Hyperhomocysteinemia (HH) and metabolic syndrome (MS) are associated with increased cardiovascular risk. However, whether there is a link between MS or its components and homocysteine levels in a population without cardiovascular disease is not well established. We conducted a case-control study in 61 MS patients (41 males, 20 females, aged 51 ± 11 years) and in 98 controls without MS (59 males, 39 females, aged 50 ± 10 years) to ascertain the association between MS and HH, and with inflammatory markers. MS was classified according to the updated ATPIII criteria . No differences in homocysteine levels were observed when comparing MS patients and controls (12.0 ± 3.18 μM vs. 11.9 ± 3.5 μM, p = 0.829). No association was found between HH (homocysteine >15 μM) and MS, its components (abdominal obesity (p = 0.635), hypertension (0.229), low-HDL cholesterol (p = 0.491), glucose >100 mg/dL (0.485), hypertriglyceridemia (p = 0.490)) or the number of MS components (p = 272). When considering glucose >110 mg/dL (NCEP-ATPIII criteria, 2001) instead of glucose intolerancen >100 mg/dl (updated ATPIII criteria, Grundy, 2005), a borderline association with HH was observed (p = 0.054) of statistical significance (p = 0.008) when glucose >126 mg/dL was considered. In a multivariate regression model, creatinine, folic acid and vitamin B12 were the only independent predictors of homocysteine levels (p < 0.05). Although MS correlated with inflammatory parameters (fibrinogen, hs-RCP, plasma viscosity and leukocyte count, p < 0.001), no association was found between HH and the above-mentioned parameters (p > 0.05). Our results do not indicate a link between SM or its individual components with HH, and diabetes was the only relevant contribution. Cardiovascular disease risk due to MS and HH seems to share no common mechanisms.
"Lipid abnormalities are unique in individuals with T2D and those are at risk of T2D (obesity, metabolic syndrome and pre-diabetes): the total cholesterol and LDL are lower in those with statins but higher in those without. In addition, in both groups the triglyceride levels are higher and the HDL levels are lower as statins have little effect on them [35-37]. In post-menopausal women with T2D and CAD who were not on lipid lowering medications, in addition to higher total and LDL cholesterol and higher triglycerides, homocysteine was also higher, suggesting a potential link between vitamin B12 and folic acid and abnormal lipid profiles [38-41]. "
[Show abstract][Hide abstract] ABSTRACT: Metformin, a standard therapy in type 2 diabetes, reduces vitamin B12 levels. Studies linking low vitamin B12 levels and cardiovascular disease are equivocal and suggest improving B12 levels may help in primary prevention. The role of vitamin B12 deficiency on cardiovascular risk factors, especially in type 2 diabetes has not been explored. The aim of this study is to investigate whether vitamin B12 deficiency in type 2 diabetes patients is associated with cardiovascular risk factors in two different ethnic groups in UK and India.
Type 2 diabetes patients from two secondary care diabetic centres (Europeans - UK and Indians - India) were studied. Serum vitamin B12, folate and biochemical parameters were measured.
The prevalence rates of vitamin B12 deficiency (<191 ng/L) were 27% and 12% in Europeans and Indians, respectively and higher in metformin treated type 2 diabetes patients. In linear regression analysis, after adjusting for all likely confounding factors, vitamin B12 independently associated with triglycerides in both the populations and cholesterol/HDL ratio in Indians. Logistic regression showed type 2 diabetes patients with vitamin B12 deficiency were at significantly higher odds of having coexisting coronary artery disease (CAD) in Europeans with similar but non-significant trend in Indians, after adjusting for all likely confounding factors.
The prevalence of vitamin B12 deficiency is common in type 2 diabetes patients and is associated with adverse lipid parameters. Type 2 diabetes management guidelines should include the recommendation for regular testing for B12 levels, especially for those on metformin.
"Okyay et al. reported that EAT thickness of >4.35 mm indicated MS according to International Diabetes Federation criteria . Although there is conflicting data regarding the association between plasma homocystene level and MS, several studies support this relationship [8-10,24,25]. In addition, in patients with coronary artery disease, plasma homocysteine levels were found to be higher in subjects with MS than in those without . "
[Show abstract][Hide abstract] ABSTRACT: Background
Increased epicardial adipose tissue thickness and plasma homocysteine levels are associated with Metabolic Syndrome (MS) and coronary artery disease. The majority of patients with MS have subclinical or manifest coronary artery disease. The aim of this study was to evaluate the relationship between MS and plasma homocysteine levels and epicardial adipose tissue thickness in subjects without epicardial coronary artery disease.
Patients who underwent coronary angiography due to angina or equivocal symptoms and/or abnormal stress test results and were found to have normal coronary arteries were evaluated for the presence of MS. The study group comprised 75 patients with normal coronary arteries and MS, and the control group included 75 age-gender matched subjects without coronary artery disease or MS.
Epicardial adipose tissue thickness (5.8 ± 1.9 mm vs. 4.3 ± 1.6 mm, p <0.001) and plasma homocysteine levels (21.6 ± 6.1 μmol/L vs. 15.1 ± 5.8 μmol/L, p <0.001) were significantly higher in the MS group. Body mass index, triglyceride level, weight, age and waist circumference were positively and HDL cholesterol level were negatively correlated with both epicardial adipose tissue thickness and plasma homocysteine level. Epicardial adipose tissue thickness had the strongest correlation with plasma homocysteine level (r = 0.584, p < 0.001). For each 1 mm increase in epicardial adipose tissue thickness, an increase of 3.51 μmol/L (95% CI: 2.24-4.79) in plasma homocysteine level was expected.
We observed a close relationship between MS and epicardial adipose tissue thickness and plasma homocysteine levels, even in the absence of overt coronary artery disease.
"Moreover, it has not been established whether there is an association between Hcy levels and microangiopathy severity in RP when determined by nailfold capillaroscopy  . These discrepancies may be due to the heterogeneity of patients, concomitant treatment, differences in cardiovascular risk factors prevalence    , age  and renal function  as all these factors are of paramount importance for Hcy levels. "
[Show abstract][Hide abstract] ABSTRACT: The association between hyperhomocysteinemia (HHcy) and Raynaud's phenomenon (RP) remains a matter of debate. In 18 primary RP, 23 secondary RP and 41 controls, we investigated homocysteine (Hcy) levels along with biochemical and inflammatory parameters. The Hcy levels in both primary and secondary RP were elevated when compared with controls (p < 0.05 and p < 0.01, respectively). As age was higher in secondary RP as compared with controls (p < 0.01), both primary and secondary RP were age-matched with a corresponding control group, and with Hcy maintaining its statistical significance (p < 0.05). No differences in creatinine, B12 vitamin or folic acid were observed between groups (p > 0.05), or in the prevalence of cardiovascular risk factors (p > 0.05). When patients were classified according to presence or absence of digital ulcers, as a sign of microangiopathy severity, the former showed higher Hcy levels than the latter (p = 0.035). Our results indicate that both primary and secondary RP patients show a mild increase in Hcy levels, which is not related to age, vitamin deficiencies or impaired renal function, but is related to microangiopathy severity. Therefore the association of HHcy and RP suggest that Hcy may contribute to endothelial dysregulation, which characterizes this disease. Specific studies should be designed to elucidate the pathogenesis of HHcy in these patients.
Clinical hemorheology and microcirculation 03/2014; DOI:10.3233/CH-131681 · 2.24 Impact Factor
Karin M. A. Swart, Annelies C. Ham, Janneke P. van Wijngaarden, Anke W. Enneman, Suzanne C. van Dijk, Evelien Sohl, Elske M. Brouwer-Brolsma, Nikita L. van der Zwaluw, M. Carola Zillikens, Rosalie A. M. Dhonukshe-Rutten, Nathalie van der Velde, Johannes Brug, André G. Uitterlinden, Lisette C. P. G. M. de Groot, Paul Lips, Natasja M. van Schoor
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