Twenty‐five years of <i>Respirology</i>: Advances in idiopathic pulmonary fibrosis

Varone, Francesco; Inoue, Yoshikazu; Richeldi, Luca

doi:10.1111/resp.13733

Cited by 6 publications

(6 citation statements)

References 14 publications

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“…[31][32][33] The incidence of some non-IPF F-ILD subtypes exceeded that of IPF (sarcoidosis in most countries, but also other F-ILD in Belgium and Denmark, and iNSIP and uIIP in Belgium). The refinement of IPF definition and the improvement of diagnostic procedures in later years, [34] may have reduced misdiagnoses of non-IPF F-ILDs as IPF, and is expected to further increase non-IPF F-ILDs estimates in the future.…”

Section: Discussionmentioning

confidence: 99%

Epidemiology of interstitial lung diseases and their progressive-fibrosing behaviour in six European countries

et al. 2021

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The PERSEIDS study aimed to estimate incidence/prevalence of interstitial lung diseases (ILDs), fibrosing Interstitial lung diseases (F-ILDs), idiopathic pulmonary fibrosis (IPF), systemic sclerosis-associated ILD (SSc-ILD), other non-IPF F-ILDs and their progressive-fibrosing (PF) forms in six European countries, as current data are scarce.This retrospective, two-phase study used aggregate data (2014–2018). In Phase 1, incident/prevalent cases of ILDs above were identified from clinical databases through an algorithm based on codes/keywords, and incidence/prevalence was estimated. For non-IPF F–ILDs, the relative percentage of subtypes was also determined. In Phase 2, a subset of non-IPF F-ILD cases was manually reviewed to determine the percentage of PF behaviour and usual interstitial pneumonia-like (UIP-like) pattern. A weighted mean percentage of progression was calculated for each country and used to extrapolate incidence/prevalence of progressive-fibrosing ILDs (PF–ILDs).In 2018, incidence/105 person-years ranged between 9.4–83.6(ILDs), 7.7–76.2(F-ILDs), 0.4–10.3(IPF), 6.6–71.7(non-IPF F-ILDs) and 0.3–1.5(SSc-ILD); and prevalence/105 persons ranged between 33.6–247.4(ILDs), 26.7–236.8(F-ILDs), 2.8–31.0(IPF), 22.3–205.8(non-IPF F-ILDs) and 1.4–10.1(SSc-ILD). Among non-IPF F-ILDs, sarcoidosis was the most frequent subtype. PF behaviour and UIP-like pattern were present in a third of non-IPF F-ILD cases each and hypersensitivity pneumonitis showed the highest percentage of progressive behaviour. Incidence of PF-ILDs ranged between 2.1–14.5/105 person-years, and prevalence between 6.9–78.0/105 persons.To our knowledge, PERSEIDS is the first study assessing incidence, prevalence and rate of progression of ILDs across several European countries. Still below the threshold for orphan diseases, the estimates obtained were higher and more variable than reported in previous studies, but differences in study design/population must be considered.

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Section: Discussionmentioning

confidence: 99%

Epidemiology of interstitial lung diseases and their progressive-fibrosing behaviour in six European countries

et al. 2021

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“…Improving the management of lung transplant candidates during the pretransplant period has been the focus of much attention, as efforts to delay the time until need for transplant are being readily developed. The emergence of highly effective, targeted pharmacologic agents for diseases such as idiopathic pulmonary fibrosis (IPF), idiopathic pulmonary arterial hypertension (PAH), and cystic fibrosis (CF) have demonstrated efficacy in slowing the otherwise-rapid progressive clinical course of these respiratory illnesses (5)(6)(7). These advances in pharmacologic treatment have made later listing possible in some patients, successfully extending the time until need for transplant and contributing to an overall decrease in time-to-death for these end-stage lung diseases (8).…”

Section: Trends In Pretransplant Evaluation Candidate Selection and Organ Allocationmentioning

confidence: 99%

Current trends in candidate selection, contraindications, and indications for lung transplantation

Arjuna¹,

Olson²,

Walia³

2021

J Thorac Dis

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Lung transplant has been established as the treatment of choice for patients with various forms of end-stage lung disease, in whom non-transplant therapeutic options have failed. Many advances in the realms of basic science, clinical research, surgical technique, and perioperative management have emerged over the past few decades; these innovations have contributed to substantial improvements in survival and quality of life for transplant recipients. However, the field of lung transplantation faces appreciable challenges, including expanding the lung donor pool and ameliorating posttransplant complications, such as primary graft dysfunction, cellular-and antibodymediated rejection, chronic lung allograft dysfunction, and infection (1). One of the most important questions

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“…Thalidomide is currently used for the treatment of diseases such as leprosy and multiple myeloma (9,10). Several studies (11)(12)(13) have found that thalidomide may also has good anti-pulmonary fibrosis effects, but the underlying pharmacological mechanisms have not been well-elucidated. Therefore, more studies on this issue are warranted.…”

Section: Original Articlementioning

confidence: 99%

Thalidomide inhibits the gene promoter of connective tissue growth factor in human embryonic lung fibroblasts

Wu¹,

Liu²,

Zhang³

et al. 2020

Ann Palliat Med

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Background: The etiology and pathogenesis of idiopathic pulmonary fibrosis (IPF) remain unclear, and the early detection and treatment are vital to the prognosis of IPF patients. It's necessary to investigate the effect of thalidomide on the gene promoter activation of connective tissue growth factor (CTGF) induced by transforming growth factor-β1 (TGF-β1) in human embryonic lung fibroblast (HELF). Methods:The gene vector of pGL3-CTGFP containing human CTGF gene promoter was constructed and transfected into HELF cells. We used different TGF-β1 (0, 2.5, 5, 10 and 20 µg/L respectively) to stimulate HELF to identify the optimal concentration for gene promoter of CTGF. The activity of luciferase was measured to observe the effect of TGF-β1 and THALIDOMIDE on the activity of CTGF gene promoter. Results:The relative luciferase activity increased significantly with the stimulation of TGF-β1, and the relative luciferase activity peaked in the 5 µg/L TGF-β1 group (all P<0.01). The thalidomide inhibited the TGF-β1-induced activation of CTGF gene promoter in HELF, and the effect peaked in the 25 µg/L group (all P<0.001).Conclusions: Thalidomide produces a significant inhibitory effect on the gene promoter activation of CTGF induced by TGF-β1 in HELF, it may be a potentially effective drug for the treatment of pulmonary fibrosis.

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Twenty‐five years of Respirology: Advances in idiopathic pulmonary fibrosis

Cited by 6 publications

References 14 publications

Epidemiology of interstitial lung diseases and their progressive-fibrosing behaviour in six European countries

Epidemiology of interstitial lung diseases and their progressive-fibrosing behaviour in six European countries

Current trends in candidate selection, contraindications, and indications for lung transplantation

Thalidomide inhibits the gene promoter of connective tissue growth factor in human embryonic lung fibroblasts

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