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Open Forum Infectious Diseases ; 8(SUPPL 1):S18-S19, 2021.
Article in English | EMBASE | ID: covidwho-1746813


Background. While COVID-19 carries substantial morbidity and mortality, the extent of long-term complications remains unclear. Reports suggest that acute lung damage associated with severe COVID-19 can result in chronic respiratory dysfunction. This study: (1) estimated the incidence of dyspnea and ILD after COVID-19 hospitalization, and (2) assessed risk factors for developing dyspnea and ILD in a real-world cohort of patients hospitalized with COVID-19 using US electronic health records (EHR). Methods. Patients in the Optum de-identified COVID-19 EHR database who were hospitalized for COVID-19 (lab confirmed or diagnosis code) between February 20 and July 2020 and had at least 6 months of follow-up were eligible for analysis. Dyspnea and ILD were identified using diagnosis codes. The effects of baseline characteristics and hospitalization factors on the risk of incident dyspnea or ILD 3 to 6 months' post discharge were evaluated. Results. Among eligible patients (n=26,339), 1705 (6.5%) had dyspnea and 220 (0.8%) had ILD 3 to 6 months after discharge. Among patients without prior dyspnea or ILD (n=22,613), 110 (0.5%) had incident ILD (Table 1) and 1036 (4.6%) had incident dyspnea (Table 2) 3 to 6 months after discharge. In multivariate analyses, median (IQR) length of stay (LOS;5.0 [3.0, 9.0] days in patients who did not develop ILD vs 14.5 [6.0, 26.0] days in patients who developed ILD;RR: 1.12, 95% CI: 1.08, 1.15;P=4.34 x 10-10) and age (RR: 1.02, 95% CI: 1.01, 1.03;P=4.63 x 10-3) were significantly associated with ILD. Median (IQR) LOS (5.0 [3.0, 9.0] days in patients who did not develop dyspnea vs 7 [4.0, 14.0] days in patients who developed dyspnea;RR: 1.04, 95% CI: 1.02, 1.06;P=8.52 x 10-4), number of high-risk comorbidities (RR: 1.18, 95% CI: 1.12, 1.24;P=3.85 x 10-9), and obesity (RR: 1.52, 95% CI: 1.25, 1.86;P=2.59 x 10-4) were significantly associated with dyspnea. Conclusion. In a real-world cohort, 4.6% and 0.5% of patients developed dyspnea and ILD, respectively, after COVID-19 hospitalization. Multivariate analyses suggested that LOS, age, obesity, and comorbidity burden may be risk factors for post-COVID-19 respiratory complications. Limitations included sensitivity of diagnosis codes, availability of labs, and care-seeking bias.

PUBMED; 2020.
Preprint in English | PUBMED | ID: ppcovidwho-292827


The recent outbreak of the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), has led to a worldwide pandemic. One week after initial symptoms develop, a subset of patients progresses to severe disease, with high mortality and limited treatment options. To design novel interventions aimed at preventing spread of the virus and reducing progression to severe disease, detailed knowledge of the cell types and regulating factors driving cellular entry is urgently needed. Here we assess the expression patterns in genes required for COVID-19 entry into cells and replication, and their regulation by genetic, epigenetic and environmental factors, throughout the respiratory tract using samples collected from the upper (nasal) and lower airways (bronchi). Matched samples from the upper and lower airways show a clear increased expression of these genes in the nose compared to the bronchi and parenchyma. Cellular deconvolution indicates a clear association of these genes with the proportion of secretory epithelial cells. Smoking status was found to increase the majority of COVID-19 related genes including ACE2 and TMPRSS2 but only in the lower airways, which was associated with a significant increase in the predicted proportion of goblet cells in bronchial samples of current smokers. Both acute and second hand smoke were found to increase ACE2 expression in the bronchus. Inhaled corticosteroids decrease ACE2 expression in the lower airways. No significant effect of genetics on ACE2 expression was observed, but a strong association of DNA- methylation with ACE2 and TMPRSS2- mRNA expression was identified in the bronchus.