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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Abnormal riboflavin status in the absence of a dietary deficiency was detected in 31 consecutive outpatients with Parkinson's disease (PD), while the classical determinants of homocysteine levels (B6, folic acid, and B12) were usually within normal limits. In contrast, only 3 of 10 consecutive outpatients with dementia without previous stroke had abnormal riboflavin status. The data for 12 patients who did not complete 6 months of therapy or did not comply with the proposed treatment paradigm were excluded from analysis. Nineteen PD patients (8 males and 11 females, mean age +/- SD = 66.2+/-8.6 years; 3, 3, 2, 5, and 6 patients in Hoehn and Yahr stages I to V) received riboflavin orally (30 mg every 8 h) plus their usual symptomatic medications and all red meat was eliminated from their diet. After 1 month the riboflavin status of the patients was normalized from 106.4+/-34.9 to 179.2+/-23 ng/ml (N = 9). Motor capacity was measured by a modification of the scoring system of Hoehn and Yahr, which reports motor capacity as percent. All 19 patients who completed 6 months of treatment showed improved motor capacity during the first three months and most reached a plateau while 5/19 continued to improve in the 3- to 6-month interval. Their average motor capacity increased from 44 to 71% after 6 months, increasing significantly every month compared with their own pretreatment status (P < 0.001, Wilcoxon signed rank test). Discontinuation of riboflavin for several days did not impair motor capacity and yellowish urine was the only side effect observed. The data show that the proposed treatment improves the clinical condition of PD patients. Riboflavin-sensitive mechanisms involved in PD may include glutathione depletion, cumulative mitochondrial DNA mutations, disturbed mitochondrial protein complexes, and abnormal iron metabolism. More studies are required to identify the mechanisms involved.
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PMID:High doses of riboflavin and the elimination of dietary red meat promote the recovery of some motor functions in Parkinson's disease patients. 1533 94

Plasma homocysteine is a risk factor for coronary artery disease, stroke, peripheral arterial disease, extracranial carotid arterial disease, aortic atherosclerosis, deep vein thrombosis, and possibly dementia and Alzheimer's disease in older persons. Randomized trials are in progress investigating whether multivitamin therapy with folic acid, vitamin B12, and vitamin B6 to reduce plasma homocysteine levels will reduce the risk for atherosclerotic vascular disease.
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PMID:Homocysteine. The association with atherosclerotic vascular disease in older persons. 1451 74

Cardiovascular diseases are the primary cause of mortality in France. Many epidemiological studies have shown that the total homocysteine concentration is a risk indicator for cardiovascular disease. Furthermore, it has been shown that the homocysteine concentration can be effectively lowered by supplementation with folic acid, vitamin B6 and B12. However, it is not yet known whether a reduction of the homocysteine concentration by such a supplementation indeed leads to a decreased risk of cardiovascular disease. Another possible dietary factor that may lower the risk of cardiovascular disease is fish-oil, which is rich in omega-3 fatty acids. These fatty acids lower platelet aggregation and triglyceride rich lipoproteins and may have antiarrhythmic effects. Some trials have investigated the effect of fish or fish-oil on cardiovascular mortality, and the results, although not conclusive, suggest a protective effect of a higher intake. In the SU.FOL.OM3 study we will evaluate the effect of supplementation at nutritional doses of folate (in the natural 5-methyl-tetrahydrofolate form) in combination with vitamin B6 and B12 and/or omega-3 fatty acids and/or placebo on recurrent ischemic diseases in a factorial design. The supplements will be randomly allocated to the participants in a double-blind fashion. In total 3,000 patients aged between 45 and 80 years who had a past history of myocardial infarction or unstable angina pectoris or an ischemic stroke will be included. The participants will be supplemented and followed up for a period of five years.
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PMID:Background and rationale of the SU.FOL.OM3 study: double-blind randomized placebo-controlled secondary prevention trial to test the impact of supplementation with folate, vitamin B6 and B12 and/or omega-3 fatty acids on the prevention of recurrent ischemic events in subjects with atherosclerosis in the coronary or cerebral arteries. 1462 23

The etiological role of hyperhomocysteinemia in the origin of neural-tube defects was proved, therefore a mandatory flour folic acid fortification program was introduced in the USA since January 1, 1998. In Hungary one kind of breads was fortified with folic acid, vitamin B12 and vitamin B6. The Hungarian randomised controlled trials of periconceptional folic acid containing micronutrient-combination supplementation also indicated a reduction in the occurrence of congenital cardiovascular malformations, urinary tract's defects and congenital limb deficiencies and these findings were confirmed by US teams. Recent studies showed a positive association between cardiovascular diseases and hyperhomocysteinemia as well, thus it is considered as an independent etiological factor in the pathogenesis of ischemic heart diseases, stroke, deep vein thrombosis, in addition of vascular diseases in the placenta during pregnancy. Other studies showed that hyperhomocysteinemia is more prevalent in demented patients and in persons with impaired cognitive performance. Some association was also found between hyperhomocysteinemia and cancers (e.g. colon). There is strong evidence that four vitamins B, such as vitamin B11 (folate-folic acid), vitamin B12, B2 and B6 can reduce the level of serum homocysteine and subsequently neural-tube defects. In addition the results of intervention studies indicated a protective effect of folic acid and other vitamins B for some other congenital abnormalities, cardiovascular diseases, senile dementia and cancers. The flour fortification with these water-soluble vitamins B is appropriate for an effective public health program for the primary prevention of these hyperhomocysteinemia-related disorders. There is no real risk for side effects on the basis of available US, Canadian and Hungarian experiences. In conclusion an urgent task is to introduce a mandatory flour fortification program in Hungary.
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PMID:[Public health control of hyperhomocysteinemia and its consequences]. 1462 40

Thrombophilia is defined as an enhanced tendency to form intravascular thrombi, which may be arterial or venous. Of the inherited thrombophilias, factor V Leiden and the prothrombin 20210 mutation have been associated with stroke, but this association is statistically significant only in children and adults under age 40. The risk of stroke in persons with these mutations is substantially increased by concomitant exposure to oral contraceptives. Hyperhomocystinemia is a major risk factor for stroke as well as Alzheimer's disease; persons with deficiencies of vitamin B12 or folic acid are especially vulnerable to these complications. Of the acquired thrombophilias, the antiphospholipid antibody syndrome is strongly associated with transient ischemic attacks, cerebral infarction, Sneddon syndrome, and dementia. The diagnosis of thrombophilia should be considered in stroke patients who are young, have a family history of thrombosis, suffer venous dural sinus thrombosis, or have recurrent strokes.
Top Stroke Rehabil 2003
PMID:Thrombophilia and stroke. 1468 17

Hyperhomocysteinemia (HHcy) is an independent risk factor for cardiovascular disease, including ischemic heart disease, stroke, and peripheral vascular disease. Mutations in the enzymes responsible for homocysteine metabolism, particularly cystathionine beta-synthase (CBS) or 5,10-methylenetetrahydrofolate reductase (MTHFR), result in severe forms of HHcy. Additionally, nutritional deficiencies in B vitamin cofactors required for homocysteine metabolism, including folic acid, vitamin B6 (pyridoxal phosphate), and/or B12 (methylcobalamin), can induce HHcy. Studies using animal models of genetic- and diet-induced HHcy have recently demonstrated a causal relationship between HHcy, endothelial dysfunction, and accelerated atherosclerosis. Dietary enrichment in B vitamins attenuates these adverse effects of HHcy. Although oxidative stress and activation of proinflammatory factors have been proposed to explain the atherogenic effects of HHcy, recent in vitro and in vivo studies demonstrate that HHcy induces endoplasmic reticulum (ER) stress, leading to activation of the unfolded protein response (UPR). This review summarizes the current role of HHcy in endothelial dysfunction and explores the cellular mechanisms, including ER stress, that contribute to atherothrombosis.
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PMID:Role of hyperhomocysteinemia in endothelial dysfunction and atherothrombotic disease. 1524 79

Evidence shows that there is a rapid increase in the production of markers of oxidative damage immediately following acute stroke and that endogenous antioxidant defences are rapidly depleted, thus permitting further tissue damage. Several studies point to an antioxidant effect of B-group vitamins and a pro-oxidant effect of elevated plasma tHcy (total homocysteine). In the present study, we assessed whether supplementary B-group vitamins during this critical period will enhance antioxidant capacity and mitigate oxidative damage. Forty-eight patients with acute ischaemic stroke within 12 h of symptom onset were assigned to receive daily oral supplements of B-group vitamins comprising 5 mg of folate, 5 mg of vitamin B2, 50 mg of vitamin B6 and 0.4 mg of vitamin B12 (n=24) or no supplements (n=24) for 14 days. The treatment group and controls were matched for stroke subtype and age. Blood samples were obtained before intervention and also at 7 and 14 days post-recruitment for measurement of the following biomarkers: red cell folate (whole blood folate corrected with haematocrit), erythrocyte glutathione reductase activity coefficient (EGRAC; measure of vitamin B2 status), plasma pyridoxal phosphate (vitamin B6 status), plasma vitamin B12, plasma alpha-tocopherol, plasma ascorbic acid, plasma TAOC (total antioxidant capacity), plasma MDA (malondialdehyde), plasma tHcy and CRP (C-reactive protein). Supplementation for 14 days with B-group vitamins significantly increased the plasma concentrations of pyridoxal phosphate and red blood cell folate and improved a measure of B2 status compared with the control group (P<0.05). Plasma tHcy decreased in both groups albeit less in the control group, but differences in cumulative changes were not significant. There was, however, a decrease in plasma MDA concentration in the treatment group, in contrast with the increase seen in the control group and these differences were significant (P=0.05). CRP concentration, a marker of tissue inflammation, was significantly lower in the treatment group compared with controls (P<0.05). In conclusion, B-group vitamin supplementation immediately post-infarct may have antioxidant and anti-inflammatory effects in stroke disease independent of a homocysteine-lowering effect.
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PMID:B-group vitamin supplementation mitigates oxidative damage after acute ischaemic stroke. 1527 19

ATP-binding cassette transporters use the free energy of ATP hydrolysis to transport structurally diverse molecules across prokaryotic and eukaryotic membranes. Computer simulation studies of the "real-time" dynamics of the ATP binding process in BtuCD, the vitamin B12 importer from Escherichia coli, demonstrate that the docking of ATP to the catalytic pockets progressively draws the two cytoplasmic nucleotide-binding cassettes toward each other. Movement of the cassettes into closer opposition in turn induces conformational rearrangement of alpha-helices in the transmembrane domain. The shape of the translocation pathway consequently changes in a manner that could aid the vectorial movement of vitamin B12. These results suggest that ATP binding may indeed represent the power stroke in the catalytic mechanism. Moreover, occlusion of ATP at one catalytic site is mechanically coupled to opening of the nucleotide-binding pocket at the second site. We propose that this asymmetry in nucleotide binding behavior at the two catalytic pockets may form the structural basis by which the transporter is able to alternate ATP hydrolysis from one site to the other.
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PMID:Conformational transitions induced by the binding of MgATP to the vitamin B12 ATP-binding cassette (ABC) transporter BtuCD. 1530 47

Hyperhomocysteinemia is an independent risk factor for atherothrombotic cerebral stroke. Vitamin B12 and folic acid are important determinants of homocysteine metabolism. We aimed to evaluate the relationship, if present, between vitamin B12 and folic acid levels and acute cerebral stroke in this study. Blood aliquots drawn within 24 hours after the stroke from hospitalized patients (n=66) with the diagnosis of acute ischemic cerebrovascular episode and also blood samples from 38 healthy controls without any vascular risk factor were analyzed. With a competitive, chemoluminescence assay, serum levels of vitamin B12 and folic acid were measured in blood samples taken within 24 hours after the stroke. The differences and correlations were tested using frequency test, student-t test and multivariate analysis. Mean serum vitamin B12 levels were significantly lower in the patients than in the control subjects, 245.40 (S.D.: 72.9) and 343.2 (S.D.: 113.0) pg/ml respectively (p=0.0001). This difference was independent from other risk factors. Likewise, mean serum folic acid levels were lower in the patients than in the control subjects, 4.62 (S.D.: 1.94) and 5.97 (S.D.: 1.19) ng/ml, respectively (p=0.003). Mean serum levels of vitamin B12 and folate at the convalescence phase were 253.05 (S.D.: 68.78) pg/ml and 4.48 (S.D.: 2.08) ng/ml, respectively; the values obtained at the acute phase were not significantly different from the values obtained at the convalescence phase. We conclude that low vitamin B12 and folic acid concentrations are associated with an increased risk of stroke, and the relationship for vitamin B12 is independent from the other known modifiable stroke risk factors. For understanding the effects of B12 and folate in stroke patients, more detailed follow-up studies with long period are needed.
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PMID:Serum vitamin B12 and folic Acid levels in acute cerebral atherothrombotic infarction. 1538 96

Mild hyperhomocysteinemia is a probable risk factor for atherosclerotic diseases and stroke. Recently, associations of elevated plasma homocysteine concentrations in the acute phase and of MTHFR 677 TT genotype with spontaneous cervical artery dissections (sCAD) have been reported. The purpose of this study was to test this hypothesis in the currently largest sample of patients with sCAD, taking into account known factors influencing plasma homocysteine levels. Ninety-five patients with past sCAD were compared with 95 age- and sex-matched healthy individuals. Homocysteine, vitamin B6, B12, folate, and polymorphisms of methylenetetrahydrofolate reductase (MTHFR C677T), cystathionine beta-synthase (CBS 844ins68bp) and methylenetetrahydrofolate dehydrogenase/methenyltetrahydrofolate cyclohydrolase/formyltetrahydrofolate synthetase (MTHFD1 G1958A) were assessed and any associations were analysed using multivariate statistics. The occurrence of sCAD was associated with elevated homocysteine levels with an odds ratio of 1.327 per 20 % percentile. Homocysteine levels were influenced by gender, smoking status, occurrence of hypertension, vitamin B12 and folate levels, and by the MTHFR TT genotype. MTHFR, CBS 844ins68bp, and MTHFD1 G1958A genotype were not independently associated with the occurrence of sCAD. These data suggest that elevated homocysteine is associated with the occurrence of sCAD. The MTHFR C677T polymorphism is associated with the homocysteine level.
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PMID:Plasma homocysteine, MTHFR C677T, CBS 844ins68bp, and MTHFD1 G1958A polymorphisms in spontaneous cervical artery dissections. 1550 5


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