scholarly journals Improvement in Subjective Symptoms and Tolerability in Response to Nintedanib Treatment in Elderly Patients with Idiopathic Pulmonary Fibrosis

2020 ◽  
Vol 9 (3) ◽  
pp. 755 ◽  
Author(s):  
Takayuki Takeda ◽  
Yusuke Kunimatsu ◽  
Nozomi Tani ◽  
Izumi Hashimoto ◽  
Yuri Kurono ◽  
...  
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Elderly Patients ◽  
The Elderly ◽  
Subjective Assessment ◽  
Phase Iii ◽  
Disease Assessment ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Phase Iii Trials

The efficacy of nintedanib treatment in patients with idiopathic pulmonary fibrosis (IPF) was demonstrated in phase III trials. However, there is limited data on the significance of nintedanib in elderly patients aged ≥75 years. We have retrospectively evaluated 54 newly nintedanib-treated patients including 32 elderly individuals. Potential changes in modified medical research council (mMRC) grade and COPD (chronic obstructive pulmonary disease) assessment test (CAT) score, as well as in forced vital capacity (FVC) were obtained 6 months before, at the time of, and 6 and 12 months after initiation of nintedanib treatment. Significant differences were observed in CAT scores between 6 months before treatment and baseline (p < 0.001), and between baseline and 6 months (p < 0.001) and 12 months (p < 0.001) after treatment. If subjective improvement is defined as an improvement in mMRC grade or CAT score by 1 or 3 points, respectively, 25 patients (46.3%) have significantly improved after 6 months of treatment. Out of these, all have improved in CAT score. The tolerability of nintedanib was similar in elderly and younger patients. These findings suggest that CAT scores could be useful in the subjective assessment during nintedanib treatment, and that nintedanib is safe and efficient for the treatment of the elderly population.

scholarly journals Non-coding RNAs as Regulators of Cellular Senescence in Idiopathic Pulmonary Fibrosis and Chronic Obstructive Pulmonary Disease

2020 ◽  
Vol 7 ◽  
Author(s):  
Norihito Omote ◽  
Maor Sauler
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Pulmonary Disease ◽  
Cell Fate ◽  
Cellular Senescence ◽  
Cellular Stress ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Non Coding Rnas

Cellular senescence is a cell fate implicated in the pathogenesis of idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD). Cellular senescence occurs in response to cellular stressors such as oxidative stress, DNA damage, telomere shortening, and mitochondrial dysfunction. Whether these stresses induce cellular senescence or an alternative cell fate depends on the type and magnitude of cellular stress, but also on intrinsic factors regulating the cellular stress response. Non-coding RNAs, including both microRNAs and long non-coding RNAs, are key regulators of cellular stress responses and susceptibility to cellular senescence. In this review, we will discuss cellular mechanisms that contribute to senescence in IPF and COPD and highlight recent advances in our understanding of how these processes are influenced by non-coding RNAs. We will also discuss the potential therapeutic role for targeting non-coding RNAs to treat these chronic lung diseases.

scholarly journals Hallmarks of the ageing lung

2015 ◽  
Vol 45 (3) ◽  
pp. 807-827 ◽  
Author(s):  
Silke Meiners ◽  
Oliver Eickelberg ◽  
Melanie Königshoff
Keyword(s):  
Lung Cancer ◽  
Chronic Obstructive Pulmonary Disease ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Pulmonary Disease ◽  
Lung Diseases ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Specific Effects ◽  
Chronic Lung Diseases

Ageing is the main risk factor for major non-communicable chronic lung diseases, including chronic obstructive pulmonary disease, most forms of lung cancer and idiopathic pulmonary fibrosis. While the prevalence of these diseases continually increases with age, their respective incidence peaks at different times during the lifespan, suggesting specific effects of ageing on the onset and/or pathogenesis of chronic obstructive pulmonary disease, lung cancer and idiopathic pulmonary fibrosis. Recently, the nine hallmarks of ageing have been defined as cell-autonomous and non-autonomous pathways involved in ageing. Here, we review the available evidence for the involvement of each of these hallmarks in the pathogenesis of chronic obstructive pulmonary disease, lung cancer, or idiopathic pulmonary fibrosis. Importantly, we propose an additional hallmark, “dysregulation of the extracellular matrix”, which we argue acts as a crucial modifier of cell-autonomous changes and functions, and as a key feature of the above-mentioned lung diseases.

scholarly journals Comorbidity in idiopathic pulmonary fibrosis - what can biomarkers tell us?

2020 ◽  
Vol 14 ◽  
pp. 175346662091009 ◽  
Author(s):  
Tiago M. Alfaro ◽  
Carlos Robalo Cordeiro
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Clinical Manifestations ◽  
Premature Death ◽  
Sleep Apnoea ◽  
Significant Loss ◽  
Diagnostic Methods ◽  
Response To Treatment ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

Idiopathic pulmonary fibrosis (IPF) is characterized by progressive parenchymal scarring, leading to dyspnoea, respiratory failure and premature death. Although IPF is confined to the lungs, the importance of IPF comorbidities such as pulmonary hypertension and ischaemic heart disease, lung cancer, emphysema/chronic obstructive pulmonary disease, gastroesophageal reflux, sleep apnoea and depression has been increasingly recognized. These comorbidities may be associated with increased mortality and significant loss of quality of life, so their identification and management are vital. The development of good-quality biomarkers could lead to numerous gains in the management of these patients. Biomarkers can be used for the identification of predisposed individuals, early diagnosis, assessment of prognosis, selection of best treatment and assessment of response to treatment. However, the role of biomarkers for IPF comorbidities is still quite limited, and mostly based on evidence coming from populations without IPF. The future development of new biomarker studies could be informed by those that have been studied independently for each of these conditions. For now, clinicians should be mostly attentive to clinical manifestations of IPF comorbidities, and use validated diagnostic methods for diagnosis. As research on biomarkers of most common diseases continues, it is expected that useful biomarkers are developed for these diseases and then validated for IPF populations. The reviews of this paper are available via the supplemental material section.

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