Background: Pirfenidone and nintedanib are the sole pharmacological therapies currently approved for idiopathic pulmonary fibrosis (IPF). Limited comparison data is available in literature, despite they are both prescribed for mild-to-moderate disease. Here, we describe our almost 10 years real-life experience with antifibrotic treatment to investigate potential differences in terms of efficacy.
Population And Methods: We retrospectively recruited patients diagnosed with IPF and treated with pirfenidone or nintedanib at Siena Referral Center. Clinical, functional, safety and radiological data was collected at baseline and during the follow-up, according to our Center protocol.
Results: We retrospectively recruited 263 IPF patients (139 treated with pirfenidone and 124 with nintedanib) in the study. After 885.3 ± 559.5 days of observation, the median survival was 1224 days. No significant differences were found between pirfenidone and nintedanib in terms of survival and time to decline of forced vital capacity >10% ( = 0.8786 and = 0.1677, respectively). A smaller lung diffusion for carbon monoxide (DL ) decrease was found after 1 year of therapy with nintedanib in respect to pirfenidone ( = 0.0167). Overall, 21 patients permanently discontinued antifibrotic treatment due to side effects (14 with pirfenidone, 7 with nintedanib); no fatal adverse events were recorded.
Discussion: Our results showed a similar effectiveness between pirfenidone and nintedanib in terms of mortality and functional disease progression. Both drugs confirmed their good tolerability profile and no new safety alerts were observed. Nintedanib was associated with a smaller reduction of DL after 1 year of follow-up compared with pirfenidone, maybe due to its antiangiogenic properties.
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http://dx.doi.org/10.3389/fmolb.2020.581828 | DOI Listing |
J Pers Med
December 2024
Department of Nephrology, Ghent University Hospital, 9000 Ghent, Belgium.
Chronic kidney disease (CKD) is a chronic disorder characterized by kidney fibrosis and extracellular matrix accumulation that can lead to end-stage kidney disease. Epithelial-to-mesenchymal transition, inflammatory cytokines, the TGF-β pathway, Wnt/β-catenin signaling, the Notch pathway, and the NF-κB pathway all play crucial roles in the progression of fibrosis. Current medications, such as renin-angiotensin-aldosterone system inhibitors, try to delay disease development but do not stop or reverse fibrosis.
View Article and Find Full Text PDFEClinicalMedicine
January 2025
Department of Pulmonology, Semmelweis University, Budapest, Hungary.
Background: Idiopathic pulmonary fibrosis (IPF) is a progressive, deadly lung disease with several factors, including respiratory tract infections (RTI), for disease worsening. There's no comprehensive data on RTI incidence in IPF patients across different therapies, including antifibrotic (nintedanib or pirfenidone), investigative or placebo treatments.
Methods: A systematic search of databases Medline, EMBASE, Cochrane Central, Web of Science and Scopus was conducted on September 30th 2024 (PROSPERO registration number: CRD42023484213).
Clin Radiol
November 2024
School of Medicine, Cork University Hospital, Cork, Ireland; Department of Respiratory Medicine, Cork University Hospital, Cork, Ireland.
Aim: Idiopathic pulmonary fibrosis (IPF) is a debilitating and fatal lung disease. Changes in body composition potentially correlate with outcomes in patients with IPF.
Materials And Methods: Patients with IPF on antifibrotic treatment attending a single institution were identified and retrospectively evaluated (n=84).
Microb Pathog
December 2024
Clinical Immunology Research Center, Zahedan University of Medical Sciences, Zahedan, Iran. Electronic address:
Indian J Pharmacol
September 2024
Department of Dermatology, Government Medical College, Patiala, Punjab, India.
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