Institutional Courage in Healthcare: An Improvement Project Exploring the Perspectives of Veterans Exposed to Airborne Hazards.

BACKGROUND: Military environmental exposures and care for subsequent health concerns have been associated with institutional betrayal, or a perception on the part of veterans that the US government has failed to adequately prevent, acknowledge, and treat these conditions and in doing so has betrayed its promise to veterans. Institutional courage is a term developed to describe organizations that proactively protect and care for their members. While institutional courage may be useful in mitigating institutional betrayal, there is a lack of definitions of institutional courage in healthcare from the patient perspective. METHODS: Using qualitative methods, we sought to explore the notions of institutional betrayal and institutional courage among veterans exposed to airborne hazards (i.e., airborne particulate matter such as open burn pits; N = 13) to inform and improve clinical practice. We performed initial interviews and follow-up interviews with veterans. RESULTS: Veterans' depictions of courageous institutions contained key themes of being accountable, proactive, and mindful of unique experiences, supporting advocacy, addressing stigma related to public benefits, and offering safety. Veterans described institutional courage as including both individual-level traits and systems or organizational-level characteristics. CONCLUSIONS: Several existing VA initiatives already address many themes identified in describing courageous institutions (e.g., accountability and advocacy). Other themes, especially views of public benefits and being proactive, hold particular value for building trauma-informed healthcare.

HIV Infection, HCV Coinfection, and Alcohol Use: Associations with Microbial Translocation and Immune Activation.

BACKGROUND: Human immunodeficiency virus (HIV) infection and heavy drinking independently promote microbial translocation and inflammation. However, it is not known how alcohol use may affect these processes in people living with HIV (PLWH). This study tested the hypothesis that alcohol exacerbates innate immune dysfunction in PLWH. METHODS: Participants were 75 PLWH and 34 uninfected controls. Groups were recruited to have similar proportions of nondrinkers, moderate drinkers, and heavy drinkers. Substance use data and plasma samples were collected at up to 3 visits over a 5-year study period. Recent alcohol use was assessed with the Timeline Followback Interview. Biomarkers of microbial translocation (lipopolysaccharide, LPS) and immune activation (lipopolysaccharide binding protein, LBP; soluble CD14, sCD14; soluble CD163, sCD163) were quantified using enzyme-linked immunosorbent assays. Analyses tested 2 hypotheses: (i) that biomarker levels would be significantly higher in PLWH than controls with comparable alcohol use and (ii) that current alcohol use would exacerbate biomarker elevations in PLWH. The second analysis included the interaction of alcohol use with hepatitis C virus (HCV) coinfection. RESULTS: Groups were matched on alcohol use, smoking, and other drug use. All biomarkers were significantly higher in PLWH relative to controls (LBP: p = 0.005; LPS: p = 0.014; sCD14: p < 0.001; sCD163: p < 0.001). In PLWH, alcohol use showed a significant, positive association with sCD163, but not with other biomarkers. However, the interaction of alcohol use with HCV coinfection was significant for all biomarkers (LBP: p = 0.002; LPS: p = 0.026; sCD14: p = 0.0004; sCD163: p = 0.001). In pairwise tests with sequential Bonferroni correction, HIV/HCV coinfected individuals who drank heavily had significantly higher sCD163 compared to coinfected nondrinkers and to HIV monoinfected nondrinkers, moderate drinkers, and heavy drinkers (ps < 0.005). Coinfected moderate drinkers had significantly higher sCD163 than each monoinfected group (ps < 0.003). In addition, sCD14 was significantly higher in coinfected moderate drinkers than coinfected nondrinkers (p = 0.027). CONCLUSIONS: As predicted, PLWH had higher levels of LBP, LPS, sCD14, and sCD163 than uninfected individuals with similar alcohol use. In PLWH, alcohol by itself was significantly associated only with higher sCD163. However, heavy or moderate alcohol use was associated with elevations in macrophage activation (sCD163) and monocyte activation (sCD14) in HIV/HCV coinfected individuals.

Heavy Alcohol Use and Age Effects on HIV-Associated Neurocognitive Function.

BACKGROUND: There is growing concern about the health impact of heavy alcohol use in people infected with human immunodeficiency virus (HIV+). Mixed findings of past studies regarding the cognitive impact of alcohol use in HIV+ adults have been mixed, with inconsistent evidence that alcohol consumption exacerbates HIV-associated brain dysfunction. This study examined contributions of current heavy drinking, lifetime alcohol use disorder (AUD), and age to cognitive deficits in HIV+ adults, and relative to other HIV-associated clinical factors. METHODS: Cognitive performance of HIV+ adults (n = 104) was assessed, and comparisons were made between heavy current to nonheavy drinkers (NIAAA criteria), lifetime AUD versus no-AUD, and older (>50 years) versus younger participants. Hierarchical regression analyses were conducted to examine the association between cognitive performance and current heavy drinking, lifetime AUD, and older age, while also correcting for HIV clinical factors and history of other substance use. RESULTS: Individuals reporting current heavy drinking and meeting criteria for lifetime AUD demonstrated the greatest degree of deficits across multiple cognitive domains. Deficits were greatest among HIV+ adults with lifetime AUD, and older age was also associated with weaker cognitive performance. Lifetime AUD and older age independently exhibited stronger associations with cognitive performance than HIV clinical factors (e.g., viral load, current CD4, and nadir CD4) or past opiate and cocaine use. CONCLUSIONS: Current heavy drinking and lifetime AUD adversely affect cognitive function in HIV+ adults. Greatest deficits existed when there was a history of AUD and continued current heavy drinking, indicating that past AUD continues to have an adverse impact and should not be ignored. That alcohol use was more strongly associated with cognitive performance than HIV clinical factors underscore clinical importance of targeting reduction in heavy alcohol consumption in HIV+ adults.