Combined vitamin B6 plus folic acid therapy in young patients with arteriosclerosis and hyperhomocysteinemia

Berg, M. van den; Franken, D. G.; Boers, G.H.J.; Blom, Henk J.; Jakobs, Cornelis; Stehouwer, Coen D.A.; Rauwerda, Jan A.

doi:10.1016/0741-5214(94)90230-5

Cited by 107 publications

(36 citation statements)

References 19 publications

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“…In young patients with coronary artery or cerebro vascular disease, the effect of pyridoxine plus folic acid on homocysteine metabolism was similar to that reported here [28].…”

Section: Van Den Berg Et Alsupporting

confidence: 70%

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

Berg¹,

Boers²,

Franken³

et al. 1995

Eur J Clin Investigation

188

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Abstract. Hyperhomocysteinaemia, defined as an abnormally high plasma homocysteine concentration after an oral methionine load, is common in young ( ^ 50 years) patients with peripheral arterial occlusive disease. It is thought to predispose to atherosclerosis by injuring the vascular endothelium. Treatment with pyridoxine and/or folic acid may lower plasma homo cysteine levels, In mildly hyperhomocysteinaemic patients with peripheral arterial occlusive disease, we studied the effect of daily treatment with pyridoxine (250 mg) plus folic acid (5 mg) on homocysteine metabolism (i.e. plasma concentrations in the fasting state and after methionine loading, in 48 patients) and on endothelial function (in 18 patients), Endothelial function was estimated as the plasma concentrations of the endothelium-derived proteins, von Willebrand factor (vWF), thrombomodulin (TM), and tissue-type plasminogen activator (tPA). At baseline, fasting homocysteine levels were above normal in 24 of the 48 patients (50%); post-load levels, by definition, were above normal in 100% of patients. After 12 weeks of treatment, fasting and post-load levels were normal in 98 and 100% of patients, respectively. Endothelial function was assessed in 18 patients who completed 1 year of treatment. At baseline, median vWF (235%) and TM (57'1 ngm L"1) levels were above normal. At follow-up, vWF levels had decreased to 170% (p = 0*01) and TM levels had decreased to 49ngmL-1 (P = 0*04). tPA levels were normal at baseline and did not change. Endothelial dysfunction is present in young patients with peripheral arterial occlusive disease and hyperhomocysteinaemia. Pyri doxine plus folic acid treatment normalizes homocys teine metabolism in virtually all patients, and appears to ameliorate endothelial dysfunction.

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“…In young patients with coronary artery or cerebro vascular disease, the effect of pyridoxine plus folic acid on homocysteine metabolism was similar to that reported here [28].…”

Section: Van Den Berg Et Alsupporting

confidence: 70%

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

Berg¹,

Boers²,

Franken³

et al. 1995

Eur J Clin Investigation

188

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“…The fasting and post-load homocysteine concentration (2.5-97.5 percentile) respectively was in control men 8-18 and 25-54 /miol/1 (n 23), in control pre-menopausal women 6-15 and 18-51 /¿mo I/I (n 46) and in control post-menopausal women 6-19 and 25-69 /¿mol/1 (n 26) [27].…”

Section: Control Subjectsmentioning

confidence: 96%

Prevalence of familial mild hyperhomocysteinemia

et al. 1996

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Previous studies have shown that elevated basal homocysteine levels are correlated among family members of patients with coronary vascular disease and juvenile venous thrombosis. This suggests the possibility of the presence of inherited basal mild hyperhomocysteinemia (mHH). We studied homocysteine levels, fasting as well as after methionine load, among 96 family members of 21 post-load hyperhomocysteinemic vascular index patients, i.e. 6 parents, 27 offspring, 38 siblings, 19 uncles and aunts and 6 cousins. In 15 out of 21 screened families post-load ml-IH was esti in at least one family member. Fa:>ting and post-load mHH was observed in 19 out of 89 (21%) screened family members (fasting homocysteine levels not measured in seven family members), and 31 out of 96 screened family members (32%), respectively. In 40% of all family members, post-load mHH was not accompanied by fasting mHH.conclude that both fasting and post-load mHH seems to be inherited in the majority of ic vascular patients.

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“…24 Hyperhomocysteinemia was defined as elevated fasting homocysteine levels (Ͼ18 mol/L) and/or a postmethionine load homocysteine level Ͼ97.5th percentile in healthy controls, ie, 51 mol/L for females and 54 mol/L for males. 25 Plasma cholesterol and triglycerides were determined by commercially available enzymatic methods (Boehringer Mannheim No. 237574 and Sera-PAK, Miles No.…”

Section: Homocysteine and Cholesterol Determinationmentioning

confidence: 99%

Carotid and Femoral Artery Wall Thickness and Stiffness in Patients at Risk for Cardiovascular Disease, With Special Emphasis on Hyperhomocysteinemia

Smilde

Berkmortel

Boers

et al. 1998

ATVB

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Abstract-Recent developments in ultrasound technology enable the noninvasive measurement of structural and functional vessel wall changes. Until now, the effect of homocysteine on the arterial wall has remained unclear: reports on intima-media thickness (IMT) yield conflicting results, whereas data on vessel wall stiffness are lacking. Because several cardiovascular risk factors result in an increased IMT or stiffness, different groups at risk for atherosclerotic disease, with special emphasis on hyperhomocysteinemia, were studied. Nineteen patients homozygous and 14 subjects heterozygous for cystathionine ␤-synthase (CBS) deficiency, 21 patients with familial hypercholesterolemia (FH), 15 patients with essential hypertension, 20 smokers, and 28 control subjects were studied. The IMT values (both right and left) of the common carotid artery (CCA), bulb (BUL), internal carotid artery (ICA), and common femoral artery (CFA) were measured in millimeters by high-resolution ultrasound (Biosound). The distensibility (DC, in 10 Ϫ3 ⅐ kPa Ϫ1) and compliance (CC in mm 2 ⅐ kPa Ϫ1) coefficients of the CCA (right and left) and CFA (right) were determined by a wall track system (Pie Medical). The mean IMT of the posterior wall in the CCA was 0.70Ϯ0.09 mm in healthy controls. For patients with vascular disease, FH, and hypertension and in smokers, the mean CCA IMT was larger, whereas no major differences in IMT were observed in patients either homozygous or heterozygous for CBS deficiency. The DC and CC in the right CCA were 23.5Ϯ6.9 (10 Ϫ3 ⅐ kPa Ϫ1) and 0.9Ϯ0.3 (mm 2 ⅐ kPa Ϫ1 ) in healthy subjects, slightly lower in patients homozygous for CBS deficiency, and clearly lower in patients with vascular disease, FH, and hypertension. No positive correlation was found between plasma homocysteine level and either IMT, CC, or DC. Because smoking was a confounder in each risk group, a stepwise regression analysis was carried out to assess the contribution of each risk factor on IMT and arterial wall stiffness. Age explained most of the variation in IMT of the CCA (coefficient of determination R 2 of 0.34), whereas R 2 values for serum low density lipoprotein cholesterol, smoking (pack-years), and systolic blood pressure were 0.08, 0.07, and 0.06, respectively. Homocysteine did not contribute to variation in IMT in both the CCA and CFA. Age and smoking contributed to the variation in IMT in the CFA. The variation in DC and CC in the right CCA and right CFA could in part be explained by age, low density lipoprotein cholesterol, and blood pressure. Plasma homocysteine concentration explained only a small proportion of the variation in DC in the CCA (R 2 ϭ0.02) and in CC in the CFA (R 2 ϭ0.04). In this study, no relationship was found between homocysteine level and the thickness of the arterial wall, with only a marginal influence on stiffness.

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Combined vitamin B6 plus folic acid therapy in young patients with arteriosclerosis and hyperhomocysteinemia

Cited by 107 publications

References 19 publications

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

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

Prevalence of familial mild hyperhomocysteinemia

Carotid and Femoral Artery Wall Thickness and Stiffness in Patients at Risk for Cardiovascular Disease, With Special Emphasis on Hyperhomocysteinemia

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