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The association between H. pylori infection and coronary artery disease (CAD) is well-known. Alterations in DNA methylation in CAD have been reported, which can be induced by H. pylori through the DNA demethylases (DNMTs). The objective was to analyze the association and interaction of H. pylori infection and DMNT3a gene polymorphisms with premature CAD (pCAD) and subclinical atherosclerosis (SA).The study included 561 patients with pCAD, 318 subjects with SA, and 599 healthy controls. Antibodies against H. pylori and DNMT3a rs13420827, rs752208, and rs1550117 polymorphisms were determined.The pCAD group presented the highest seroprevalence of H. pylori infection (87.7%) compared to the SA (74.5%, p = 1 × 10According to the model adjusted for more confounding variables, H. pylori infection was associated with almost three times the risk of developing pCAD. The rs13420827G allele was associated with an increased risk of H. pylori infection in the whole population and in individuals with SA. Individuals in whom H. pylori infection and the rs13420827GG genotype coexist are at increased risk of pCAD.

Interleukin IL-15 (IL-15) has been implicated in the development of coronary artery disease (CAD). The aim of the present study was to evaluate the role of IL-15 gene polymorphisms as susceptibility markers for development of subclinical atherosclerosis (SA) and cardiovascular risk factors in Mexican population. Four IL-15 gene polymorphisms (rs4956403, rs3806798, rs1057972 and rs10833) were analyzed in a group of 397 individuals with SA and 1120 controls. Under different inheritance models adjusted by traditional risk factors, the rs10833T allele was associated with increased risk of developing SA [OR=1.42, Pcodom1=0.046; OR=1.48, Pdom=0.021; OR=1.43, Padd=0.014]. Under a dominant model, the rs1057972 polymorphism was associated with central obesity (P=0.045) and fatty liver (P=0.021), while the rs10833 polymorphism was associated with metabolic syndrome (P=0.007) in individuals with SA. The TAC haplotype was significantly associated with a decreased risk of SA. Individuals with rs10833CC genotype exhibited higher levels of IL-15 than individuals with CT+TT genotypes. The results suggest that IL-15 polymorphisms are involved in the risk of developing SA and are associated with metabolic syndrome, central obesity and fatty liver in our study population. The rs10833 polymorphism could be involved in regulating IL-15 production in SA.

The aim of this study was to evaluate the potential use of the I148M/PNPLA3 (rs738409) gene polymorphism as a susceptibility marker for premature coronary artery disease (pCAD) and/or cardiovascular risk factors in Mexican type 2 diabetes mellitus patients (T2DM). The polymorphism was genotyped by 5′ exonuclease TaqMan assays in a group of 2572 subjects (1103 with pCAD and 1469 healthy controls) belonging to the Genetics of Atherosclerotic Disease (GEA) Mexican Study. Anthropometric and biochemical measurements were performed in all individuals. The association between the I148M/PNPLA3 (rs738409) gene polymorphism with pCAD and other metabolic and cardiovascular risk factors was evaluated using logistic regression analysis under different statistical approaches including dominant, recessive, heterozygous, additive, and co-dominant models. The polymorphism was not associated with pCAD in the whole group of participants, however, when patients and controls were divided into those with and without T2DM, under additive model, the polymorphism was associated with the presence of pCAD only in patients with T2DM (OR = 1.20, 95% CI: 1.01–1.42, Padd = 0.042). On the other hand, under several models adjusted for age, gender, body mass index and T2DM, the polymorphism was associated with increased risk of fatty liver and elevated levels of alanine transaminase (ALT) in the whole group of pCAD patients and controls. In the control group, the polymorphism was associated with insulin resistance and coronary artery calcification (CAC) score ≥ 10 under several models. The results suggest that the I148M/PNPLA3 (rs738409) polymorphism is associated with the presence of pCAD in T2DM patients and with some cardiometabolic parameters. The association detected with CAC in the control group indicates that this polymorphism could be a marker for subclinical atherosclerosis.

The receptor-interacting protein 2 (Rip2) is a serine/threonine kinase involved in multiple nuclear factor-κB (NFκB) activation pathways and is a key regulator of cellular lipid metabolism and cardiovascular disease. The aim of the present study was to evaluate the role of RIP2 gene polymorphisms as susceptibility markers for subclinical atherosclerosis (SA). Using an informatics analysis, four RIP2 gene polymorphisms with predicted functional effects (rs2293808, rs43133, rs431264, and rs16900627) were selected. The polymorphisms were genotyped in 405 individuals with SA (calcium score>0 assessed by computed tomography) and 1099 controls (calcium score=0). Clinical, anthropometric, tomographic and biochemical traits were measured. The association between the RIP2 polymorphisms and SA was evaluated using logistic regression analyses. Pair wise linkage disequilibrium (LD, D') estimations between polymorphisms and haplotype reconstruction were performed with Haploview version 4:1. Under different models adjusted by age, gender, body mass index, hypertension, diabetes mellitus, smoking habit, total cholesterol, HDL-cholesterol, LDL-cholesterol and triglyceride levels, rs43133 (OR=1.43, 95% CI: 1.05-1.94, P=0.022), and rs16900627 (OR=1.59, 95% CI: 1.00-2.54, Pdom=0.048 and OR=1.60, 95% CI: 1.05-2.54, Padd=0.028) were associated with increased risk of developing SA. Moreover, rs2293808, and rs431264 were associated with clinical or metabolic parameters in SA individuals and in healthy controls. The four polymorphisms were in high linkage disequilibrium and the GAAG haplotype was associated with increased risk of developing SA (OR=1.47, P=0.027). This study shows for the first time, that RIP2 polymorphisms are associated with increased risk of SA and with some clinical and metabolic parameters.

Background Postprandial triglyceridemia may transitory affect the structure of HDL subclasses and probably their antiatherogenic properties but little is known in this field. We analyzed the HDL subclasses lipid content along postprandial period. Methods Fifteen metabolic syndrome (MS) patients and 15 healthy controls were enrolled. HDL were isolated from plasma samples obtained at fasting and every 2-h up to 8-h, after a 75-g fat meal. Cholesterol (C), triglycerides (TAG), and phospholipid (Ph) plasma concentrations of five HDL subclasses were determined by densitometry of electrophoresis gels enzymatically stained. Results The increase of postprandial triglyceridemia expressed as the incremental area under the curve (iAUC) was twice in MS patients than in controls. Only large HDL2b-TAG were higher in MS than controls at 4, 6 and 8 h after meal intake, whereas cholesterol of HDL2a, 3a and 3b were lower at 8 h. HDL size distribution shifted towards large HDL and HDL3a-, 3b- and 3c-subclasses had a lower content of cholesterol (estimated by the C-to-Ph ratio) in subjects whose iAUC > 289.5 mg h/dl (n = 15) in comparison with those subjects with iAUC below this cutoff point (n = 15), independently of the MS status and fasting TAG. Triglycerides content of HDL subclasses changed only discreetly along the postprandial period, whereas paraoxonase-1 remained unchanged. Conclusions A high postprandial triglyceridemia conditions the shift of HDL size distribution towards large particles and the decrease of cholesterol in HDL3 subclasses. These data demonstrate that postprandial hypertriglyceridemia contributes to a transitory hypoalphalipoproteinemia that may increase the risk of cardiovascular disease.

Background and Aims Adiponectin (ADPN) is a cardioprotective adipocytokine, and its association with atherosclerosis development is controversial. The aim of the present study was to assess the association of low ADPN plasma levels with the presence of subclinical atherosclerosis in a Mexican-Mestizo population without history of diabetes or coronary artery disease (CAD). Methods In 818 subjects (53.4 ± 9 years; 49.9% women) anthropometry, subcutaneous and visceral adipose tissue, lipids, glucose, C-reactive protein (CRP), insulin, and ADPN levels were determined. Carotid artery intima-media thickness (CIMT) was measured with ultrasound in B mode and the sex-age specific value higher than 75th percentile defined the presence of subclinical atherosclerosis. Low ADPN was considered when plasma concentrations were lower than 25th percentile (8.67 μg/mL in women, 5.30 μg/mL in men). Results Prevalence of low ADPN was 43.6% (42.9% in women and 44.4% in men; p = 0.66) and elevated CIMT (eCIMT) was 23.8% (25.8% in women and 21.9% in men; p = 0.184). In addition to their higher prevalence of low ADPN, subjects with eCIMT had higher values of body mass index, blood pressure, total cholesterol, triglycerides, glucose, insulin, and CRP. Multivariate analysis revealed that independent of these factors, low ADPN was associated with eCIMT (OR [95% CI]: 1.505 [1.051–2.153]). Conclusions In the studied population, low adiponectin concentrations are associated with a higher prevalence of subclinical atherosclerosis, independent of traditional cardiovascular risk factors.

Ulcerative colitis (UC) is a chronic condition of unknown etiology and a polygenic disease. The interleukin 27 (IL-27) have been implicated in the pathogenesis of several autoimmune diseases including inflammatory bowel disease. Several polymorphisms of IL-27 have been associated with several types of cancer and immune disorders. The aim of the present study was to evaluate the association between IL-27 gene polymorphisms and the development of UC. Four polymorphisms of IL-27p28 gene (rs181206, rs26528, rs17855750, and rs40837) and three of the Epstein-Barr virus-induced gene 3 (EBI3) (rs428253, rs4740, and rs4905) were genotyped by 5′ exonuclease TaqMan genotyping assays on an ABI Prism 7900HT Fast Real-Time PCR System in 375 Mexican patients with UC and 1599 Mexican Mestizo healthy unrelated individuals. IL-27 levels were determined in 458 healthy controls. Under recessive model adjusted by age and gender, the IL-27p28 rs17855750 polymorphism was associated with decreased risk of developing UC (OR = 0.27, 95% CI: 0.06–1.13, P = 0.031). On the other hand, under recessive models adjusted by age and gender, the EBI3 rs428253 (OR = 0.54, 95% CI: 0.29–0.99, P = 0.035), rs4740 (OR = 0.60, 95% CI: 0.36–1.01, P = 0.046) and rs4905 (OR = 0.59, 95% CI: 0.35–1.01, P = 0.043) were associated with decreased risk of developing UC. Similar levels of IL-27 were observed among the genotypes of the studied polymorphisms. IL-27 polymorphisms might play a protective role for the development of UC in the Mexican population.

Objective : To determine whether HDL size distribution and HDL subclasses are associated with coronary calcium scores. Methods : We screened 677 apparently healthy individuals by coronary tomography. One hundred twenty subjects were then recruited for the study and grouped by coronary artery calcification scores (CAC). Forty asymptomatic patients with atherosclerosis with CAC scores ≥75th percentile for gender and age were placed in the first group. Forty patients with CAC scores ≤25th percentile and 40 matched controls (CAC = 0) made up the two remaining groups. HDL samples were separated via sequential ultracentrifugation, followed by electrophoresis: they were then enzymatically stained and densitometrically analyzed to determine the triglycerides ( Tg ), phospholipids (Ph), and plasma cholesterol (C) concentrations corresponding to each HDL subclass. Results : HDL size distribution, lipid and non-lipid risk factors for atherosclerosis were similar among the three groups: HDL-cholesterol and HDL-phospholipids were significantly lower in the CAC ≥75th percentile group, whereas HDL-lipids in the CAC ≤25th group were comparable to the controls. HDL2b- and HDL2a-cholesterol were decreased, whereas phospholipids were lower in patients constituting 4 of the 5 HDL subclasses. The Ph-to- Tg ratios of small HDL were higher in both experimental groups compared with the controls, suggesting that these lipoproteins had abnormal structures. In spite of the significant differences between the high-CAC score subjects and the controls, statistical analyses demonstrated no substantial relationship between CAC scores and HDL parameters: other lipid and non-lipid risk factors for atherosclerosis were not statistically linked to CAC scores. Only male gender and age contributed to CAC scores in our study population. Conclusions : Our results suggest that CAC scores and traditional lipid profiles are independent aspects of atherosclerosis and that only lipids may be biomarkers of coronary calcification during the asymptomatic stages of the disease; however, HDL subclasses do not contribute to CAC scores.

Nephrolithiasis is a complex disease in which its pathophysiology is strongly influenced by genetics. Polymorphisms of the vitamin D receptor (VDR) gene have been reported to be associated with the development of kidney stones which in most cases are composed predominantly of calcium salts. For the purpose of this study, we performed a systematic review and meta-analysis to analyze the association of BsmI (rs1544410), ApaI (rs7975232), TaqI (rs731236) and FokI (rs2228570) polymorphisms with nephrolithiasis. A systematic search was performed up to June 2018 using PubMed, Embase and ISI Web of Knowledge databases. The keywords used for the search were “vitamin D receptor or VDR” and “polymorphisms or SNPs” combined with “urolithiasis or nephrolithiasis”. A meta-analysis was performed with the results of the selected and included studies. After analyzing 23 publications, we observed that BsmI polymorphism (rs1544410) has a protective association against nephrolithiasis (Allelic model: OR = 0.84, CI 95% 0.73–0.96, Z p-value 0.015; homozygous model: OR = 0.72, CI 95% 0.54–0.97, Z p-value 0.033). Furthermore, we observed that FokI polymorphism (rs2228570) has a decreased risk of nephrolithiasis in the heterozygous model in the presence of heterogeneity (OR = 0.69, CI 95% 0.48–0.99, Z p-value 0.044), as well as in the absence of heterogeneity (OR = 0.81, CI 95% 0.66–0.99, Z p-value 0.045). Additionally, TaqI polymorphism (rs731236) was associated with a decreased risk of nephrolithiasis in the heterozygous model (OR = 0.77, CI 95% 0.63–0.94, Z p-value 0.010), and no overall association was observed with ApaI polymorphism (rs7975232). This meta-analysis provided comprehensive evidence that VDR polymorphisms are associated with upper urinary tract stones incidence and the genetic variants we studied provide protection against nephrolithiasis.

Purpose To examine the prevalence of coronary risk factors in Mexican adolescents, and their relations to school type, gender, and residence in urban and rural areas. Methods A cross-sectional survey was conducted in 3121 junior high school students, aged 12 to 16 years, attending urban schools (eight public, n=1850, two private, n=480) and three rural public (n = 791) schools. Weight, height, waist circumference, blood pressure, and fasting glucose and lipid-lipoprotein levels were measured. Tobacco smoking and physical activity were also ascertained. The prevalence rates of cardiovascular risk factors were determined by gender and school type. Results Obesity, overweight, high blood pressure, cigarette smoking, and physical inactivity were higher for urban than rural adolescents. The prevalence of the low HDL-C level was exceedingly high in adolescents of three school types (> 30%) but particularly in male rural students (48.9%). Compared with rural students, high LDL-cholesterol was twice as high in private schoolchildren. The prevalence of impaired fasting glucose was .35% in the whole population and much higher in obese males (1.6%) and obese females (2.4%). Conclusions Our findings highlight an epidemic of coronary risk factors mainly in adolescents living in the urban area, suggesting the importance of environmental factors.