Objective. To examine low-density lipoprotein (LDL) size, LDL susceptibility to oxidation, and plasma insulin levels in children with systemic lupus erythematosus (SLE).Methods. Fifty-nine SLE patients and 59 healthy, age-matched control subjects were studied. LDL size was determined by gradient gel electrophoresis. LDL oxidizability was assessed by lag time for conjugated diene formation during copper incubation. Plasma levels of fasting insulin, glucose, lipids, lipoproteins, apolipoproteins B and A-I, and fatty acids were also measured.Results. Compared with control subjects, SLE patients showed significantly higher plasma insulin levels and increased susceptibility of LDLs to oxidation. Patients with active disease were more likely than patients with inactive disease or control subjects to have the following lipid characteristics: small, dense LDL subclass, elevated total cholesterol levels, elevated LDL cholesterol levels, elevated triglyceride levels, and low levels of high-density lipoprotein cholesterol (HDL-C). Statistically significant direct correlations were observed between disease activity and triglyceride levels and between disease activity and lag time, whereas significant inverse correlations were found between disease activity and HDL-C levels and between disease activity and LDL size. Prednisone dosage explained only 15.6% of the variance in insulin levels.Conclusion. SLE patients have higher plasma insulin levels and increased LDL oxidizability compared with healthy control subjects. These abnormalities may contribute to the accelerated atherosclerosis observed in patients with SLE.
A regulatory single nucleotide polymorphism (SNP) PD1.3G/A located on programmed cell death 1 (PDCD1) gene, was shown to be involved in susceptibility to systemic lupus erythematosus (SLE) in Swedish, European American, and Mexican cases. However, association to childhood-onset SLE has not been analyzed. The aim of this study was to investigate the association of PDCD1 polymorphisms and haplotypes with susceptibility to childhood-onset SLE in Mexican population. Three PDCD1 SNPs, PD1.3G/A, PD1.5C/T, PD1.6G/A, were analyzed in 250 childhood-onset SLE Mexican patients and 355 healthy controls in a case-control association study. Polymorphisms were genotyped by TaqMan technology. Stratification analysis was performed on the SLE cohort to investigate the SNP association with renal disorder. In addition, haplotypes were constructed with these three SNPs. The PD1.3A allele was significantly associated to childhood-onset SLE (P ¼ 0.0019, odds ratio (OR) 2.73, 95% confidence interval (95% CI) 1.35-5.56). The other PDCD1 SNPs did not show association. A total of 155 patients (62%) had nephritis, and no association was observed with PDCD1 SNPs. The ACG haplotype (PD1.3A, PD1.5C, PD1.6G) included almost all PD1.3A alleles, and it was more frequent in SLE patients (5.5%) than in controls (2.1%) (P ¼ 0.003; OR 2.73, 95% CI 1.37-5.46). The haplotype structure in Mexican controls was significantly different from those reported in Spanish and Swedish. Our results support association of the PD1.3A SNP to susceptibility of childhood-onset SLE in Mexican population and does not show association to lupus nephritis in this age group.
Background Introduction: The metabolic syndrome (MS) is a cluster of the most dangerous risk factors for cardiovascular disease and type 2 diabetes, which include abdominal obesity, high cholesterol, high blood pressure, diabetes or raised fasting plasma glucose. Metabolic syndrome is a risk factor that increases cardiovascular morbidity and mortality in adults and increased morbidity in children and adolescents. The prevalence of metabolic syndrome in healthy Mexican adolescents it had been reported up to 13% according International Diabetes Federation (IDF). Objectives Objective: To investigate the prevalence of metabolic syndrome in a pediatric population with SLE and its association with lupus activity versus healthy controls. Methods Patients and methods: we studied 37 children (women 32 and men 5) with SLE and 100 healthy children (women 48 and men 52) with age between 10 to 16 years old and complete clinical charts. Exclusion criteria: primary antiphospholipid syndrome, overlap syndrome of connective tissue disease, patients in treatment with drugs to decrease lipids and glucose. The following were determined: total cholesterol (TC), high density cholesterol (HDLc), triglycerides, glucose, antinuclear antibodies, blood cell count and somatometry. For the diagnosis of MS we applied the criteria of the IDF and for the SLE activity we used Mex-SLEDAI. Results Results: There were 37 children with age of 12.2±1.9 year and control 12.1 ± 1.5 year. The mean evolution time of SLE was 2.8±2.5 years. MS was found in 11 of 37 (32%) versus control 11 of 100 (10.78%), p = 0.0021. When we analyzed the components of the MS we find statistical differences in triglyceride levels 151 mg/dl [71-504 mg/dl] vs 91 mg/dl [32-504 mg/dl] (p= 0.0001), arterial hypertension according to age and gender percentile (>95) we found 19 of 37 (37.14%) in SLE patients vs 16 of 100 ( 15.6%) healthy control, (p=0.0037) and glucose levels 79.05 mg/dl + 10.82mg/dl vs 83.7 mg/dl + 7.31 mg/dl (p=0.0001) respectively. We did not find statistical significance between SLE activity and metabolic syndrome with active SLE 31.03% versus 37.5% cases with non active SLE (p= 0.47) Conclusions Conclusion: The prevalence of MS in Mexican pediatric patients with SLE was 32% in comparison with healthy children in 11%. The MS was not associated with SLE activity. It is important to identify children with SLE and MS, implementing therapeutic strategies for the prevention of diabetes or cardiovascular disease in the future. Disclosure of Interest: None Declared
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