Journal Article Review Epublish
PubMed: 40806851 DOI: 10.3390/jcm14155229
Hematologic and Immunologic Overlap Between COVID-19 and Idiopathic Pulmonary Fibrosis.
J Clin Med 14(15)
Authors: Gabriela Mara, Gheorghe Nini, Stefan Marian Frenț, Coralia Cotoraci
Affiliations
- Multidisciplinary Doctoral School, Vasile Goldis Western University of Arad, 310414 Arad, Romania.
- Pneumology Department, Vasile Goldis Western University of Arad, 310414 Arad, Romania.
- Centre for Research and Innovation in Precision Medicine of Respiratory Diseases, Department of Pulmonology, University of Medicine and Pharmacy Timisoara, 300041 Timisoara, Romania.
- Clinical Hematology Department, Vasile Goldis Western University of Arad, 310025 Arad, Romania.
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive fibrosing lung disease characterized by chronic inflammation, vascular remodeling, and immune dysregulation. COVID-19, caused by SARS-CoV-2, shares several systemic immunohematologic disturbances with IPF, including cytokine storms, endothelial injury, and prothrombotic states. Unlike general comparisons of viral infections and chronic lung disease, this review offers a focused analysis of the shared hematologic and immunologic mechanisms between COVID-19 and IPF. Our aim is to better understand how SARS-CoV-2 infection may worsen disease progression in IPF and identify converging pathophysiological pathways that may inform clinical management. We conducted a narrative synthesis of the peer-reviewed literature from PubMed, Scopus, and Web of Science, focusing on clinical, experimental, and pathological studies addressing immune and coagulation abnormalities in both COVID-19 and IPF. Both diseases exhibit significant overlap in inflammatory and fibrotic signaling, particularly via the TGF-β, IL-6, and TNF-α pathways. COVID-19 amplifies coagulation disturbances and endothelial dysfunction already present in IPF, promoting microvascular thrombosis and acute exacerbations. Myeloid cell overactivation, impaired lymphocyte responses, and fibroblast proliferation are central to this shared pathophysiology. These synergistic mechanisms may accelerate fibrosis and increase mortality risk in IPF patients infected with SARS-CoV-2. This review proposes an integrative framework for understanding the hematologic and immunologic convergence of COVID-19 and IPF. Such insights are essential for refining therapeutic targets, improving prognostic stratification, and guiding early interventions in this high-risk population.
MeSH
Idiopathic Pulmonary Fibrosis, Lung, Fibrosis, Cytokine Release Syndrome, Covid-19, Pulmonary Fibrosis, Thrombosis, Lung Diseases, Infections