BACKGROUNDHydroxychloroquine has been widely administered to patients with Covid-19 without robust evidence supporting its use. METHODSWe examined the association between hydroxychloroquine use and intubation or death at a large medical center in New York City. Data were obtained regarding consecutive patients hospitalized with Covid-19, excluding those who were intubated, died, or discharged within 24 hours after presentation to the emergency department (study baseline). The primary end point was a composite of intubation or death in a time-to-event analysis. We compared outcomes in patients who received hydroxychloroquine with those in patients who did not, using a multivariable Cox model with inverse probability weighting according to the propensity score. RESULTSOf 1446 consecutive patients, 70 patients were intubated, died, or discharged within 24 hours after presentation and were excluded from the analysis. Of the remaining 1376 patients, during a median follow-up of 22.5 days, 811 (58.9%) received hydroxychloroquine (600 mg twice on day 1, then 400 mg daily for a median of 5 days); 45.8% of the patients were treated within 24 hours after presentation to the emergency department, and 85.9% within 48 hours. Hydroxychloroquine-treated patients were more severely ill at baseline than those who did not receive hydroxychloroquine (median ratio of partial pressure of arterial oxygen to the fraction of inspired oxygen, 223 vs. 360). Overall, 346 patients (25.1%) had a primary end-point event (180 patients were intubated, of whom 66 subsequently died, and 166 died without intubation). In the main analysis, there was no significant association between hydroxychloroquine use and intubation or death (hazard ratio, 1.04, 95% confidence interval, 0.82 to 1.32). Results were similar in multiple sensitivity analyses.
The coronavirus disease 2019 (COVID-19) can result in a hyperinflammatory state, leading to acute respiratory distress syndrome (ARDS), myocardial injury, and thrombotic complications, among other sequelae. Statins, which are known to have anti-inflammatory and antithrombotic properties, have been studied in the setting of other viral infections, but their benefit has not been assessed in COVID-19. This is a retrospective analysis of patients admitted with COVID-19 from February 1st through May 12th, 2020 with study period ending on June 11th, 2020. Antecedent statin use was assessed using medication information available in the electronic medical record. We constructed a multivariable logistic regression model to predict the propensity of receiving statins, adjusting for baseline sociodemographic and clinical characteristics, and outpatient medications. The primary endpoint includes in-hospital mortality within 30 days. A total of 2626 patients were admitted during the study period, of whom 951 (36.2%) were antecedent statin users. Among 1296 patients (648 statin users, 648 non-statin users) identified with 1:1 propensity-score matching, statin use is significantly associated with lower odds of the primary endpoint in the propensity-matched cohort (OR 0.47, 95% CI 0.36–0.62, p < 0.001). We conclude that antecedent statin use in patients hospitalized with COVID-19 is associated with lower inpatient mortality.
The coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), can result in a hyperinflammatory state, leading to acute respiratory distress syndrome (ARDS), myocardial injury, and thrombotic complications, among other sequelae. Statins, which are known to have anti-inflammatory and antithrombotic properties, have been studied in the setting of other viral infections and ARDS, but their benefit has not been assessed in COVID-19. Thus, we sought to determine whether antecedent statin use is associated with lower in-hospital mortality in patients hospitalized for COVID-19. This is a retrospective analysis of patients admitted with COVID-19 from February 1st through May 12th, 2020 with study period ending on June 11th, 2020. Antecedent statin use was assessed using medication information available in the electronic medical record. We constructed a multivariable logistic regression model to predict the propensity of receiving statins, adjusting for baseline socio-demographic and clinical characteristics, and outpatient medications. The primary endpoint included in-hospital mortality within 30 days. A total of 2626 patients were admitted during the study period, of whom 951 (36.2%) were antecedent statin users. Among 1296 patients (648 statin users, 648 non-statin users) identified with 1:1 propensity-score matching, demographic, baseline, and outpatient medication information were well balanced. Statin use was significantly associated with lower odds of the primary endpoint in the propensity-matched cohort (OR 0.48, 95% CI 0.36 – 0.64, p<0.001). We conclude that antecedent statin use in patients hospitalized with COVID-19 was associated with lower inpatient mortality. Randomized clinical trials evaluating the utility of statin therapy in patients with COVID-19 are needed.
The diversity of a social network is potentially more protective against PTSD than the perception of strong social support. This suggests that programs, which engage individuals in social groups and activities may effectively attenuate the risk of PTSD. A better understanding of how these networks operate with respect to PTSD prevention and mitigation holds promise for improving psychiatric health.
There is ample evidence that social support is protective against posttraumatic stress (PTS) symptoms through social causation processes. It is also likely that PTS is associated with decreased social support through social selection processes. Few studies, however, have examined the longitudinal and bidirectional associations between social support and PTS in a postdisaster context, and whether such associations vary by type of support (e.g., emotional, informational, or tangible). We examined these relationships using Galveston Bay Recovery Study data. Participants (N = 658) were interviewed 2–6 months (W1), 5–9 months (W2), and 14–19 months (W3) after Hurricane Ike in 2008. Longitudinal relationships between each support type and PTS were examined in cross-lagged models. W1 emotional support was negatively associated with W2 PTS (Estimate = −.13, p = .007), consistent with social causation. W1 PTS was negatively associated with W2 emotional support (Estimate = −.14, p = .019), consistent with social selection. In contrast, pathways were nonsignificant at subsequent waves and for informational and tangible support. Results suggested that postdisaster social causation and selection were limited to emotional support and diminish over time. Based on these findings, postdisaster services should emphasize restoring supportive social connections to minimize the psychiatric consequences of disaster, especially among those with prior evidence of distress.
Objective Little is known about the relationship between cigarette smoking and long-term substance use disorder (SUD) outcomes. The current study examined the association between smoking and SUD relapse among adults with remitted SUDs. Method Analyses were conducted on respondents who completed Waves 1 and 2 of the National Epidemiologic Survey on Alcohol and Related Conditions and met DSM-IV criteria for substance abuse and/or prior to but not during the year before the Wave 1 interview (n=5,515). Relationships between smoking status (Wave 2 smoking versus non-smoking among Wave 1 smokers; Wave 2 smoking versus non-smoking among Wave 1 non-smokers) and Wave 2 substance use and SUD relapse were examined using logistic regression analyses. Analyses were adjusted for demographics; psychiatric and alcohol use disorders; nicotine dependence; and SUD severity. Results In the fully adjusted models, among Wave 1 smokers, continued smoking at Wave 2 was associated with significantly greater odds of substance use (OR=1.56, 95% CI=1.10-2.20) and SUD relapse (OR=2.02, 95% CI=1.65-2.47) compared to Wave 2 non-smoking. In the fully adjusted model, among Wave 1 non-smokers, smoking at Wave 2 was associated with significantly greater odds of SUD relapse compared to Wave 2 non-smoking (OR=4.86, 95% CI=3.11-7.58). Conclusion Continued smoking for smokers and smoking initiation for non-smokers was associated with greater odds of SUD relapse. More research is needed to examine the timing of SUD relapse in relation to smoking behaviors. Incorporating smoking cessation and prevention efforts into substance abuse treatment may improve long-term substance use outcomes for adult smokers with SUDs.
Importance Despite long-standing interest in the association of psychiatric disorders with intelligence, few population-based studies of psychiatric disorders have assessed intelligence. Objectives To investigate the association of fluid intelligence with past-year and lifetime psychiatric disorders, disorder age-of-onset, and disorder severity in a nationally-representative sample of U.S. adolescents. Design Dual-frame national sample of adolescents ascertained from schools and households from the National Comorbidity Survey Replication-Adolescent Supplement, collected 2001–2004. Setting Face-to-face household interviews with adolescents and questionnaires from parents. Participants The sample included 10,073 adolescents with valid data on fluid intelligence. Exposures DSM-IV mental disorders were assessed with the World Health Organization Composite International Diagnostic Interview, and included a broad range of fear, distress, behavior, substance use and other disorders. Disorder severity was measured with the Sheehan Disability Scale. Main Outcomes Fluid intelligence quotient (IQ) measured with Kaufman Brief Intelligence Test, normed within the sample by six-month age groups. Results Lower mean IQ was observed among adolescents with past-year bipolar disorder (predicted Mean [M]=94.2, p<0.01), attention-deficit/hyperactivity disorder (M=96.3, p<0.01), oppositional defiant disorder (M=97.3, p<0.01), conduct disorder (M=97.1, p=0.02) substance disorders (M=96.5–97.6, p=0.02 to <0.01) and specific phobia (M=97.1, p<0.01) after adjustment for a wide range of potential confounders. Intelligence was not associated with post-traumatic stress disorder, eating disorders, and anxiety disorders other than specific phobia, and was positively associated with major depression. Associations of fluid intelligence with lifetime disorders that had remitted were attenuated compared to past-year disorders, with the exception of separation anxiety disorder. Across disorders, higher disorder severity was associated with lower fluid intelligence. Conclusions Numerous psychiatric disorders are associated with reductions in fluid intelligence; associations are generally small in magnitude. Stronger associations of current than past disorders with intelligence suggest that active symptoms of psychopathology interfere with cognitive functioning, although longitudinal studies are needed to determine the extent to which changes in fluid intelligence precede or follow the onset of psychiatric disorders. Early identification and treatment of children with mental disorders in school settings is critical to promote academic achievement and long-term success.
Mood disorders, such as depression and anxiety, are more prevalent among women than men. This disparity may be partially due to the effects of structural gender discrimination in the work force, which acts to perpetuate gender differences in opportunities and resources and may manifest as the gender wage gap. We sought to quantify and operationalize the wage gap in order to explain the gender disparity in depression and anxiety disorders, using data from a 2001–2002 US nationally representative survey of 22,581 working adults ages 30–65. Using established Oaxaca-Blinder decomposition methods to account for gender differences in individual-level productivity, our models reduced the wage gap in our sample by 13.5%, from 54% of men’s pay to 67.5% of men’s pay. We created a propensity-score matched sample of productivity indicators to test if the direction of the wage gap moderated the effects of gender on depression or anxiety. Where female income was less than the matched male counterpart, odds of both disorders were significantly higher among women versus men (major depressive disorder OR: 2.43, 95% CI: 1.95–3.04; generalized anxiety disorder OR: 4.11, 95% CI: 2.80–6.02). Where female income was greater than the matched male, the higher odds ratios for women for both disorders were significantly attenuated (Major Depressive Disorder OR: 1.20; 95% CI: 0.96–1.52) (Generalized Anxiety Disorder OR: 1.5; 95% CI: 1.04–2.29). The test for effect modification by sex and wage gap direction was statistically significant for both disorders. Structural forms of discrimination may explain mental health disparities at the population level. Beyond prohibiting overt gender discrimination, policies must be created to address embedded inequalities in procedures surrounding labor markets and compensation in the workplace.
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