Persistence of a SARS-CoV-2 T-cell response in patients with long COVID and lung sequelae after COVID-19.

1 year after an acute COVID-19 episode, patients with either lung sequelae or long COVID show a stronger SARS-CoV-2-specific T-cell response than fully recovered individuals, suggesting persistent cell stimulation by residual viral reservoirs https://bit.ly/40bPZm7.

Validity of prognostic models of critical COVID-19 is variable. A systematic review with external validation.

OBJECTIVES: To identify prognostic models which estimate the risk of critical COVID-19 in hospitalized patients and to assess their validation properties. STUDY DESIGN AND SETTING: We conducted a systematic review in Medline (up to January 2021) of studies developing or updating a model that estimated the risk of critical COVID-19, defined as death, admission to intensive care unit, and/or use of mechanical ventilation during admission. Models were validated in two datasets with different backgrounds (HM [private Spanish hospital network], n = 1,753, and ICS [public Catalan health system], n = 1,104), by assessing discrimination (area under the curve [AUC]) and calibration (plots). RESULTS: We validated 18 prognostic models. Discrimination was good in nine of them (AUCs ≥ 80%) and higher in those predicting mortality (AUCs 65%-87%) than those predicting intensive care unit admission or a composite outcome (AUCs 53%-78%). Calibration was poor in all models providing outcome's probabilities and good in four models providing a point-based score. These four models used mortality as outcome and included age, oxygen saturation, and C-reactive protein among their predictors. CONCLUSION: The validity of models predicting critical COVID-19 by using only routinely collected predictors is variable. Four models showed good discrimination and calibration when externally validated and are recommended for their use.

Inhaled corticosteroids for the treatment of COVID-19.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has caused severe illness and mortality for millions worldwide. Despite the development, approval and rollout of vaccination programmes globally to prevent infection by SARS-CoV-2 and the development of coronavirus disease 2019 (COVID-19), treatments are still urgently needed to improve outcomes. Early in the pandemic it was observed that patients with pre-existing asthma or COPD were underrepresented among those with COVID-19. Evidence from clinical studies indicates that the inhaled corticosteroids (ICS) routinely taken for asthma and COPD could have had a protective role in preventing severe COVID-19 and, therefore, may be a promising treatment for COVID-19. This review summarises the evidence supporting the beneficial effects of ICS on outcomes in patients with COVID-19 and explores the potential protective mechanisms.

Real-life burden of hospitalisations due to COPD exacerbations in Spain.

Background: Patients with chronic obstructive pulmonary disease (COPD) often suffer episodes of exacerbation of symptoms (ECOPD) that may eventually require hospitalisation due to several, often overlapping, causes. We aimed to analyse the characteristics of patients hospitalised because of ECOPD in a real-life setting using a "big data" approach. Methods: The study population included all patients over 40 years old with a diagnosis of COPD (n=69 359; prevalence 3.72%) registered from 1 January 2011 to 1 March 2020 in the database of the public healthcare service (SESCAM) of Castilla-La Mancha (Spain) (n=1 863 759 subjects). We used natural language processing (Savana Manager version 3.0) to identify those who were hospitalised during this period for any cause, including ECOPD. Results: During the study 26 453 COPD patients (38.1%) were hospitalised (at least once). Main diagnoses at discharge were respiratory infection (51%), heart failure (38%) or pneumonia (19%). ECOPD was the main diagnosis at discharge (or hospital death) in 8331 patients (12.0% of the entire COPD population and 31.5% of those hospitalised). In-hospital ECOPD-related mortality rate was 3.11%. These patients were hospitalised 2.36 times per patient, with a mean hospital stay of 6.1 days. Heart failure was the most frequent comorbidity in patients hospitalised because of ECOPD (52.6%). Conclusions: This analysis shows that, in a real-life setting, ECOPD hospitalisations are prevalent, complex (particularly in relation to heart failure), repetitive and associated with significant in-hospital mortality.

SARS-CoV-2 T-cell response in COVID-19 convalescent patients with and without lung sequelae.

A specific T-cell response persists in the majority of COVID-19 patients 6 months after hospital discharge. This response is more prominent in those who required critical care during the acute COVID-19 episode but is reduced in patients with lung sequelae. https://bit.ly/3fBuVA4.

COVID-19 and COPD: lessons beyond the pandemic.

Early in the COVID pandemic there were concerns about the outcomes for patients with COPD who developed COVID-19. Although the pandemic has made the diagnosis and routine management of COPD more difficult, the risk of patients developing COVID or of having poor outcomes is less than anticipated and there have been some unexpected findings that may lead to significant improvements in the management of COPD in future.

Elevated plasma levels of epithelial and endothelial cell markers in COVID-19 survivors with reduced lung diffusing capacity six months after hospital discharge.

BACKGROUND: Some COVID-19 survivors present lung function abnormalities during follow-up, particularly reduced carbon monoxide lung diffusing capacity (DLCO). To investigate risk factors and underlying pathophysiology, we compared the clinical characteristics and levels of circulating pulmonary epithelial and endothelial markers in COVID-19 survivors with normal or reduced DLCO 6 months after discharge. METHODS: Prospective, observational study. Clinical characteristics during hospitalization, and spirometry, DLCO and plasma levels of epithelial (surfactant protein (SP) A (SP-A), SP-D, Club cell secretory protein-16 (CC16) and secretory leukocyte protease inhibitor (SLPI)), and endothelial (soluble intercellular adhesion molecule 1 (sICAM-1), soluble E-selectin and Angiopoietin-2) 6 months after hospital discharge were determined in 215 COVID-19 survivors. RESULTS: DLCO was < 80% ref. in 125 (58%) of patients, who were older, more frequently smokers, had hypertension, suffered more severe COVID-19 during hospitalization and refer persistent dyspnoea 6 months after discharge. Multivariate regression analysis showed that age ≥ 60 years and severity score of the acute episode ≥ 6 were independent risk factors of reduced DLCO 6 months after discharge. Levels of epithelial (SP-A, SP-D and SLPI) and endothelial (sICAM-1 and angiopoietin-2) markers were higher in patients with reduced DLCO, particularly in those with DLCO ≤ 50% ref. Circulating SP-A levels were associated with the occurrence of acute respiratory distress syndrome (ARDS), organizing pneumonia and pulmonary embolisms during hospitalization. CONCLUSIONS: Reduced DLCO is common in COVID-19 survivors 6 months after hospital discharge, especially in those older than 60 years with very severe acute disease. In these individuals, elevated levels of epithelial and endothelial markers suggest persistent lung damage.

SARS-CoV-2 T-cell response in COVID-19 convalescent patients with and without lung SEQUELAE

Patients infected by SARS-CoV-2 may develop pneumonia (COVID19) and require hospital admission and, eventually, critical care [1]. This has been related with a weaker innate immune response with impaired production of type I interferons [2]. In this setting, an antigen specific T-cell response is needed for the elimination of SARS-CoV-2, as well as to develop long-lasting memory to respond to potential future SARS-CoV-2 infections [3, 4]. However, this response needs to be contained once the virus is eradicated to avoid further damaging the host.

Is asthma associated with COVID-19 infection? A UK Biobank analysis.

BACKGROUND: The relationship between asthma and coronavirus disease 2019 (COVID-19) risk is not clear and may be influenced by level of airway obstruction, asthma medication and known COVID-19 risk factors. We aimed to investigate COVID-19 risk in people with asthma. METHODS: We used UK Biobank data from all participants tested for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (n=107 412; 17 979 test positive). Questions at baseline defined ever asthma and asthma medications. Baseline forced expiratory volume in 1 s (FEV1) was categorised into quartiles. Logistic regression modelled relationships between asthma, and asthma categories (age at onset, medications, FEV1 quartiles), and risk of SARS-CoV-2 positive test. We investigated modification by sex, ethnic group, smoking and body mass index. RESULTS: There was a reduced risk of a positive test associated with early-onset asthma (<13 years) (OR 0.91, 95% CI 0.84-0.99). This was found for participants with early-onset asthma who were male (OR 0.87, 95% CI 0.78-0.98), nonsmokers (OR 0.87, 95% CI 0.78-0.98), overweight/obese (OR 0.85, 95% CI 0.77-0.93) and non-Black (OR 0.90, 95% CI 0.82-0.98). There was increased risk amongst early-onset individuals with asthma in the highest compared to lowest quartile of lung function (1.44, 1.05-1.72). CONCLUSION: Amongst male, nonsmoking, overweight/obese and non-Black participants, having early-onset asthma was associated with lower risk of a SARS-CoV-2 positive test. We found no evidence of a protective effect from asthma medication. Individuals with early-onset asthma of normal weight and with better lung function may have lifestyle differences placing them at higher risk. Further research is needed to elucidate the contribution of asthma pathophysiology and different health-related behaviour, across population groups, to the observed risks.