Social support and Quality of Life: a cross-sectional study on survivors eight months after the 2008 Wenchuan earthquake

<p>Abstract</p> <p>Background</p> <p>The 2008 Wenchuan earthquake resulted in extensive loss of life and physical and psychological injuries for survivors. This research examines the relationship between social support and health-related quality of life for the earthquake survivors.</p> <p>Methods</p> <p>A multistage cluster sampling strategy was employed to select participants from 11 shelters in nine counties exposed to different degrees of earthquake damage, for a questionnaire survey. The participants were asked to complete the Short Form 36 and the Social Support Rating Scale eight months after the earthquake struck. A total of 1617 participants returned the questionnaires. The quality of life of the survivors (in the four weeks preceding the survey) was compared with that of the general population in the region. Multivariate logistic regression analysis and canonical correlation analysis were performed to determine the association between social support and quality of life.</p> <p>Results</p> <p>The earthquake survivors reported poorer quality of life than the general population, with an average of 4.8% to 19.62% reduction in scores of the SF-36 (p < 0.001). The multivariate logistic regression analysis showed that those with stronger social support were more likely to have better quality of life. The canonical correlation analysis found that there was a discrepancy between actual social support received and perceived social support available, and the magnitude of this discrepancy was inversely related to perceived general health (rs = 0.467), and positively related to mental health (rs = 0.395).</p> <p>Conclusion</p> <p>Social support is associated with quality of life in the survivors of the earthquake. More attention needs to be paid to increasing social support for those with poorer mental health.</p

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.