Hemorheology and Hemostasis Unit, Service of Clinical Pathology, La Fe University Hospital, Valencia, Spain. vaya
Clin Hemorheol Microcirc. 2011;47(1):59-66. doi: 10.3233/CH-2010-1366.
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 [17]. 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.
高同型半胱氨酸血症（HH）和代谢综合征（MS）与心血管风险增加有关。然而，在没有心血管疾病的人群中，MS 或其成分与同型半胱氨酸水平之间是否存在联系尚不清楚。我们对 61 名 MS 患者（41 名男性，20 名女性，年龄 51±11 岁）和 98 名无 MS 的对照者（59 名男性，39 名女性，年龄 50±10 岁）进行了病例对照研究，以确定 MS 与 HH 以及与炎症标志物之间的关系。MS 根据更新的 ATPIII 标准进行分类[17]。比较 MS 患者和对照组时，同型半胱氨酸水平无差异（12.0±3.18μM 与 11.9±3.5μM，p=0.829）。HH（同型半胱氨酸>15μM）与 MS 及其成分（腹部肥胖（p=0.635）、高血压（0.229）、低 HDL 胆固醇（p=0.491）、血糖>100mg/dL（0.485）、高甘油三酯血症（p=0.490））或 MS 成分数量（p=0.272）之间无关联。当考虑血糖>110mg/dL（NCEP-ATPIII 标准，2001）而不是血糖不耐受>100mg/dl（更新的 ATPIII 标准，Grundy，2005）时，HH 与 HH 之间存在边缘关联（p=0.054），具有统计学意义（p=0.008）。在多元回归模型中，肌酐、叶酸和维生素 B12 是同型半胱氨酸水平的唯一独立预测因子（p<0.05）。尽管 MS 与炎症参数（纤维蛋白原、hs-RCP、血浆粘度和白细胞计数，p<0.001）相关，但 HH 与上述参数之间无关联（p>0.05）。我们的结果表明，SM 或其单个成分与 HH 之间没有联系，糖尿病是唯一的相关贡献。MS 和 HH 引起的心血管疾病风险似乎没有共同的机制。
