Search

Objective: There are no data about the main factors associated with metabolic syndrome in young premenopausal systemic lupus erythematosus (SLE) patients. The aim of the study was to evaluate the frequency of metabolic syndrome and disease- or therapy-related factors in premenopausal young SLE patients.Methods: A total of 103 premenopausal SLE patients ages <40 years were selected and compared to 35 healthy premenopausal age-matched women. Metabolic syndrome was defined according to the 2009 Joint Interim Statement.Results: A higher frequency of metabolic syndrome (22.3% versus 5.7%; P = 0.03) was observed in the SLE group. Metabolic syndrome-SLE patients had higher SLE Disease Activity Index scores (mean ± SD 5.9 ± 7.6 versus 1.9 ± 2.7; P = 0.006), more frequently had previous renal disease (73.9% versus 51.2%; P = 0.05) and current renal disease (34.8% versus 10.0%; P = 0.008), and had higher current prednisone dose (median [range] 20 [0-60] versus 5 [0-60] mg/dl; P = 0.018) and cumulative prednisone dose (mean ± SD 41.48 ± 27.81 versus 24.7 ± 18.66 gm; P = 0.023) than those without metabolic syndrome. Chloroquine was less frequently used in metabolic syndrome-SLE patients (65.2% versus 90.0%; P = 0.008). In multivariate analysis, only current chloroquine use (prevalence ratio [PR] 0.29, 95% confidence interval [95% CI] 0.13-0.64) and cumulative prednisone were associated with metabolic syndrome (PR 1.02, 95% CI 1.01-1.04). Further estimated prevalence analysis identified the fact that antimalarial use promoted continuous decrease in the progressive metabolic syndrome prevalence associated with glucocorticoid cumulative dose.Conclusion: The prevalence of metabolic syndrome is high in premenopausal young adult SLE patients. Chloroquine has a protective effect on the prevalence of metabolic syndrome in these patients, and this benefit counteracts the deleterious effect of glucocorticoids in a dose-dependent manner. [ABSTRACT FROM AUTHOR]

Objectives. The aim of this study was to assess the cumulative incidence, risk and protective factors and impact on mortality of primary cardiac disease in SLE patients (disease duration ≤2 years) from a multi-ethnic, international, longitudinal inception cohort (34 centres, 9 Latin American countries).Methods. Risk and protective factors of primary cardiac disease (pericarditis, myocarditis, endocarditis, arrhythmias and/or valvular abnormalities) were evaluated.Results. Of 1437 patients, 202 (14.1%) developed one or more manifestations: 164 pericarditis, 35 valvulopathy, 23 arrhythmias, 7 myocarditis and 1 endocarditis at follow-up; 77 of these patients also had an episode of primary cardiac disease at or before recruitment. In the multivariable parsimonious model, African/Latin American ethnicity [odds ratio (OR) 1.80, 95% CI 1.13, 2.86], primary cardiac disease at or before recruitment (OR 6.56, 95% CI 4.56, 9.43) and first SLICC/ACR Damage Index for SLE assessment (OR 1.31, 95% CI 1.14, 1.50) were risk factors for the subsequent occurrence of primary cardiac disease. CNS involvement (OR 0.44, 95% CI 0.25, 0.75) and antimalarial treatment (OR 0.62, 95% CI 0.44, 0.89) at or before recruitment were negatively associated with the occurrence of primary cardiac disease risk. Primary cardiac disease was not independently associated with mortality.Conclusion. Primary cardiac disease occurred in 14.1% of SLE patients of the Grupo Latino Americano de Estudio de Lupus cohort and pericarditis was its most frequent manifestation. African origin and lupus damage were found to be risk factors, while CNS involvement at or before recruitment and antimalarial treatment were protective. Primary cardiac disease had no impact on mortality. [ABSTRACT FROM PUBLISHER]

Objective. To assess the efficacy and safety of pandemic 2009 influenza A (H1N1) in SLE under different therapeutic regimens.Methods. A total of 555 SLE patients and 170 healthy controls were vaccinated with a single dose of a non-adjuvanted preparation. According to current therapy, patients were initially classified as SLE No Therapy (n = 75) and SLE with Therapy (n = 480). Subsequent evaluations included groups under monotherapy: chloroquine (CQ) (n = 105), prednisone (PRED) &geq;20 mg (n = 76), immunosuppressor (IS) (n = 95) and those with a combination of these drugs. Anti-H1N1 titres and seroconversion (SC) rate were evaluated at entry and 21 days post-vaccination.Results. The SLE with Therapy group had lower SC compared with healthy controls (59.0 vs 80.0%; P < 0.0001), whereas the SLE No Therapy group had equivalent SC (72 vs 80.0%; P = 0.18) compared with healthy controls. Further comparison revealed that the SC of SLE No Therapy (72%) was similar to the CQ group (69.5%; P = 0.75), but it was significantly reduced in PRED &geq;20 mg (53.9%; P = 0.028), IS (55.7%; P = 0.035) and PRED &geq;20 mg + IS (45.4%; P = 0.038). The concomitant use of CQ in each of these later regimens was associated with SC responses comparable with SLE No Therapy group (72%): PRED &geq;20 mg + CQ (71.4%; P = 1.00), IS + CQ (65.2%; P = 0.54) and PRED &geq;20 mg + IS + CQ (57.4%; P = 0.09).Conclusion. Pandemic influenza A H1N1/2009 vaccine response is diminished in SLE under immunosuppressive therapy and antimalarials seems to restore this immunogenicity.Trial registration. www.clinicaltrials.gov, NCT01151644. [ABSTRACT FROM PUBLISHER]

Autoimmunity and inflammation are associated with marked changes in lipid and lipoprotein metabolism in SLE. Autoantibodies and cytokines are able to modulate lipoprotein lipase (LPL) activity, a key enzyme in lipid metabolism, with a consequent “lupus pattern” of dyslipoproteinemia characterized by elevated levels of very low-density lipoprotein cholesterol (VLDL) and triglycerides (TG) and lower high-density lipoprotein cholesterol (HDL) levels. This pattern favors an enhanced LDL oxidation with a subsequent deleterious foam cell formation. Autoantibodies and immunocomplexes may aggravate this oxidative injury by inducing accumulation and deposition of oxLDL in endothelial cells. Drugs and associated diseases usually magnify the close interaction of these factors and further promote the proatherogenic environment of this disease. [ABSTRACT FROM AUTHOR]