Objectives: To describe the challenges inherent in diagnosing fibrosing lung diseases (FLD) on CT imaging and methodologies by which the diagnostic process may be simplified.
Methods: Extensive searches in online scientific databases were performed to provide relevant and contemporary evidence that describe the current state of knowledge related to FLD diagnosis. This includes descriptions of the utility of a working diagnosis for an individual case discussed in a multidisciplinary team (MDT) setting and challenges associated with the lack of consensus guidelines for diagnosing chronic hypersensitivity pneumonitis.
Results: As well as describing imaging features that indicate the presence of a fibrosing lung disease, those CT characteristics that nuance a diagnosis of the various FLDs are considered. The review also explains the essential information that a radiologist needs to convey to an MDT when reading a CT scan. Lastly, we provide some insights as to the future directions the field make take in the upcoming years.
Conclusions: This review outlines the current state of FLD diagnosis and emphasizes areas where knowledge is limited, and more evidence is required. Fundamentally, however, it provides a guide for radiologists when tackling CT imaging in a patient with FLD.
Advances In Knowledge: This review encompasses advice from recent guideline statements and evidence from the latest studies in FLD to provide an up-to-date manual for radiologists to aid the diagnosis of FLD on CT imaging in an MDT setting.
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http://dx.doi.org/10.1259/bjro.20190009 | DOI Listing |
Trends Pharmacol Sci
January 2025
Department of Surgery, University of California, San Francisco, San Francisco, CA, USA; Center for Bioengineering and Tissue Regeneration, University of California, San Francisco, San Francisco, CA, USA; UCSF Helen Diller Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA, USA; Department of Radiation Oncology, Eli and Edythe Broad Center for Regeneration Medicine and Stem Cell Research, University of California, San Francisco, San Francisco, CA, USA.
Fibrosis accounts for approximately one-third of disease-related deaths globally. Current therapies fail to cure fibrosis, emphasizing the need to identify new antifibrotic approaches. Fibrosis is defined by the excessive accumulation of extracellular matrix (ECM) and resultant stiffening of tissue stroma.
View Article and Find Full Text PDFStem Cells Int
January 2025
Department of Respiratory Medicine Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing 400014, China.
Pulmonary fibrosis (PF) is a lethal pathological change of fibrotic interstitial lung diseases (ILDs) with abundant fibroblasts proliferation after severely or continually alveolar epithelial cells (AECs) injury. Barely therapies are helpful for PF. Here we use bleomycin intratracheally injection to model PF with or without human umbilical cord-mesenchymal stem cells (hUC-MSCs) and/or nintedanib intervention.
View Article and Find Full Text PDFMycoses
January 2025
Unité de Parasitologie-Mycologie, Département de Prévention, Diagnostic et Traitement Des Infections, CHU Henri Mondor, Assistance Publique Des Hôpitaux de Paris (APHP), Creteil, France.
Background: The airways of patients with cystic fibrosis (pwCF) harbour complex fungal and bacterial microbiota involved in pulmonary exacerbations (PEx) and requiring antimicrobial treatment. Descriptive studies analysing bacterial and fungal microbiota concomitantly are scarce, especially using both culture and high-throughput-sequencing (HTS).
Objectives: We analysed bacterial-fungal microbiota and inter-kingdom correlations in two French CF centres according to clinical parameters and antimicrobial choices.
Gen Physiol Biophys
January 2025
Institute of Histology and Embryology, Faculty of Medicine, University of Ostrava, Ostrava, Czech Republic.
Pulmonary alveolar proteinosis (PAP) is a rare disease characterised by excessive accumulation of surfactant components in alveolar macrophages, alveoli, and peripheral airways. The accumulation of surfactant is associated with only a minimal inflammatory response but can lead to the development of pulmonary fibrosis. Three clinical forms of PAP are distinguished - primary, secondary and congenital.
View Article and Find Full Text PDFAlveolar type 2 (AT2) cells maintain lung health by acting as stem cells and producing pulmonary surfactant. AT2 dysfunction underlies many lung diseases, including interstitial lung disease (ILD), in which some inherited forms result from the mislocalization of surfactant protein C (SFTPC) variants. Lung disease modeling and dissection of the underlying mechanisms remain challenging due to complexities in deriving and maintaining human AT2 cells ex vivo.
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