Rationale: Coronavirus disease (COVID-19) is an ongoing pandemic, in which obesity, hypertension, and diabetes have been linked to poor outcomes. Obstructive sleep apnea (OSA) is associated with these conditions and may influence the prognosis of adults with COVID-19. Objectives: To determine the effect of OSA on clinical outcomes in patients with COVID-19. Methods: The current prospective observational study was conducted in three hospitals in Istanbul, Turkey from March 10 to June 22, 2020. The participants were categorized as high-risk or low-risk OSA according to the Berlin questionnaire that was administered in the out-patient clinic, in hospital, or shortly after discharge from hospital blinded to the clinical outcomes. A modified high-risk (mHR)–OSA score based on the snoring patterns (intensity and/or frequency), breathing pauses, and morning/daytime sleepiness, without taking obesity and hypertension into account, were used in the regression models. Results: The primary outcome was the clinical improvement defined as a decline of two categories from admission on a 7-category ordinal scale that ranges from 1 (discharged with normal activity) to 7 (death) on Days 7, 14, 21, and 28, respectively. Secondary outcomes included clinical worsening (an increase of 1 category), need for hospitalization, supplemental oxygen, and intensive care. In total, 320 eligible patients (median [interquartile range] age, 53.2 [41.3–63.0] yr; 45.9% female) were enrolled. In all, 121 (37.8%) were categorized as known (n = 3) or high-risk OSA (n = 118). According to the modified scoring, 70 (21.9%) had mHR-OSA. Among 242 patients requiring hospitalization, clinical improvement within 2 weeks occurred in 75.4% of the mHR-OSA group compared with 88.4% of the modified low-risk–OSA group (P = 0.014). In multivariate regression analyses, mHR-OSA (adjusted odds ratio [OR], 0.42; 95% confidence interval [CI], 0.19–0.92) and male sex (OR, 0.39; 95% CI, 0.17–0.86) predicted the delayed clinical improvement. In the entire study population (n = 320), including the nonhospitalized patients, mHR-OSA was associated with clinical worsening (adjusted hazard ratio, 1.55; 95% CI, 1.00–2.39) and with the need for supplemental oxygen (OR, 1.95; 95% CI, 1.06–3.59). Snoring patterns, especially louder snoring, significantly predicted delayed clinical improvement, worsening, need for hospitalization, supplemental oxygen, and intensive care. Conclusions: Adults with mHR-OSA in our COVID-19 cohort had poorer clinical outcomes than those with modified low-risk OSA independent of age, sex, and comorbidities. Clinical trial registered with www.clinicaltrials.gov (NCT04363333).

COVID-19,idiopathic pulmonary fibrosis,exacerbation

Turkthoracj, Turkish Thoracic Journal

Turkthoracj, Turkish Thoracic Journal

Objectives: We aimed to describe the cardiopulmonary function during exercise and the health-related quality of life (HRQoL) in patients with a history of COVID-19 pneumonia, stratified by chest computed tomography (CT) findings at baseline. Methods: Among 77 consecutive patients with COVID-19 who were discharged from the Pulmonology Ward between March 2020 and April 2021, 28 (mean age 54.3 ± 8.6 years, 8 females) agreed to participate to the current study. The participants were analyzed in two groups based on pulmonary involvement (PI) at baseline chest CT applying a threshold of 25%. A consequent artificial intelligence (AI)-guided total opacity score (TOS) was calculated in a subgroup of 22 patients. A cardiopulmonary exercise test (CPET) was conducted on average 8.4 (±1.9) months after discharge from the hospital. HRQoL was defined using the short-form (SF-36) questionnaire. The primary outcome was exercise intolerance that was defined as a peak oxygen uptake (V′O_2peak) < 80% predicted. Secondary outcomes were ventilatory limitation, defined as breathing reserve < 15%, circulatory limitation, defined as oxygen pulse predicted below 80%, and deconditioning, defined as exercise intolerance in the absence of ventilatory and circulatory limitations. Other secondary outcomes included the SF-36 domains. Results: In all, 15 patients had at least 25% PI (53.6%) at baseline chest CT. Exercise intolerance was observed in ten patients (35.7%), six due to deconditioning and four due to circulatory limitation; none had ventilatory limitation. AI-guided TOS was 30.1 ± 24.4% vs. 6.1 ± 4.8% (p < 0.001) at baseline, and 1.7 ± 3.0% vs. 0.2 ± 0.7% (nonsignificant) at follow-up in high and low PI groups, respectively. The physical functioning (PF) domain score of the SF-36 questionnaire was 66.3 ± 19.4 vs. 85.0 ± 13.1 in high and low PI groups, respectively (p = 0.007). Other SF-36 domains did not differ significantly between the groups. A high PI at baseline was inversely correlated with V′O_2peak (standardized β coefficient = −0.436; 95% CI −26.1; −0.7; p = 0.040) and with PF scores (standardized β coefficient −0.654; 95% CI −41.3; −7.6; p = 0.006) adjusted for age, sex, body mass index and lung diffusion capacity. Conclusions: One-third of participants experienced exercise intolerance eight months after COVID-19 pneumonia. A higher PI at baseline was significantly associated with exercise intolerance and PF. Notwithstanding, the radiological PI was resolved, and the exercise intolerance was mainly explained not by ventilatory limitation but by circulatory limitation and deconditioning.

Background: Relapse remains a major challenge in the long-term management of pulmonary sarcoidosis, yet predictors of relapse-free survival in patients with early-stage disease are incompletely understood. We investigated the clinical determinants of time to relapse in a biopsy-confirmed cohort of patients with pulmonary sarcoidosis followed for up to 15 years. Methods: This retrospective cohort study included 200 adults (mean age 42.0 ± 11.2 years, 72.0% women) with biopsy-confirmed Stage I–II pulmonary sarcoidosis. The primary outcome was relapse requiring re-initiation or escalation of systemic therapy after remission. Relapse-free survival was evaluated using Kaplan–Meier analysis and compared by the log-rank test. Cox proportional hazards models were used to identify independent predictors of relapse. Results: During long-term follow-up, 36 patients (18.0%) experienced disease relapse. Relapse-free survival was significantly lower among patients who received systemic treatment at baseline than among untreated patients (log-rank p < 0.001). In multivariable Cox analysis, baseline systemic treatment (adjusted hazard ratio [HR] 4.27, 95% confidence interval [CI] 1.39–13.09; p = 0.011) and Scadding Stage II disease (HR 2.58, 95% CI 1.26–5.29; p = 0.010) independently predicted relapse. Increasing age was associated with a lower relapse risk (HR 0.70 per 10-year increase, 95% CI 0.50–1.00; p = 0.047). Baseline FVC and sex were not independently associated with relapse, while extrapulmonary involvement showed a borderline association (HR 2.16, 95% CI 0.97–4.80; p = 0.059). Conclusions: Long-term relapse-free survival in early pulmonary sarcoidosis is primarily determined by baseline disease phenotype. Stage II disease identifies patients at increased relapse risk, whereas the association between systemic treatment and relapse most likely reflects confounding by indication rather than a detrimental treatment effect. Time-to-event analysis provides a clinically relevant framework for long-term risk stratification in early-stage sarcoidosis.