The G/C polymorphism of the IL6 gene does not predispose patients to pSS, but the circulating IL-6 concentration is related to specific manifestations of the disease and the levels of IL-6 are regulated by the IL6 promoter polymorphism in pSS.

Abstract-Limited and partly controversial data are available regarding the relationship of arterial pulse wave velocity and childhood cardiovascular risk factors. We studied how risk factors identified in childhood and adulthood predict pulse wave velocity assessed in adulthood. The study cohort consisted of 1691 white adults aged 30 to 45 years who had risk factor data available since childhood. Pulse wave velocity was assessed noninvasively by whole-body impedance cardiography. The number of conventional childhood and adulthood risk factors (extreme quintiles for low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, systolic blood pressure, body mass index, and smoking) was directly associated with pulse wave velocity in adulthood (Pϭ0.005 and PϽ0.0001, respectively). In multivariable regression analysis, independent predictors of pulse wave velocity were sex (PϽ0.0001), age (PϽ0.0001), childhood systolic blood pressure (Pϭ0.002) and glucose (Pϭ0.02), and adulthood systolic blood pressure (PϽ0.0001), insulin (Pϭ0.0009), and triglycerides (Pϭ0.003). Reduction in the number of risk factors (PϽ0.0001) and a favorable change in obesity status (Pϭ0.0002) from childhood to adulthood were associated with lower pulse wave velocity in adulthood. Conventional risk factors in childhood and adulthood predict pulse wave velocity in adulthood. Favorable changes in risk factor and obesity status from childhood to adulthood are associated with lower pulse wave velocity in adulthood. These results support efforts for a reduction of conventional risk factors both in childhood and adulthood in the primary prevention of atherosclerosis. (Hypertension. 2010;55:806-811.)Key Words: cardiovascular health Ⅲ risk factors Ⅲ elasticity Ⅲ epidemiology Ⅲ pulse wave velocity I t is well recognized that atherosclerosis has its roots in childhood. Risk factors identified in childhood predict the occurrence of preclinical carotid atherosclerosis in adulthood. 1-3 Risk factors have also been associated with decreased arterial elasticity in cross-sectional studies. 4 -6 We have demonstrated previously a link between youth risk factor exposure and decreased carotid elasticity in adulthood. 7 Arterial pulse wave velocity (PWV) is commonly used as a marker of arterial stiffness. In various patient categories, including patients with hypertension, 8 end-stage renal failure, 9 and diabetes mellitus, 10 PWV is an independent predictor of all-cause and cardiovascular mortality. Furthermore, aortic PWV is associated with higher cardiovascular mortality, coronary heart disease, and stroke among generally healthy older adults. 11 Previous observations concerning the relationship between risk factors identified in childhood/adolescence and arterial PWV in adulthood have been controversial. Li et al 12 (835 participants, aged 24 to 44 years) reported a direct correlation between childhood blood pressure and PWV in adulthood, whereas Oren et al 13 (524 participants, aged 27 to 30 years) did not find an association between adolescent blo...

Background— Genome-wide association studies have recently identified a locus on chromosome 9p21 that influences risk of coronary artery disease (CAD). The effect of the locus on early markers of atherosclerosis is unknown. We examined its association with carotid intima-media thickness (CIMT) and brachial flow-mediated dilatation (FMD). Methods and Results— We genotyped 2277 individuals, age 24 to 39 years, from the Cardiovascular Risk in Young Finns Study with CIMT and FMD measurements and 1295 individuals, age 46 to 76 years, from the Health 2000 Survey with CIMT for rs1333049, the chromosome 9p21 variant showing the strongest association with CAD. Both mean and maximum CIMT were significantly higher ( P <0.001) in the older subjects of the Health 2000 Survey compared with the Young Finns Study. However, there was no association of the rs1333049 genotype with either mean or maximum CIMT at either age ( P =0.959 and 0.977 for the 2 phenotypes in the Young Finns Study and P =0.714 and 0.725 in the Health 2000 Survey). Similarly, there was no association of the locus with variation in FMD in the Young Finns cohort ( P =0.521). Conclusions— The chromosome 9p21 locus does not influence CAD risk through a mechanism that also affects CIMT or induces early changes in FMD.