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ObjectiveAt least half of patients with systemic lupus erythematosus (SLE) develop organ damage as a consequence of autoimmune disease or long-term therapeutic steroid use. This study synthesised evidence on the association between organ damage and mortality in patients with SLE.DesignSystematic review and meta-analysis.MethodsElectronic searches were performed in PubMed, Embase, Cochrane Library and Latin American and Caribbean Health Sciences Literature for observational (cohort, case-control and cross-sectional) studies published between January 2000 and February 2017. Included studies reported HRs or ORs on the association between organ damage (measured by the Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (SDI) score) and mortality. Study quality was assessed using the modified Newcastle-Ottawa assessment. Pooled HRs were obtained using the DerSimonian and Laird random-effects model. Heterogeneity was assessed using the Cochrane Q (Q) and I2 statistics.ResultsThe search yielded 10 420 articles, from which 21 longitudinal studies were selected. Most studies (85%) were of high quality. For 10 studies evaluating organ damage (SDI) as a continuous variable and reporting HR as a measure of association, a 1-unit increase in SDI was associated with increased mortality; pooled HR was 1.34 (95% CI: 1.24 to 1.44, p<0.001; Q p=0.027, I2=52.1%). Exclusion of one potential outlying study reduced heterogeneity with minimal impact on pooled HR (1.33 (95% CI: 1.25 to 1.42), p<0.001, Q p=0.087, I2=42.0%). The 11 remaining studies, although they could not be aggregated because of their varying patient populations and analyses, consistently demonstrated that greater SDI was associated with increased mortality.ConclusionsOrgan damage in SLE is consistently associated with increased mortality across studies from various countries. Modifying the disease course with effective therapies and steroid-sparing regimens may reduce organ damage, improve outcomes and decrease mortality for patients with SLE.

A43was to assess the association of the depression as a risk factor for coronary heart disease (CHD) based on prospective studies included in published systematic reviews. Methods: A systematic review to identify systematic reviews was conducted in MEDLINE, Cochrane library and Embase databases, with no limit on the start date until December 2015, using keywords for depression, coronary events and risk factors. The selection of the reviews that included prospective studies was realized by two researchers independently; primary data from prospective studies analyzing the relationship of depression and CHD were extracted. The Hazard Ratios (HRs) were pooled using random effects model. The subgroup analysis was carried out considering fatal CHD, myocardial infarction, gender, and follow-up duration. Results: It was selected twenty one systematic reviews comprising thirty five prospective studies that were extracted. The number of people included in the studies was 900,226. The main differences among the studies were the age, gender, measurement of depression, length of follow-up and CHD fatality. The meta-analysis found that the depression behavior is a risk factor for CHD, although the heterogeneity is substantial. The analysis by subgroup found low heterogeneity for myocardial infarction and fatal CHD. The analysis suggested that depression increases the risk for fatal CHD AND myocardial infarction (HR 1.13 95%CI: 1.06-1.20 and HR 1.29 95%CI: 1.19-1.39, respectively). In the subgroup analysis by length of follow-up, the HR of CHD was 1.24 (95%CI 1.01-1.47) for the studies with less than 15 years of follow-up and 1.18 (95%CI 1.12-1.24) for those with more than 15 years of followup. ConClusions: The results of meta-analysis suggest that depression increases the risk of CHD significantly, although the evidence has substantial heterogeneity. PCV24CardioVasCular risks of ExogEnous TEsTosTEronE usE among mEn: a sysTEmaTiC rEViEw and mETa-analysis

Background-Some classes of drugs have lower than optimal uptake of generic products. We aimed to understand the determinants of generic drug substitution across classes.Methods-We conducted a cross-sectional analysis of data from the 2013 MarketScan Commercial Claims and Encounters Database from Truven Health Analytics. We quantified generic substitution rates (GSR) for 26 drug classes, choosing one representative week in November 2013. We used mixed-effects logistic regression to estimate the independent relationship between the determinants of interest and generic substitution for 8 classes with low generic utilization.Results-The GSRs for most classes exceeded 90%, although some were much lower including thyroid hormones (64%), androgens (74%), estrogens (71%), and hydantoin-type anticonvulsants (72%). The determinants of generic substitution varied across classes, albeit with important patterns. Patients using a mail order pharmacy had significantly less generic substitution than patients filling at retail pharmacies for 5 of the 8 studied classes; two additional classes showed no relationship between pharmacy type and generic use. Men relative to women and patients taking more medications were more likely to use generics for most classes. State substitution laws and patient consent laws were largely inconsequential regarding generic substitution.