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Background: Persistent dyspnoea and pulmonary function impairment are common after coronavirus disease 2019 (COVID-19). However, long-term outcomes beyond 2 years of infection are unknown. Methods: In this single-center study, we observed the trend of self-reported dyspnoea and pulmonary functions among subjects attending a post-COVID clinic in India after 2 years of COVID-19 illness. Using logistic regression, we explored the clinico-demographic factors associated with persistent dyspnoea and impaired lung functions beyond 2 years. Results: Among 231 included subjects (68.8% male) with a mean [standard deviation (SD)] age of 44.8 (13.2) years, 119 (51.5%) had recovered from moderate-to-severe COVID-19. The median [inter-quartile range (IQR)] time intervals from COVID-19 diagnosis (T0) to clinical enrolment (T1) and final follow-up (T2) were 3.3 (1.9-5.5) months and 29.5 (27.2-32.2) months, respectively. Between T1 and T2, the prevalence of self-reported dyspnoea remained stable in the whole cohort (39.4% vs. 36.4%, P = 0.26) but declined in the sub-group with moderate-to-severe COVID-19 (63% vs. 54.6%, P = 0.03). Persistent dyspnoea at T2 was associated with female sex (P = 0.007), moderate-to-severe COVID-19 (P < 0.001), and infection during the delta wave (P < 0.001). At T2, impairment in forced vital capacity (FVC) was seen in 48.1% subjects. Persistently impaired FVC was associated with older age (P value = 0.047), female sex (P value <0.001), and infection during the delta wave (P value = 0.02). Conclusion: Persistent self-reported dyspnoea and impaired pulmonary functions were common in COVID-19 survivors beyond 2 years of infection. Female sex and infection during the delta wave were associated with long-term impairments. [ABSTRACT FROM AUTHOR]

Introduction: The dysregulated host immune response in sepsis is orchestrated by peripheral blood leukocytes. This study explored the associations of the peripheral blood leukocyte subpopulations with early clinical deterioration and mortality in sepsis. Methods: We performed a prospective observational single-center study enrolling adult subjects with sepsis within 48 h of hospital admission. Peripheral blood flow cytometry was performed for the patients at enrolment and after 5 days. The primary outcome was to explore the association between various leukocyte subpopulations at enrolment and early clinical deterioration [defined as an increase in the sequential organ failure assessment (SOFA) score between enrolment and day 5, or death before day 5]. Other pre-specified outcomes explored associations of leukocyte subpopulations at enrolment and on day 5 with in-hospital mortality. Results: A total of 100 patients, including 47 with septic shock were enrolled. The mean (SD) age of the patients was 53.99 (14.93) years. Among them, 26 patients had early clinical deterioration, whereas 41 died during hospitalization. There was no significant association between the leukocyte subpopulations at enrolment and early clinical deterioration on day 5. On multivariate logistic regression, a reduced percentage of CD8 + CD25+ T-cells at enrolment was associated with in-hospital mortality [odds ratio (OR), 0.82 (0.70-0.97); p-value = 0.02]. A reduced lymphocyte percentage on day 5 was associated with in-hospital mortality [OR, 0.28 (0.11-0.69); p-value = 0.01]. In a post-hoc analysis, patients with "very early" deterioration within 48 h had an increased granulocyte CD64 median fluorescent intensity (MFI) [OR, 1.07 (1.01-1.14); p-value = 0.02] and a reduced granulocyte CD16 MFI [OR, 0.97 (0.95-1.00); p-value = 0.04] at enrolment. Conclusions: None of the leukocyte subpopulations showed an association with early clinical deterioration at day 5. Impaired lymphocyte activation and lymphocytopenia indicative of adaptive immune dysfunction may be associated with in-hospital mortality. [ABSTRACT FROM AUTHOR]

Study Objectives: Rapid growth in childhood predisposes to obesity and cardiometabolic diseases in adulthood. While obstructive sleep apnea (OSA) is bidirectionally linked to obesity, its developmental origins are sparsely studied. We examined associations between postnatal growth and the risk of OSA in adulthood., Methods: We included adults whose childhood anthropometric data was collected in the New Delhi Birth Cohort study. The risk of OSA was defined by the Berlin Questionnaire (BQ) with and without the obesity criterion. Using logistic regression, we studied associations of OSA risk with conditional growth parameters, which are statistically independent measures of gain in height, weight, and body mass index (BMI), during infancy (0-2 years), early childhood (2-5 years), and late childhood (5-11 years)., Results: Among 521 subjects (58.9% males) with a mean (SD) age of 40.9 (1.7) years, 30.9% had a high risk of OSA. On multivariate analysis, a high risk of OSA was associated with a higher conditional BMI in infancy (odds ratio: 1.25; 95% confidence interval: 1.00-1.57; p = 0.048) and early childhood (1.35; 1.07-1.69; p = 0.011). Higher risk of OSA was associated with greater conditional weight in early childhood (1.34; 1.06-1.68; p = 0.013). Using the modified BQ definition without obesity, adult risk of OSA was significantly associated with a higher adult BMI instead of childhood conditional BMIs., Conclusions: Greater gain in conditional BMI or weight in early childhood is associated with a high risk of OSA in middle age, which is mediated by a higher attained adult BMI., (© 2024 Wiley Periodicals LLC.)