Background: Hospitalization with community‐acquired pneumonia (CAP) is associated with an increased risk of cardiovascular disease (CVD) events in patients uninfected with HIV. We evaluated whether people living with HIV (PLWH) have a higher risk of CVD or mortality than individuals uninfected with HIV following hospitalization with CAP. Methods and Results: We analyzed data from the Veterans Aging Cohort Study on US veterans admitted with their first episode of CAP from April 2003 through December 2014. We used Cox regression analyses to determine whether HIV status was associated with incident CVD events and mortality from date of admission through 30 days after discharge (30‐day mortality), adjusting for known CVD risk factors. We included 4384 patients (67% [n=2951] PLWH). PLWH admitted with CAP were younger, had less severe CAP, and had fewer CVD risk factors than patients with CAP who were uninfected with HIV. In multivariable‐adjusted analyses, CVD risk was similar in PLWH compared with HIV‐uninfected (hazard ratio [HR], 0.89; 95% CI, 0.70–1.12), but HIV infection was associated with higher mortality risk (HR, 1.49; 95% CI, 1.16–1.90). In models stratified by HIV status, CAP severity was significantly associated with incident CVD and 30‐day mortality in PLWH and patients uninfected with HIV. Conclusions: In this study, the risk of CVD events during or after hospitalization for CAP was similar in PLWH and patients uninfected with HIV, after adjusting for known CVD risk factors and CAP severity. HIV infection, however, was associated with increased 30‐day mortality after CAP hospitalization in multivariable‐adjusted models. PLWH should be included in future studies evaluating mechanisms and prevention of CVD events after CAP.

Chronic obstructive pulmonary disease (COPD) is common in people living with HIV (PLWH). We sought to evaluate the appropriateness of COPD diagnosis and management in PLWH, comparing results to HIV-uninfected persons. We conducted a cross-sectional analysis of Veterans enrolled in the Examinations of HIV-Associated Lung Emphysema study, in which all participants underwent spirometry at enrollment and reported respiratory symptoms on self-completed surveys. Primary outcomes were misdiagnosis and under-diagnosis of COPD, and the frequency and appropriateness of inhaler prescriptions. Misdiagnosis was defined as having an International Classification of Diseases (ICD)-9 diagnosis of COPD without spirometric airflow limitation (post-bronchodilator forced expiratory volume in 1-second [FEV1]/Forced vital capacity [FVC] < 0.7). Under-diagnosis was defined as having spirometry-defined COPD without a prior ICD-9 diagnosis. The analytic cohort included 183 PLWH and 152 HIV-uninfected participants. Of 25 PLWH with an ICD-9 diagnosis of COPD, 56% were misdiagnosed. Of 38 PLWH with spirometry-defined COPD, 71% were under-diagnosed. In PLWH under-diagnosed with COPD, 85% reported respiratory symptoms. Among PLWH with an ICD-9 COPD diagnosis as well as in those with spirometry-defined COPD, long-acting inhalers, particularly long-acting bronchodilators (both beta-agonists and muscarinic antagonists) were prescribed infrequently even in symptomatic individuals. Inhaled corticosteroids were the most frequently prescribed long-acting inhaler in PLWH (28%). Results were overall similar amongst the HIV-uninfected. COPD was frequently misdiagnosed and under-diagnosed in PLWH, similar to uninfected-veterans. Among PLWH with COPD and a likely indication for therapy, long-acting inhalers were prescribed infrequently, particularly guideline-concordant, first-line long-acting bronchodilators. Although not a first-line controller therapy for COPD, inhaled corticosteroids were prescribed more often.

Rationale: Post-tuberculosis lung disease (PTLD), which includes restrictive and obstructive patterns of impairment, develops in 50% or more of survivors of tuberculosis (TB), yet mechanisms and associated risk factors are poorly understood. Objectives: We sought to identify clinical and transcriptomic risk factors for PTLD phenotypes. Methods: In a prospective, observational, cohort study, we enrolled adults (month 0) with newly diagnosed pulmonary TB in Nairobi, Kenya, and evaluated clinical and transcriptomic risk factors for PTLD. Participants completed 6 months of standard anti-TB therapy. PTLD was defined as abnormal spirometry at month 12 (ie, 6 months posttreatment) with either a restrictive or obstructive pattern. Measurements and Main Results: We enrolled 205 participants, of whom 103 (50.2%) had PTLD, including 60 with restrictive PTLD and 43 obstructive PTLD. Participants with PTLD had lower mid-upper arm circumference (MUAC) and cough peak flow. In multivariable analyses, having more lung quadrants involved on radiograph at diagnosis was a risk factor for both restrictive PTLD (adjusted odds ratio [aOR], 2.1; P <.001) and obstructive PTLD (aOR, 2.2; P <.001). Prior TB was associated with obstructive PTLD (aOR, 5.4; P <.001). Gene expression improved clinical predictive models. In transcriptomic analyses, restrictive PTLD was associated with upregulation of IL-6/JAK/STAT3 and TNF-α signaling at diagnosis (false discovery rate [FDR] <0.2). In contrast, obstructive PTLD was associated with transcriptomic upregulation of IFN-α and IFN-γ signaling responses (FDR <0.2) at month 6. Conclusions: Despite common clinical risk factors (lower MUAC, radiographic lung involvement), PTLD phenotypes have unique transcriptional signatures. Restrictive PTLD is marked by early profibrotic inflammation. In contrast, obstructive PTLD is characterized by persistent inflammation at treatment completion.