Background: Fibrosing interstitial lung diseases can evolve into acute exacerbations, which significantly impact morbidity and mortality. Currently, no routinely used clinical biomarkers can discern the potential progression in these patients. This study aims to analyze different biological markers used in routine clinical practice as possible predictive biomarkers for patients with acute fibrosing interstitial lung disease exacerbation. Methods: We conducted a retrospective, single-center study including patients diagnosed with acute exacerbation of fibrosing interstitial lung disease who required hospitalization between 2018 and 2019 at Vall d’Hebron Hospital, Spain. Patient demographics, clinical data, respiratory function, and comorbidities were collected at baseline. The primary outcome was survival at 30 days, 90 days, and 365 days, using Kaplan–Meier survival analysis and Cox regression. Results: Twenty-nine patients were included (mean age 70.4 years). At the 3-month follow-up, patients with ischemic heart disease showed higher survival rates (p = 0.02). Identifying an infection as the etiology of the exacerbation was associated with worse one-year survival rates compared to idiopathic cases (p = 0.03). Elevated levels of leukocytes (p < 0.01), neutrophils (p < 0.01), and fibrinogen (p = 0.03) were predictors of mortality. Additionally, patients who received a cumulative dose of corticosteroids between 501 and 1000 mg during the exacerbation showed higher one-year survival (p < 0.01). Conclusions: Routine clinical markers can help predict outcomes in AE-f-ILD. Further multicenter studies should validate these findings and assess the role of therapies in its management.

Introduction: Dexamethasone has been shown to reduce 28-day mortality in COVID-19 patients requiring oxygen, but its effect on long-term pulmonary complications remains unclear. This study aimed to assess whether treatment with dexamethasone in the acute phase of SARS-CoV-2 pneumonia improves post-COVID clinical outcomes. Methods: This longitudinal retrospective study analysed patients hospitalized for SARS-CoV-2 pneumonia between March 2020 and April 2021. Patients were stratified according to dexamethasone treatment during hospitalization. They were evaluated 3– 9 months post- discharge using clinical assessments, pulmonary function tests, and imaging studies. We compared the demographic, clinical, and functional characteristics according to dexamethasone treatment. Multivariate linear and logistic regression models were used to assess the association between dexamethasone and main outcome follow-up variables. Results: In a study of 1,011 patients hospitalized for SARS-CoV-2 pneumonia, 663 received dexamethasone treatment while 348 did not. During post-COVID follow-up, dexamethasone-treated patients reported less dyspnea (28.4% vs 37.6%, p=0.003); showed better lung function, particularly in DLCO (76.9% vs 69.9%, p< 0.001), and better performance in the 6-minute walk test (435 meters vs 405 meters, p=0.002) Radiologically, these patients had lower degrees of reticulation (4,4% vs 9,5%; p=0,009), septal thickening (5,8% vs 10,5%; p=0,012) and fibrosis (3,5% vs 15,6%; p=< 0,001). Although rates of bronchial involvement were similar, dexamethasone-treated patients had less bronchiolitis but more bronchiectasis and bronchial thickening. Dexamethasone treatment increased DLCO by 9.25 points (95% CI: 0.50– 18.00; p=0.038) and significantly reduced the risk of fibrosis (OR=0.24; 95% CI: 0.12– 0.49) in multivariate analysis. Conclusion: Patients treated with dexamethasone showed improved post-COVID respiratory outcomes, including less dyspnea, better lung function, and fewer signs of fibrosis. These findings suggest that dexamethasone is associated with improved outcomes after severe COVID-19 pneumonia.

Patients with asthma do not present more respiratory sequelae than a control population after SARS-CoV-2 pneumonia. However, patients with asthma do seem to present more symptoms and a distinct involvement of the airway https://bit.ly/47E6Hze.

Background: Organizing pneumonia (OP) is an interstitial lung disease linked to infections and other conditions. Cryptogenic OP (COP) is a rarer, idiopathic form. OP has become one of the most frequent respiratory complications following SARS-CoV-2 pneumonia. Standard treatment involves the use of glucocorticoids. The objective of the study is to determine the optimal dosage of oral corticosteroids for the treatment of this disease. Methods: Randomized, open-label, assessor-blinded, parallel-group, single-center, non-inferiority clinical trial with an active control group comparing two oral prednisone regimens. The control group received prednisone 0.75 mg·Kg ⁻¹ ·day ⁻¹ for 4 weeks; 0.5 mg·Kg ⁻¹ ·day ⁻¹ 4 weeks; 20 mg·day ⁻¹ 4 weeks; 10 mg·day ⁻¹ 6 weeks; 5 mg·day ⁻¹ 6 weeks (6 months) and the experimental group prednisone 0.5 mg·Kg ⁻¹ ·d ⁻¹ 3 weeks, 20 mg·day ⁻¹ 3 weeks; 15 mg·day ⁻¹ 2 weeks; 10 mg·day ⁻¹ 2 weeks, 5 mg·day ⁻¹ 2 weeks (3 months). Visits were carried out at baseline and at 3, 6 and 12 months, recording clinical history, physical examination, pulmonary function tests and chest CT. The primary outcome was non-inferiority with a margin of 10% in DLCO at 6 months. Results: Seventy-nine patients were randomized according to intention to treat, 40 to the experimental group and 39 to the control group. Mean baseline DLCO was 59.3% ( sd 16.7) in the experimental group and 55.5% ( sd 16.5) in the control group, with mean improvements at 6 months of 11.7% (95%CI 7.18–16.17) and 12.8% (95%CI 8.57–17.11) respectively. The difference between groups at 6 months was 1.23% [(95%CI −5.13–7.59], the experimental regimen being non-inferior to the control group with the margin of 10%. Patients in the experimental group had fewer than half as many adverse effects as controls: 9 (23%) versus 22 (56%) (p=0.0027). Conclusions: Treatment with oral corticosteroids lasting three months (initial dose of prednisone 0.5 mg·Kg ⁻¹ ·day ⁻¹ ) may be recommended in patients with post-COVID OP.

Introduction: Hypersensitivity pneumonitis (HP) is an interstitial lung disease that may present as fibrotic (fHP) or non-fibrotic (nfHP). Fibrosis is associated with progression and poor outcomes; however, the transition to progressive pulmonary fibrosis (PPF) and its predictors remain unclear. Methods: We retrospectively reviewed adult patients diagnosed with HP at a tertiary hospital (2010 and 2022). Patients were classified as having fHP or nfHP and were followed up for at least 1 year. Clinical, functional, radiological, and histological variables were analyzed. PPF was defined according to the 2022 clinical practice guideline of the American Thoracic Society (ATS), European Respiratory Society (ERS), Japanese Respiratory Society (JRS), and Asociación Latinoamericana de Tórax (ALAT). Results: Of 298 HP patients, 191 were included (153 fHP and 38 nfHP). Among patients with fHP, 76 (49.7%) developed PPF after a median of 3.2 years. Median survival was 4.8 years in fHP with PPF versus 6.3 years without, with 1.6 years from PPF onset to death or transplantation. The independent predictors of PPF and survival were lower forced vital capacity, elevated lactate dehydrogenase, fibroblastic foci, and microscopic honeycombing. Conclusion: Nearly half of fHP patients progressed to PPF within a few years, with markedly reduced survival. Early recognition of high-risk patients may support timely antifibrotic treatment and improve outcomes.