Hyperhomocysteinaemia and endothelial dysfunction in young patients with peripheral arterial occlusive disease

Berg, M. van den; Boers, G.H.J.; Franken, D. G.; Blom, Henk J.; Kamp, Gerard J. van; Jakobs, Cornelis; Rauwerda, Jan A.; Kluft, C.; Stehouwert, C. D. A.

doi:10.1111/j.1365-2362.1995.tb01545.x

Cited by 188 publications

(10 citation statements)

References 28 publications

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“…Accordingly, it is reasonable to suggest that patients with hyperthyroidism experience endothelial cell dysfunction. On the other hand, although our ®ndings of decreased basal t-PA levels in plasma in patients with endothelial dysfunction are in accordance with those obtained by some investigators [8,20,21], contradictory results have been reported in different diseases by others [9,10,19]. The reasons for the contradiction are not clear.…”

Section: Discussionsupporting

confidence: 77%

Impaired release of tissue plasminogen activator from the endothelium in Graves' disease — indicator of endothelial dysfunction and reduced fibrinolytic capacity

Chen

Tan

et al. 1998

Eur J Clin Investigation

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Section: Discussionsupporting

confidence: 77%

Impaired release of tissue plasminogen activator from the endothelium in Graves' disease — indicator of endothelial dysfunction and reduced fibrinolytic capacity

Chen

Tan

et al. 1998

Eur J Clin Investigation

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“…In our study, the plasma level of homocysteine was significantly higher in patients with Buerger’s disease as compared to atherosclerosis and healthy cases before treatment. (p < 0.001) The higher values of plasma homocysteine levels in Buerger’s disease patients and simultaneously the higher prevalence of tobacco usage in this group (90.9% of cases) and also higher plasma levels of homocysteine in smoker cases of 3 groups was compared to the initial measurement in all patients, suggests that tobacco could be the principle cause of hyperhomocysteinemia in such patients, which also has been revealed in other studies (4, 6, 12, 14). The effect of folic acid therapy on elevated homocysteine levels in some medical conditions has been evaluated in a variety of studies.…”

Section: Discussionsupporting

confidence: 76%

Effect of Folic Acid therapy on Homocysteine Level in patients with Atherosclerosis or Buerger’s Disease and in Healthy individuals: A clinical trial

et al. 2016

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BackgroundHyperhomocysteinemia is considered a risk factor for atherosclerosis and some other vascular diseases such as Buerger’s disease.ObjectiveThe aim of this study was to measure the Homocysteine levels in 3 different groups of participants (Buerger’s disease, atherosclerosis patients, and healthy cases) and determine the therapeutic effect of folic acid therapy on homocysteine levels for these three groupsMethodsThis nonrandomized clinical trial study was conducted in the vascular and endovascular surgery research center of Mashhad University of Medical Sciences in Mashhad, Iran. This interventional study consisted of 44 participants of which 22 patients had Buerger’s disease and a control group of 22 healthy individuals, all of which were enrolled in this study. All of the study’s participants had their serum homocysteine levels measured both before and after 12 weeks of folic acid (5mg/day) therapy. The data analysis used fo data analysis was a Chi square and t-test or their non-parametrical equivalents for data analysis by means of Statistical Package for the Social Sciences (SPSS) version 16ResultsThe homocysteine levels were found to be significantly higher in patients with Buerger’s disease as compared to other groups before treatment with folic acid (Buerger = 21.8 ± 8.5 Mm/L, atherosclerosis = 17.3 ± 6.9, healthy = 13.8 ± 3.1; p < 0.001). After treatment with folic acid at 5 mg/daily for 12 weeks, the new plasma homocysteine levels did not show any significant difference (p = 0.38) between the Buerger’s disease group (14.6 ± 4.5 Mm/L) and atherosclerosis group (13.9 ± 4.7), but it was found to besignificantly higher in both groups when compared to the healthy group (10.7 ± 3.9, p<0.05). The plasma homocysteine level was reduced significantly when compared to its initial level in all 3 groups. The comparison of differences among three groups was found not to be significant (p=0.41)ConclusionsIt seems that supplementary therapy with folic acid at a dose of 5 mg daily may reduce the serum homocysteine levels significantly and may have a role in the development of vascular diseases such as Buerger’s disease. We suggest that folic acid should be considered as a routine agent in the Buerger’s disease therapeutic regimeClinical trial registrationThe trial was registered at the Thai Clinical Trials Registry (http://www.clinicaltrials.in.th) with the ID: TCTR20160601003.FundingThis study was not funded by any organization.

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“…Homocysteine can build up in the arteries, which may increase the risk of blood clots, heart attack, and stroke. Vitamin B 6, B12, and folic acid are essential for reducing total homocysteine and reverse endothelial dysfunction induced by high total homocysteine levels [ 8 - 9 ]. In a few prospective studies, total homocysteine levels >10.2µmol/L were found to be associated with the doubling of vascular risk, whereas >20µmol/L was associated with an eight to nine-fold increase in vascular risk [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

Effect of Vitamin B6, B9, and B12 Supplementation on Homocysteine Level and Cardiovascular Outcomes in Stroke Patients: A Meta-Analysis of Randomized Controlled Trials

Kataria

Yadav

Kumar

et al. 2021

Cureus

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Globally, stroke is the fifth-most leading cause of mortality and also the third leading cause of disability. This study aimed to assess the effect of vitamin B 6 , B 9 , and B 12 supplementation on homocysteine level, risk of stroke, cardiovascular disorders, and vascular death among stroke participants. An extensive literature search was done through PubMed, Medline, Embase, and Clinical key database from 1 January 2000 to 1 January 2020. Effect of vitamin B (B 6 , B 9 , and B 12 ) supplementation on homocysteine was assessed with a mean difference in both vitamin and placebo groups. Risk ratio (RR) was calculated for determining the risk of stroke, major cardiovascular disorder, and vascular death by using a fixed-effect model. A total of eight trials with 8513 participants were included for the final analysis. Vitamin B supplementation intervention was found to have a significant benefit in reducing homocysteine in stroke patients (mean difference -3.84; p<0.00001). The intervention of vitamin B supplementation showed a significant risk reduction of 11% for combined risk of stroke, myocardial infarction, and vascular death among stroke patients, 13% for stroke and 17% for vascular death, whereas no beneficial effect was seen for cardiovascular disorders. This metaanalysis demonstrated up-to-date evidence on the beneficial effect of vitamin B supplementations in reducing homocysteine and preventing the combined risk of stroke, myocardial infarction, and vascular death among stroke patients.

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Hyperhomocysteinaemia and endothelial dysfunction in young patients with peripheral arterial occlusive disease

Cited by 188 publications

References 28 publications

Impaired release of tissue plasminogen activator from the endothelium in Graves' disease — indicator of endothelial dysfunction and reduced fibrinolytic capacity

Impaired release of tissue plasminogen activator from the endothelium in Graves' disease — indicator of endothelial dysfunction and reduced fibrinolytic capacity

Effect of Folic Acid therapy on Homocysteine Level in patients with Atherosclerosis or Buerger’s Disease and in Healthy individuals: A clinical trial

Effect of Vitamin B6, B9, and B12 Supplementation on Homocysteine Level and Cardiovascular Outcomes in Stroke Patients: A Meta-Analysis of Randomized Controlled Trials

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