7 research outputs found

    Delineating associations of progressive pleuroparenchymal fibroelastosis in patients with pulmonary fibrosis

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    BACKGROUND: Computer quantification of baseline computed tomography (CT) radiological pleuroparenchymal fibroelastosis (PPFE) associates with mortality in idiopathic pulmonary fibrosis (IPF). We examined mortality associations of longitudinal change in computer-quantified PPFE-like lesions in IPF and fibrotic hypersensitivity pneumonitis (FHP). METHODS: Two CT scans 6-36 months apart were retrospectively examined in one IPF (n=414) and one FHP population (n=98). Annualised change in computerised upper-zone pleural surface area comprising radiological PPFE-like lesions (Δ-PPFE) was calculated. Δ-PPFE >1.25% defined progressive PPFE above scan noise. Mixed-effects models evaluated Δ-PPFE against change in visual CT interstitial lung disease (ILD) extent and annualised forced vital capacity (FVC) decline. Multivariable models were adjusted for age, sex, smoking history, baseline emphysema presence, antifibrotic use and diffusion capacity of the lung for carbon monoxide. Mortality analyses further adjusted for baseline presence of clinically important PPFE-like lesions and ILD change. RESULTS: Δ-PPFE associated weakly with ILD and FVC change. 22-26% of IPF and FHP cohorts demonstrated progressive PPFE-like lesions which independently associated with mortality in the IPF cohort (hazard ratio 1.25, 95% CI 1.16-1.34, p<0.0001) and the FHP cohort (hazard ratio 1.16, 95% CI 1.00-1.35, p=0.045). INTERPRETATION: Progression of PPFE-like lesions independently associates with mortality in IPF and FHP but does not associate strongly with measures of fibrosis progression

    The Spectrum of Infections in Patients with Lung Cancer

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    Although diagnostic and therapeutic advances in lung cancer (LC) have increased the survival of patients, infection and its complications are still among the most important causes of mortality. The disruption of tissue caused by tumor mass, management of cancer therapy and alteration in the humoral/cellular immune systems due to both cancer itself and therapy considerably increase susceptibility to infection in cancer patients. Particularly, opportunistic microorganisms should be considered, then applying rapid and sensitive diagnostic methods for them. Thus, cancer patients who are already exposed to difficult, long-term and expensive treatments can be prevented from dying from complications related to infections.TUBITAK; [120N924]This work is supported by TUBITAK with Project No: 120N924

    Temporal progression of mediastinal lymphadenopathy in idiopathic pulmonary fibrosis

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    [No Abstract Available]NIHR Southampton Biomedical Research Centre; Wellcome Trust [209553/Z/17/Z]; NIHR UCLH Biomedical Research Centre, UKJ.M. Wallis receives a research fellowship from the NIHR Southampton Biomedical Research Centre. This research was funded in whole or in part by the Wellcome Trust (209553/Z/17/Z). For this project, J. Jacob and E. Gudmundsson were also supported by the NIHR UCLH Biomedical Research Centre, UK. Funding information for this article has been deposited with the Crossref Funder Registry

    Prognostic Imaging Biomarker Discovery in Survival Analysis for Idiopathic Pulmonary Fibrosis

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    Imaging biomarkers derived from medical images play an important role in diagnosis, prognosis, and therapy response assessment. Developing prognostic imaging biomarkers which can achieve reliable survival prediction is essential for prognostication across various diseases and imaging modalities. In this work, we propose a method for discovering patch-level imaging patterns which we then use to predict mortality risk and identify prognostic biomarkers. Specifically, a contrastive learning model is first trained on patches to learn patch representations, followed by a clustering method to group similar underlying imaging patterns. The entire medical image can be thus represented by a long sequence of patch representations and their cluster assignments. Then a memory-efficient clustering Vision Transformer is proposed to aggregate all the patches to predict mortality risk of patients and identify high-risk patterns. To demonstrate the effectiveness and generalizability of our model, we test the survival prediction performance of our method on two sets of patients with idiopathic pulmonary fibrosis (IPF), a chronic, progressive, and life-threatening interstitial pneumonia of unknown etiology. Moreover, by comparing the high-risk imaging patterns extracted by our model with existing imaging patterns utilised in clinical practice, we can identify a novel biomarker that may help clinicians improve risk stratification of IPF patients.</p

    Delineating associations of progressive pleuroparenchymal fibroelastosis in patients with pulmonary fibrosis

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    Background Computer quantification of baseline computed tomography (CT) radiological pleuroparenchymal fibroelastosis (PPFE) associates with mortality in idiopathic pulmonary fibrosis (IPF). We examined mortality associations of longitudinal change in computer-quantified PPFE-like lesions in IPF and fibrotic hypersensitivity pneumonitis (FHP). Methods Two CT scans 6–36 months apart were retrospectively examined in one IPF (n=414) and one FHP population (n=98). Annualised change in computerised upper-zone pleural surface area comprising radiological PPFE-like lesions (Δ-PPFE) was calculated. Δ-PPFE >1.25% defined progressive PPFE above scan noise. Mixed-effects models evaluated Δ-PPFE against change in visual CT interstitial lung disease (ILD) extent and annualised forced vital capacity (FVC) decline. Multivariable models were adjusted for age, sex, smoking history, baseline emphysema presence, antifibrotic use and diffusion capacity of the lung for carbon monoxide. Mortality analyses further adjusted for baseline presence of clinically important PPFE-like lesions and ILD change. Results Δ-PPFE associated weakly with ILD and FVC change. 22–26% of IPF and FHP cohorts demonstrated progressive PPFE-like lesions which independently associated with mortality in the IPF cohort (hazard ratio 1.25, 95% CI 1.16–1.34, p<0.0001) and the FHP cohort (hazard ratio 1.16, 95% CI 1.00–1.35, p=0.045). Interpretation Progression of PPFE-like lesions independently associates with mortality in IPF and FHP but does not associate strongly with measures of fibrosis progression
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