration and protein synthesis. This research will test the hypothesis that a combination of GAA with homocysteine lowering nutrients attenuates the elevation of T-hcy, and will further display the size-effect of each additive used.

NCT ID: NCT00877227 Completed - Clinical trials for Mild Hyperhomocysteinemia

Does B Vitamin Supplementation Decrease Homocysteine Concentrations in Newborns

Start date: January 2003
Phase: Phase 1
Study type: Interventional

The purpose of this study is to determine whether supplementation with folinic acid, a B vitamin, lowers the concentrations of total homocysteine in newborns. Increased homocysteine concentrations are associated with an increased risk of cerebrovascular accidents in adult, children and newborns. These increased concentrations can easily and safely be lowered by folic acid in adults.

NCT ID: NCT00755664 Completed - Clinical trials for Hyperhomocysteinemia

Effects of Low-dose Complex B-vitamins on Homocysteine and Framingham Risk Score Among Chinese Elderly

Start date: July 2007
Phase: Phase 3
Study type: Interventional

The purpose of this study is to evaluate whether low dose complex B-vitamins (folic acid,vitamin B6 and vitamin B12) can lower the risk of developing hyperhomocysteinemia in an apparently healthy population with low folate/B12 and high Hcy status.

NCT ID: NCT00737126 Completed - Clinical trials for Diabetic Nephropathies

The Effect of Folic Acid Administration in the Progression of Microalbuminuria

Start date: January 2004
Phase: N/A
Study type: Interventional

The development of diabetic nephropathy has been linked to several genetic polymorphisms, including those related with homocysteine metabolism such as the methylenetetrahydrofolate reductase (MTHFR)and the cystathionine-beta-synthase genes. Such alterations are associated with hyperhomocysteinemia, which is a known independent risk factor for the development of endothelial dysfunction and cardiovascular disease. In the Mexican population there is a high prevalence of the C677T MTHFR mutation. The investigators performed this study to evaluate the prevalence of this polymorphism in type 2 diabetic patients with diabetic nephropathy compared with type 2 diabetic patients without nephropathy, besides evaluating the relationship of hyperhomocysteinemia with endothelial dysfunction and microalbuminuria before and after the administration of folic acid. We proposed that the endothelial dysfunction caused by the hyperhomocysteinemia could be reversed after the administration of folic acid.

NCT ID: NCT00626223 Completed - Inflammation Clinical Trials

5-methyltetrahydrofolate Survival and Inflammation in ESRD Patients

Start date: January 1998
Phase: N/A
Study type: Interventional

A randomized prospective study was done to determine whether i.v. 5-methyltetrahydrofolate vs oral folate improved survival in ESRD patients. Homocysteine, CRP, Lp(a), albumin, folates, vitamin B6 and B12 were checked. The 5-MTHF treated group was associated with lowered C reactive protein and higher survival than the folate treated group.

NCT ID: NCT00473200 Completed - Clinical trials for Hyperhomocysteinemia

Effect of S-adenosylmethionine (SAMe) on Blood Levels of Homocysteine

Start date: August 2009
Phase: Phase 1
Study type: Interventional

The purpose of this study is to investigate whether S-adenosylmethionine (SAMe), a natural substance available as a nutritional supplement, can influence blood levels of homocysteine (Hcy). More specifically, we will determine if chronic oral SAMe administration affects homocysteine metabolism in patients with vascular disease who have mild to moderate hyperhomocysteinemia.

NCT ID: NCT00317005 Completed - Clinical trials for Cardiovascular Disease

Uremic Hyperhomocysteinemia -A Folate Trial for Possible Prevention of Cardiovascular Events

Start date: April 2003
Phase: Phase 4
Study type: Interventional

Homocysteine recently gained access to the category of risk factor for the development of atherosclerotic cardiovascular disease in the general population. Chronic renal failure patients, even before being introduced to dialysis therapy have almost universal elevation of serum homocysteine; when on dialysis their mortality is above 50% related to cardiovascular disease that we might now speculate, with a contribution of potentially toxic levels of the aminoacid homocysteine.