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Chronic Obstructive Pulmonary Disease (COPD) is a serious pulmonary condition. Many patients experience exacerbations and some require Emergency Room visits and hospitalization. In Portugal, hospitalizations due to COPD between 2009 and 2016 decreased by 8%, but they still represented 8049 hospitalized patients in 2016. Appropriate management of COPD exacerbations presents a clinical challenge and, in order to guide therapy, it is important to identify the underlying cause; however, this is not possible in about a third of severe COPD exacerbations. There are several diagnostic tools that can be used to assess an exacerbation and its severity, which will in turn guide treatment, and prognostic scores should be used to predict the risk of future exacerbations. After an exacerbation is appropriately managed, a suitable discharge plan should be prepared. This should generally include reclassification of the patient according to GOLD criteria, optimization of pharmacological therapy, management of comorbidities, patient (or caregiver) education on the correct use of medications, referral to a Pulmonology Outpatient Clinic, if they are not already attending one, and a smoking cessation and respiratory rehabilitation program. In this paper, we will focus on the pharmacological strategies for the management of COPD exacerbations, risk stratification and a hospital discharge plan proposal.

BackgroundThe AGE h IV cohort study is a prospective cohort study evaluating the occurrence of age-related comorbidities in people living with and without HIV. We previously reported a lower forced vital capacity (FVC) in HIV-positive compared with HIV-negative participants in those without heavy smoking exposure at time of enrolment in the AGE h IV cohort study. In this study we evaluate longitudinal changes in spirometry indices in the same AGE h IV cohort accounting for smoking behaviour and other risk factors.Methods We obtained pre-bronchodilator spirometry measurements in AGE h IV cohort participants during biennial visits over a median of 5•9 years (IQR 5•7-6•0). Adjusted declines in forced expiratory volume in 1 s (FEV 1 ), FVC, and FEV 1 /FVC ratio were modelled using linear mixed-effects models and compared by HIV status and smoking status. To evaluate whether changes in spirometry measurements could be driven by increased levels of chronic inflammation, we assessed associations between rates of FEV 1 and FVC decline and CD4 and CD8 T-cell counts, and plasma concentrations of C-reactive protein (CRP), interleukin 6, soluble CD14, soluble CD163, and intestinal fatty-acidbinding protein in separate models. The study is registered at ClinicalTrials.gov, NCT01466582.Findings 500 HIV-positive and 481 HIV-negative participants were included with spirometry data from Oct 29, 2010, to Aug 14, 2018. HIV-positive participants were virally suppressed (<40 copies per mL) during 1627 (95%) study visits, and 159 (32%) HIV-positive and 183 (38%) HIV-negative participants had never smoked. Adjusted declines in FEV 1 were 10•0 mL per year faster in HIV-positive non-smokers (95% CI 4•2 to 15•7, p=0•00066) compared with HIV-negative non-smokers, and 11•1 mL per year faster in HIV-positive smokers (95% CI 0•7 to 21•4, p=0•036) compared with HIV-negative smokers. In comparison, smoking was associated with a 16•4 mL per year steeper decline in FEV 1 among HIV-positive participants (95% CI 8•0 to 24•7, p=0•00012), and 15•3 mL per year steeper decline among HIV-negative participants (95% CI 6•7-24•0, p=0•00052) compared with not smoking. Adjusted yearly declines in FEV₁ and FVC, but not FEV₁/FVC, were significantly greater in HIV-positive than HIVnegative participants overall (additional decline in HIV-positive participants, FEV₁ 10•5 mL per year [95% CI 4•7 to 16•3], p=0•00040; FVC 11•5 mL per year [2•8 to 20•3], p=0•0096; FEV₁/FVC 0•07% per year [-0•05 to 0•19], p=0•26), with a similar observation for never-smokers (FEV₁ 6•0 mL per year [-1•8 to 13•7], p=0•13; FVC 9•1 mL per year [-3•0 to 21•1], p=0•14; FEV 1 /FVC ratio 0•00% per year [-0•18 to -0•18], p=0•97). Higher CRP concentrations during follow-up were associated with accelerated declines in FEV 1 and FVC among HIV-positive participants but not among HIV-negative participants.Interpretation Treated HIV infection was associated with faster declines in both FEV 1 and FVC, but not in the FEV 1 /FVC ratio. These changes were independent of smoking and might have been drive...

Background Prior studies have found that HIV infection is associated with impaired lung function and increased risk of chronic lung disease, but few have included large numbers of women. In this study, we investigate whether HIV infection is associated with differences in lung function in women. Methods This was a cross-sectional analysis of participants in the Women’s Interagency HIV Study (WIHS), a racially and ethnically diverse multicenter cohort of women with and without HIV. In 2018–2019, participants at all nine clinical sites were invited to perform spirometry. Single-breath diffusing capacity for carbon monoxide (DLCO) was also measured at selected sites. The primary outcomes were the post-bronchodilator forced expiratory volume in one second (FEV1) and DLCO. Multivariable regression modeling was used to analyze the association of HIV infection and lung function outcomes after adjustment for confounding exposures. Results FEV1 measurements from 1,489 women (1,062 HIV+, 427 HIV-) and DLCO measurements from 671 women (463 HIV+, 208 HIV-) met standards for quality and reproducibility. There was no significant difference in FEV1 between women with and without HIV. Women with HIV had lower DLCO measurements (adjusted difference, −0.73  mL/min/mmHg, 95% CI -1.33 to -0.14). Among women with HIV, lower nadir CD4 + cell counts and hepatitis C virus infection were associated with lower DLCO measurements. Conclusions HIV infection was associated with impaired respiratory gas exchange in women. Among women with HIV, lower nadir CD4 + cell counts and hepatitis C infection were associated with decreased respiratory gas exchange.