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Literatura científica selecionada sobre o tema "Idiopathic pulmonary fibrosi"

Autor: Grafiati

Publicado: 14 de março de 2023

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Artigos de revistas sobre o assunto "Idiopathic pulmonary fibrosi"

Lettieri, Christopher J., Ganesh R. Veerappan, Donald L. Helman, Charles R. Mulligan e Andrew F. Shorr. "Safety of Surgical Lung Biopsy in Suspected Idiopathic Pulmonary Fibrosi". Chest 124, n.º 4 (janeiro de 2003): 116S. http://dx.doi.org/10.1378/chest.124.4_meetingabstracts.116s.

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Plataki, Maria, Anastassios Koutsopoulos, John Drossitis, George Delides, Nikolaos M. Siafakas e Demosthenes Bouros. "Expression of Apoptosis-Regulatory Genes in Epithelial Cells in Patients With Idiopathic Pulmonary Fibrosi". Chest 124, n.º 4 (janeiro de 2003): 192S. http://dx.doi.org/10.1378/chest.124.4_meetingabstracts.192s-b.

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Bell, Amanda M., Steven D. Nathan, Andrew F. Shorr, Scott D. Barnett e Donald L. Helman. "The Effect of Interferon Alone vs Interferon Plus Corticosteroids in Patients With Idiopathic Pulmonary Fibrosi". Chest 124, n.º 4 (janeiro de 2003): 117S. http://dx.doi.org/10.1378/chest.124.4_meetingabstracts.117s-a.

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NS, Mahesh, Sadanand C. D e Durga Lawande. "Clinical Profile of Idiopathic Pulmonary Fibrosis". Academia Journal of Medicine 2, n.º 2 (24 de julho de 2019): 86–89. http://dx.doi.org/10.21276/ajm.2019.2.2.22.

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N, Mahesh, Sadanand C. D e Durga Lawande. "Management of Idiopathic Pulmonary Fibrosis Cases at a Tertiary Care Hospital". Academia Journal of Medicine 2, n.º 2 (24 de julho de 2019): 90–95. http://dx.doi.org/10.21276/ajm.2019.2.2.23.

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Nakanishi, Yu, Yasushi Horimasu, Kakuhiro Yamaguchi, Shinjiro Sakamoto, Takeshi Masuda, Taku Nakashima, Shintaro Miyamoto et al. "IL-18 binding protein can be a prognostic biomarker for idiopathic pulmonary fibrosis". PLOS ONE 16, n.º 6 (4 de junho de 2021): e0252594. http://dx.doi.org/10.1371/journal.pone.0252594.

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Idiopathic pulmonary fibrosis is a chronic, fibrosing interstitial pneumonia that presents with various clinical courses and progression ranging from rapid to slow. To identify novel biomarkers that can support the diagnosis and/or prognostic prediction of idiopathic pulmonary fibrosis, we performed gene expression analysis, and the mRNA of interleukin-18 binding protein was increasingly expressed in patients with idiopathic pulmonary fibrosis compared with healthy controls. Therefore, we hypothesized that the interleukin-18 binding protein can serve as a diagnostic and/or prognostic biomarker for idiopathic pulmonary fibrosis. We investigated the expression of interleukin-18 binding protein in lung tissue, bronchoalveolar lavage fluid, and serum. Additionally, the correlation between interleukin-18 binding protein expression levels and the extent of fibrosis was investigated using mouse models of lung fibrosis induced by subcutaneous bleomycin injections. Serum interleukin-18 binding protein levels were significantly higher in idiopathic pulmonary fibrosis patients (5.06 ng/mL, interquartile range [IQR]: 4.20–6.35) than in healthy volunteers (3.31 ng/mL, IQR: 2.84–3.99) (p < 0.001). Multivariate logistic regression models revealed that the correlation between serum interleukin-18 binding protein levels and idiopathic pulmonary fibrosis was statistically independent after adjustment for age, sex, and smoking status. Multivariate Cox proportional hazard models revealed that serum interleukin-18 binding protein levels were predictive of idiopathic pulmonary fibrosis disease prognosis independent of other covariate factors (hazard ratio: 1.655, 95% confidence interval: 1.224–2.237, p = 0.001). We also demonstrated a significant positive correlation between lung hydroxyproline expression levels and interleukin-18 binding protein levels in bronchoalveolar lavage fluid from bleomycin-treated mice (Spearman r = 0.509, p = 0.004). These results indicate the utility of interleukin-18 binding protein as a novel prognostic biomarker for idiopathic pulmonary fibrosis.

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Gavrysyuk, V. K., Y. O. Dziublyk, E. O. Merenkova, O. V. Strafun e O. V. Bychenko. "PROGRESSIVE PULMONARY FIBROSIS IN LIGHT OF THE ATS/ERS/JRS/ALAT 2022 CLINICAL GUIDELINES". Ukrainian Pulmonology Journal 30, n.º 4 (2022): 51–57. http://dx.doi.org/10.31215/2306-4927-2022-30-4-51-57.

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Idiopathic pulmonary fibrosis – is a specific form of chronic, progressive, fibrosing interstitial pneumonia of unknown cause, which occurs primarily in 50 years and older patients, limited to the lungs, and is associated with the histopathologic and/or radiologic pattern of usual interstitial pneumonia (UIP). In 2000 American thoracic society (ATS) and European respiratory society (ERS) published the first international; statement on diagnosis and treatment of IPF American Thoracic Society, European Respiratory Society. Idiopathic pulmonary fibrosis: diagnosis and treatment. International consensus statement. In 2011 there was published a new statement on diagnosis and treatment of IPF, approved by Japan respiratory society (JTS) and Latin American thoracis society (ALTS) – An Official ATS/ERS/JRS/AL : Idiopathic Pulmonary Fibrosis: Evidence-based Guidelines for Diagnosis and Management. In 2015 section “Treatment” and in 2018 section “Diagnosis” were revised. It is known that in part of patients with such interstitial lung diseases (ILD) as idiopathic interstitial pneumonia, systemic sclerosis, pneumoconiosis, chronic hypersensitivity pneumonitis, sarcoidosis the disease may acquire a progressive uncontrolled development with the combination of symptoms called progressive pulmonary fibrosis (PPF). At the same time the results of successful use of antifibrotic therapy have been published recently (SENSCIS, INBUILD studies). All this provided the rationale for extended indications for use of antifibrotic therapy to cover other ILDs with the features of PPF. In this connection, ATS, ERS, JRS and ALAT experts published in May 2022 An Official ATS/ERS/JRS/ALAT Clinical Practice Guideline. Idiopathic Pulmonary Fibrosis (an Update) and Progressive Pulmonary Fibrosis in Adults, in which along with the partial changes regarding the principles of diagnosis and treatment of IPF, the definition, diagnosis criteria and management of PPF due to other fibrosing ILDs were presented. The article presents the major statements of new guideline regarding the terminology, diagnosis and treatment of PPF. Key words: progressive pulmonary fibrosis, definition, diagnosis criteria, treatment.

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Rawahi, Yasmeen. "Pirfenidone Experience in Idiopathic Pulmonary Fibrosis at a Tertiary Hospital in Oman". Journal of Thoracic Disease and Cardiothoracic Surgery 1, n.º 1 (12 de junho de 2020): 01–06. http://dx.doi.org/10.31579/2693-2156/001.

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Baddini-Martinez, José, Bruno Guedes Baldi, Cláudia Henrique da Costa, Sérgio Jezler, Mariana Silva Lima e Rogério Rufino. "Update on diagnosis and treatment of idiopathic pulmonary fibrosis". Jornal Brasileiro de Pneumologia 41, n.º 5 (outubro de 2015): 454–66. http://dx.doi.org/10.1590/s1806-37132015000000152.

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Idiopathic pulmonary fibrosis is a type of chronic fibrosing interstitial pneumonia, of unknown etiology, which is associated with a progressive decrease in pulmonary function and with high mortality rates. Interest in and knowledge of this disorder have grown substantially in recent years. In this review article, we broadly discuss distinct aspects related to the diagnosis and treatment of idiopathic pulmonary fibrosis. We list the current diagnostic criteria and describe the therapeutic approaches currently available, symptomatic treatments, the action of new drugs that are effective in slowing the decline in pulmonary function, and indications for lung transplantation.

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Averyanov, A. V., e V. N. Lesnyak. "FROM IDIOPATHIC FIBROSING ALVEOLITIS TO IDIOPATIC LUNGS FIBROSIS". Journal of Clinical Practice 7, n.º 4 (15 de dezembro de 2016): 58–65. http://dx.doi.org/10.17816/clinpract7458-65.

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The second part of the analytical review devoted to features of the clinical course and diagnosis of idiopathic pulmonary fibrosis. Special attention is paid to the specific CT symptoms allows diagnosis without lung biopsy. Current approaches to invasive diagnostics and perspectives of cryoprobe are discussed.

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Teses / dissertações sobre o assunto "Idiopathic pulmonary fibrosi"

Vuljan, Stefania Edith. "Idiopathic Pulmonary Fibrosis (IPF): tissue identification of crucial biomarkers by RNA-Sequencing approach". Doctoral thesis, Università degli studi di Padova, 2019. http://hdl.handle.net/11577/3422229.

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Background. Idiopathic pulmonary fibrosis (IPF) is one of the most common idiopathic interstitial lung diseases characterized by progressive lung scarring and a very poor overall prognosis with a median survival of 2-3 years. Despite extensive research efforts, the etiopathogenesis and pathophysiology of IPF are still little understood and consequently only slight improvement has been made for appropriate management and effective therapies. Some advances have been made in understanding the multiple interrelated pathogenic pathways underlying IPF and the disease is now considered to result from complex interactions among genetic, epigenetic, transcriptional, post-transcriptional, metabolic and environmental factors. Thus, the discovery and validation of theranostic biomarkers are necessary to enable a more precise and earlier diagnosis of IPF and to improve the prediction of future disease behavior. Usual interstitial pneumonia (UIP) is the histopathological pattern of IPF characterized by spatial/temporal heterogeneous histological lesions. Fibroblastic focus (FF) areas include fibroblasts and myofibroblasts arranged in a linear fashion with a pale staining matrix, with metaplastic epithelial cells lining on top of them. They are usually detected in the transitional area from dense scarring to normal lung and are considered an “active” component in IPF pathogenesis. Aim of the research. The main goal of the present PhD research project was the identification of crucial biomarkers in IPF pathogenesis by extracting RNA from FF areas (FF plus metaplastic epithelial cells lining FF). The main steps of the study were the following: 1) validation of a protocol for the isolation of FF areas by laser microdissection of formalin-fixed and paraffin-embedded (FFPE) tissues of IPF patients and controls; 2) total RNA extraction, quality and quantity evaluation; 3) creation of cDNA libraries starting from the extracted RNAs; 4) transcriptomic analysis by a Next-Generation Sequencing (NGS) approach (RNA-sequencing; RNA-Seq); 5) validation of the biomarker emerged from the transcriptomic analysis in a more extensive (retrospective) cases series using immunohistochemistry. Material and Methods. Total RNA was extracted from fibroblastic focus areas isolated with laser microdissection in 10 FFPE IPF lung tissues: 8 from lung transplanted patients and 2 from surgical biopsy. Microdissected fibroblastic focus areas from 2 patients with recurrent pneumothorax were also analyzed and considered as controls. The RNA was extracted using a modified protocol which provides an overnight tissue incubation at 43°C with 10 μl proteinase K. RNA was then preserved by adding RNase inhibitors at the end of the extraction procedure. This was a custom-made protocol (RNeasy® FFPE kit; Qiagen, Hilden, Germany) with additional procedures optimized during my PhD research study. The final RNAs quality and quantity were valuated with an Agilent RNA 6000 Pico Kit using a 2100 Bioanalyzer instrument. Quality was expressed as DV200 (percentage of RNA fragments > 200 nucleotides). Libraries were obtained with the SMARTer Stranded Total RNA-Seq Kit pico input mammalian of Takara Bio. DNA library was sequenced with a paired-end sequencing 2x150 bp on a HiSeq 4000 System sequencer of Illumina. MUC5B immunohistochemistry (clone 4A10-H2; 1:200, Novus Biologicals, Centennial, Colorado, USA) was performed in 44 interstitial lung disease (ILD) cases (39 UIP/IPF and 5 ILD with no UIP pattern) and 6 controls (5 spontaneous pneumothorax and 1 emphysema) following the antibody manufacturer's protocol using a Leica Bond-III Autostainer. Results. Considering the whole population the mean quantity of extracted RNA was 2992.8 pg/µl±2473 (mean ± SD), ranging from 840 pg/µl to 7530 pg/µl. Quality evaluation showed 42% of total cases with a medium/high quality (DV200>50%). In all cases molecular analyses were performed and final libraries were obtained with a concentration ranging from 3.4 to 22.6 ng/ul and a mean cDNA fragment length of 289 nucleotides. RNA-Seq analysis showed that 323 genes were differentially expressed in UIP/IPF cases than controls: 14 of them were up-regulated and 309 down-regulated. The most significant up-regulated gene was MUC5B, the other up-regulated genes were those involved in epithelial-to-mesenchymal transition (EMT) and epithelial carcinogenesis process. Gene Ontology Enrichment Analysis (GOEA) was performed to identify the most enriched Gene Ontology (GO) categories for the down-regulated genes. We found that extracellular matrix structure and organization were the principally down-regulated pathways. The overexpressed gene MUC5B was validated by immunohistochemistry. MUC5B was expressed only in IPF/UIP and ILDs, never in control group. The MUC5B expression was mainly detected in metaplastic epithelial cells lining: a) honeycomb areas, b) other alveolar spaces and c) in the metaplastic epithelial cells lining FF. Interestingly, a gradient of MUC5B expression was detected both in IPF/UIP and ILDs samples where MUC5B was overexpressed in lower lobes. Interestingly, MUC5B was overexpressed in upper and middle lobes of IPF/UIP compared with the same lobes of other ILDs. Conclusion. The principal results obtained from the present research study offer interesting insights into the complex molecular system signature of IPF: 1) adequate quantity and quality of RNA was extracted from microdissected FF areas of FFPE IPF lung tissues. The quantity/quality of RNA was suitable to create cDNA libraries for transcriptomic analysis by RNA-seq: this represents an important step forward in tissue molecular investigation of this disease characterized by high tissue heterogeneity. Only a very few papers in the literature have used lung FFPE tissue for molecular analysis, in particular, this molecular approach on specific affected IPF tissues has not previously used. 2) Comparative analysis performed on selected areas found an overexpression of epithelial proliferation/cancer progression and EMT transcripts: this highlights the crucial role of metaplastic epithelial cells that are the key actors also in the FF areas, considered the active injured lesion in IPF. 3) The up-regulated transcript MUC5B, validated also by immunohistochemistry, confirms the crucial role of this mucin in the disease. Indeed previous works, mainly performed in blood samples, had highlighted the importance of this gene in the disease. Selective regulation of MUC5B in experimental models could open up an entire line of investigation that could bring us closer to understanding regulation of MUC5B and providing novel therapeutic options.

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FRAGNI, DEBORA. "Identification of novel readouts to assess anti-fibrotic efficacy of new compounds in a bleomycin-induced pulmonary fibrosis mouse model". Doctoral thesis, Università di Siena, 2022. http://hdl.handle.net/11365/1190103.

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Idiopathic pulmonary fibrosis (IPF) is a fatal interstitial lung disease with a poor prognosis and very limited therapeutic options. To date, Pirfenidone and Nintedanib are the only two therapies approved for IPF worldwide. However, these drugs can slow-down lung function decline without really stopping or reverting the fibrotic process, and in addition their use is associated with a series of side effects. The incomplete understanding of the disease and the limitations of current treatments make IPF a disease with a high medical need requiring novel treatment approaches. For these reasons, the new drugs coming from the research and development pipelines will be crucial to get new treatments for patients. Despite widely used, the current animal models of IPF need to be improved in order to be as much predictive as possible in identifying new promising treatments for pulmonary fibrosis. One of the most challenging aspects of drug discovery for IPF is the identification of new therapies that can be translated effectively to the clinic, implying that very few compounds that have shown efficacy in animal models have been successful in human clinical trials and concluding that most of the preclinical models are poorly predictive and scarcely resembling the human disease. Currently the majority of new drugs investigated in preclinical models of IPF are dosed using a prophylactic dosing regimen, whereas patients are almost always treated after the fibrosis is well established. Moreover, the most popular endpoints examined in preclinical models of IPF are histological scoring and lung collagen content; however, lung function tests are more commonly used as primary endpoints in IPF patients. In this scenario, considering the high unmet medical need and some limits that the preclinical research has to face, the main goal of this PhD project was to generate a robust and reliable preclinical model of pulmonary fibrosis, introducing novel readouts, suitable to select and to identify new pharmacological treatments for IPF with an higher translational potential. The approach pursued by this study could be very impactful to identify new potential treatments for IPF. To achieve the goal of this PhD project, performed in collaboration with Chiesi Farmaceutici, we (1) reproduced the most described preclinical model for IPF, the bleomycin (BLM)-induced pulmonary fibrosis mouse model by intratracheal (IT) administration, and we analyzed its main limitations; (2) looking at the clinic, we optimized the BLM model with the introduction of clinically more relevant parameters (i.e., lung function tests, lung imaging, oximetry (Sp02), and fibrotic biomarkers) through a new BLM oropharyngeal (OA) protocol and finally, (3) we explored the added value of these more relevant readouts by investigating the efficacy of Nintedanib, which was tested under therapeutic regimen. The characterization of the BLM IT model proved to be useful in better understanding the development of BLM-induced lung fibrosis and allowed to define the therapeutic protocol to test the anti-fibrotic efficacy of Nintedanib in the model; however, it highlighted several limitations such as a patchy distribution of fibrotic lesions and poor sensitivity to pharmacological treatment using the two traditional preclinical readouts, histology and hydoxyproline (Hyp) lung content. Those limitations were overcome by the use of the OA administration of BLM which led to a more homogeneous fibrosis throughout the lung lobes and by the introduction of more clinically relevant endpoints such as micro-computer tomography (CT) imaging and lung function measurements that are the same tests used to diagnose and monitor patients with IPF, as well as of emerging biomarkers currently under evaluation in the clinical setting, with the final aim to create a link between the preclinical model and the clinical practice. All these new readouts showed the same profile over time observed with histology in terms of development of fibrotic disease, and Nintedanib was able to significantly modulate them, confirming their relevance for monitoring lung fibrosis as well as the efficacy of new treatments. Among them, the measurement of lung function, in particular the forced vital capacity (FVC), demonstrated to be the most sensitive readout to assess the compounds efficacy and was selected also in our preclinical studies as the primary endpoint as for clinical trials, thus creating an important link between the preclinical model and the clinical setting. In addition, we also worked to refine the histological analysis which still remains an important complementary evaluation to be coupled to the functional readouts. Currently the common histological analysis utilized in preclinical models of lung fibrosis is represented by the Ashcroft scoring system, which revealed some disadvantages such as a time-consuming process, operator-dependent results, limited sensitivity and, most critical, inability to get a direct link to clinics. Therefore, we introduced an automated image analysis by using an artificial intelligence (AI) approach, which improved this analysis recognizing histological features with more accuracy and consistency, reducing significantly the time of the analysis and making the evaluation independent from the operator. In summary, this project demonstrated that in the mouse BLM-induced lung fibrosis model it has been possible to explore the same clinically relevant parameters used in IPF patients; in particular lung function tests such as FVC, that for its high translational value together with the high sensitivity to assess the efficacy of the compounds has been chosen as the primary endpoint to support the selection of novel treatments within our internal drug discovery IPF projects. Furthermore, the introduction of these different readouts, that all go to the same direction, has from one side increased the robustness of the model and from the other side has allowed to bring this preclinical model to a level of complexity that mirrors the one observed in human IPF. Overall, this PhD work has enhanced the translational value of the data obtained with the mouse BLM model increasing the chance of selecting promising compounds to advance to clinical trials and has concretely led to significant benefits to drug discovery process in the IPF research, improving the quality and the reliability of the search of novel anti-fibrotic drugs.

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Fahim, Ahmed. "The pathogenesis of idiopathic pulmonary fibrosis". Thesis, University of Hull, 2011. http://hydra.hull.ac.uk/resources/hull:5296.

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Idiopathic pulmonary fibrosis (IPF) is a restrictive pulmonary disorder of unknown aetiology with a relentless disease course and a median survival of 3 years after the diagnosis. It is the most common idiopathic interstitial lung disease (ILD) with a basal and peripheral predominance associated with temporal and geographical heterogeneity. As the pathogenesis of this disease is poorly understood, the aim of this work was to investigate the pathobiology of IPF in a prospective manner. There is evidence of a strong association of gastro-esophageal reflux and vascular disease with IPF. Moreover, a proportion of patients have evidence of immunological antibodies without any evidence of connective tissue or autoimmune disease. The data presented in this thesis suggest that platelet-monocyte complexes may be involved in the pathogenesis of IPF at molecular level as suggested by the flow cytometric data utilizing monoclonal antibodies to platelets (CD42a) and monocytes (CD14). Moreover, expression of CD40L, P-selectin and PSGL-1 on platelets and subpopulation of leukocytes suggested that platelet expression of these molecules is not significantly different in IPF as compared to ILD other than IPF or non-ILD controls. Furthermore, platelet mediated injury hypothesis is supported by significant elevation of platelet endothelial cell adhesion molecule in plasma of IPF patients. Reflux of gastric secretions into the tracheo-bronchial tree is another attractive hypothesis in light of remarkably high prevalence of gastro-esophageal reflux disease (GERD) in IPF. The data suggest that patients with IPF have significantly higher gastro and extra-esophageal reflux symptoms when assessed by Hull airway reflux questionnaire (HARQ). However, there was a lack of objective evidence of extra-esophageal reflux measured by exhaled breath pepsin concentration or significantly higher prevalence of Helicobacter Pylori. Furthermore, there was evidence of immune mediated injury in IPF by indirect immunofluorescence study of alveolar epithelial (A549) cells as significant membranous enhancement of A549 cells by anti-IgG antibodies was demonstrated in IPF patients’ sera. However, Human umbilical vein endothelial cells (HUVEC) did not show any differential staining pattern with either anti-IgG or IgM. Hence, there is a suggestion of alveolar epithelial disruption mediated by immune mechanisms with a predominant involvement of IgG antibodies. Furthermore, epithelial derangement may extend into the respiratory epithelium with release of carcinoembryonic antigen (CEA) in peripheral circulation as evidenced by a significant correlation of raised CEA level and lung function impairment in IPF. These findings provide clinical and molecular evidence of novel mechanisms of pathogenesis of IPF with increased platelet-monocyte aggregation. Moreover, immune mediated alveolar epithelial dysfunction involving IgG antibodies may provide further insight into the understanding of the pathogenesis and natural history of this fibrotic disease.

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Jo, Helen Eun-Ae. "Predicting Prognosis in Idiopathic Pulmonary Fibrosis". Thesis, The University of Sydney, 2018. http://hdl.handle.net/2123/20029.

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Idiopathic pulmonary fibrosis (IPF) is a specific fibrosing, interstitial lung disease (ILD) of unknown aetiology. In recent years, immunosuppressive therapy, used for the treatment of a majority of ILDs has been shown to be harmful in IPF, while new antifibrotic treatments that can slow IPF progression have become widely available. The accurate distinction of IPF from other ILDs has therefore become of utmost importance as it has important managements and prognostic implications. While the prognosis of IPF is universally poor with a median survival of only 3-5 years, the disease course is heterogeneous with some patients having rapidly progressive disease, while other have slow progression. In many patients, there are periods of stability interspersed with periods of rapid progression however at present, it is not possible to predict a patient’s disease course. The main objective of this thesis is to find factors that predict the prognosis in patients with IPF. In order to achieve this objective, this thesis is divided into two main sections. In the first section, we concentrate on the ILD multidisciplinary meeting (MDM). The diagnosis of IPF can often be challenging as it shares many clinical, radiological and histopathological features with the other ILDs. A multidisciplinary discussion between clinicians, radiologist and histopathologists is therefore recommended for accurate diagnosis. Unfortunately, there is no “gold standard” for IPF diagnosis and while significant emphasis is placed on the importance of the ILD MDM, there is little to actually guide the structure and function, or to standardise the output of this diagnostic process. In Chapter 2 of this thesis, we survey expert ILD MDMs internationally to assess current practices and find features common to most MDMs. We also assess features that differ and may potentially result in bias and thus inconsistencies in the performance of ILD MDMs. We introduce suggestions based on our findings that may be core features to the development of MDMs (presence of core clinical groups, structure and frequency of meetings) and areas that require consideration and further assessment as to their potential impact. In Chapter 3, we assess the impact of the ILD multidisciplinary service at 2 Australian centres and find there is a significant impact on IPF diagnosis and thus subsequent management. This section of the thesis therefore highlights the fact that before we can explore features that predict prognosis in IPF, we must also improve methods by which IPF is diagnosed as this can be difficult and result in inaccuracies when predicting prognosis and instituting therapies for IPF. In Chapters 4 to 8 of this thesis we concentrate on clinical, physiological and radiological factors that predict prognosis in IPF patients. Using the Australian IPF Registry, we find that more severe physiological impairment, as well as higher symptoms scores at baseline are associated with worse prognosis. We also find however, that the progression of disease in patients with mild physiological impairment, measured as an annual decline in FVC % predicted, is the same in those with mild and more severe impairment. This suggests that the worse prognosis in those with greater physiological impairment may be related to patients being at a later stage of IPF disease. We also find that the presence of honeycombing on radiology, but not the classification of the radiological UIP pattern, predicts poorer prognosis and that the presence or treatment of gastroesophageal reflux disease has no impact of IPF outcomes. Overall, this thesis has contributed to the field by highlighting the impact of the ILD MDM and assessing features that may contribute to accuracy of diagnosis and subsequent prognosis of IPF. We also found factors that predict IPF prognosis in real-world cohorts. While these results are useful and at times, reinforce factors that have been found in other IPF cohorts, the ability to accurately diagnose and predict the IPF course of an individual patient remains elusive. Further studies, particularly focusing on the pathobiology of IPF and translation to potential biomarkers are needed in order to improve and refine our understanding of the factors that predict prognosis in IPF.

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Hutchinson, Nicola-Xan. "Studies of cough in Idiopathic Pulmonary Fibrosis". Thesis, Cardiff University, 2016. http://orca.cf.ac.uk/94471/.

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A dry cough is a common symptom described in patients with IPF and impairs quality of life. The exact mechanisms causing cough in IPF remain unclear, however there is evidence that altered cough neurophysiology and sensitisation plays a roleY IPF patients have an enhanced cough reflex sensitivity to the inhalation of capsaicin. It was hypothesised that IPF patients have increased airway expression of the capsaicin receptor TRPVF1 and a coFexpressed receptor TRPAF1. Bronchial biopsies were obtained in 16 IPF patients, 11 chronic cough patients and 8 controls. Quantitative PCR was used to detect TRPVF1 and TRPAF1 gene expression, with immunohistochemistry demonstrating protein expression. Mean TRPVF1 and TRPAF1 gene expression was higher in IPF patients compared with controls, but the difference did not reach statistical significance. Immunostaining supported these findings. Gastroesophageal reflux is common in IPF patients and has also been implicated. An inFvitro study using cultured pulmonary epithelial cells was conducted to assess the expression of these receptors in a cell model of gastric reflux. TRPVF1 and TRPAF1 gene expression was demonstrated in pulmonary epithelial cells of bronchial and alveolar origin. No significant difference in receptor expression level was seen in either cell line when exposed to the major constituents of gastric refluxate. This study suggests that a structural upFregulation of central airway TRP receptors is not the key mechanism for cough in IPF patients. Similarly, it does not support the role of the individual constituents of gastric refluxate resulting in cough hypersensitivity through a physical upFregulation of receptors in pulmonary epithelial cells. Overall this thesis outlines the complexity of the cough reflex. It is probable that cough in IPF results from the cumulative manifestation of various physiological changes and mechanisms.

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Hutchinson, John. "International comparative epidemiology of idiopathic pulmonary fibrosis". Thesis, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/40715/.

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Background Evidence from the UK suggests the incidence of idiopathic pulmonary fibrosis is increasing, but there is a lack of data from elsewhere in the World. The cause of the disease remains unknown. New anti-fibrotic therapies may increase the use of surgical lung biopsy for accurate diagnosis, although the risks of this (and other surgery) are not clear. Methods Collated international mortality statistics and a systematic review of the literature were used to assess the incidence and mortality of idiopathic pulmonary fibrosis worldwide. Primary care data from the United Kingdom were used to assess the association between recent major surgery and a new diagnosis of idiopathic pulmonary fibrosis. Secondary care data from the United States and United Kingdom were used to assess the risk of surgical lung biopsy for the diagnosis of interstitial lung disease, and the risk of other major surgery in those with idiopathic pulmonary fibrosis. Results Mortality from idiopathic pulmonary fibrosis in increasing steadily worldwide. Incidence varies worldwide but is in the range of 3-9 per 100,000 in the West. No association was identified between recent major surgery and a new diagnosis of idiopathic pulmonary fibrosis. Surgical lung biopsy for the diagnosis of interstitial lung disease has an in-hospital mortality of under 2% for elective procedures, but this is higher for non-elective surgery, and in those who are older with co-morbidities. In those with idiopathic pulmonary fibrosis undergoing major surgery, in-hospital mortality was higher than the general population. Conclusion Idiopathic pulmonary fibrosis seems to be increasingly common worldwide. Surgery has risks, particularly in unwell older patients, and less invasive diagnostic methods are needed.

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Luk, Sheung Fung Simon. "Alveolar macrophage heterogeneity in idiopathic pulmonary fibrosis". Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/29433.

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Idiopathic Pulmonary Fibrosis (IPF) involves excess extracellular matrix (ECM) deposition within the lung interstitium, caused by non-resolving chronic inflammation and dysregulated repair. Alveolar macrophage (AMφ) may contribute to IPF through releasing various mediators by different subsets, investigated here in vitro, and ex vivo using a mouse model of bleomycin (BLM)-induced pulmonary fibrosis. The role of foamy AMφ in the reported increased susceptibility of Hermansky Pudlak Syndrome (HPS) 1 mice to BLM-induced pulmonary fibrosis was also assessed. Novel characterisation studies revealed that terminally differentiated AMφ are inducible into M1-like [nitric oxide synthase 2 (NOS2)hi interleukin (IL)-1βhi IL-12 p40 (total)hi major histocompatibility protein (MHC)-IIhi mannose receptor C, type 1 (MRC1)-] or M2-like [Arginase 1 (Arg1)hi Fibronectinhi IGF-1hi MHC-IIlo MRC1-/+] phenotypes following IFN-γ or IL-13 priming respectively. Lipopolysccharide (LPS) altered these AMφ subset phenotypes. AMφ heterogeneity in a novel multiple oropharyngeal dose, BLM-induced pulmonary fibrosis was evaluated from days 7 to 21. Accumulation of M1-like AMφ at day 7, and M1/M2-hybrid AMφ [Arg1hi IL-12 p40 (total)hi fibronectinhi MHC-IIlo MRC1-/+] from days 7 to 21, may promote inflammation and fibrosis respectively. Toll-like Receptor (TLR) 9 messenger ribonucleic acid (mRNA) and TLR2 surface protein, and both TLRs2 and 9 ex vivo activities were increased in BLM-challenged mice from days 7 to 21, suggesting their roles in inflammation and fibrosis. Foamy AMφ accumulated in BLM-induced pulmonary fibrosis, and their potential role in the reported increased susceptibility to BLM-induced pulmonary fibrosis of HPS1 mice was evaluated. BLM-challenged HPS1 mice (days 7-21) had increased weight loss indicating reduced BLM tolerance from days 7 to 11, but little/no difference in collagen accumulation, suggesting that reduced BLM tolerance is not correlated with increased pulmonary fibrosis. In conclusion AMφ alter their phenotype in response to their environment that contributes to different stages of BLM-induced pulmonary fibrosis. Reduced BLM tolerance in HPS1 mice is not correlated with increased pulmonary fibrosis.

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Maduli, Elvis. "Polypharmacology approaches for treatment of idiopathic pulmonary fibrosis". Thesis, University of Sheffield, 2016. http://etheses.whiterose.ac.uk/15540/.

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Patrucco, Filippo. "Idiopathic pulmonary fibrosis: from monocyte and macrophage inflammation to a novel, non-invasive measurement of pulmonary density". Doctoral thesis, Università del Piemonte Orientale, 2022. http://hdl.handle.net/11579/144064.

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The anti-fibrotic drug nintedanib (NTD) has been approved for the management of Idiopathic Pulmonary Fibrosis (IPF), a rare progressive interstitial lung disease. Monocytes/macrophages and alveolar macrophages have been demonstrated to contribute to the wound healing process, promoting inflammation and collagen deposition. Aim: We intend to evaluate the effects of NTD on phenotype and responsiveness of monocytes/macrophages isolated from IPF patients before (TO) and after 3 months of treatment (T1) with the drug. In this thesis the results obtained from patients at TO will be showed. Samples from healthy volunteers and from patients will be challenged in vitro with NTD. Methods: Monocytes were isolated from peripheral blood and differentiated into M1 and M2 macrophages; cell viability, superoxide anion production and surface markers expression were evaluated. Results: we included 10 IPF patients and 5 healthy volunteers. For in vitro experiments, we used increasing concentrations of NTD up to the highest of 15nM. In monocytes from both healthy volunteers and patients NTD reduced the basal production of superoxide anion and at 15nM the effect was similar in both populations. After NTD treatment we observed a reduction of non classical monocytes percentage, with a relative reduction of classical monocytes. NTD did not significantly affect the basal 02- production in M1 neither in M2, but it reduced in a dose dependent manner the PMA-induced burst in both macrophage populations. Among surface markers' expression, we observed a reduction of CD206 in M2 macrophages of IPF subjects after NTD stimulation. Conclusions: Our results could build the basis to verify if in IPF patients monocyte production of oxidative stress would influence macrophages polarization, and to support the antifibrotic effects of NTB also by the reduction of CD206 profibrotic marker expression in M2 cells.

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Duffy, Emma. "Approaches to lead generation for idiopathic pulmonary fibrosis targets". Thesis, University of Strathclyde, 2016. http://digitool.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=27489.

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Livros sobre o assunto "Idiopathic pulmonary fibrosi"

Meyer, Keith C., e Steven D. Nathan, eds. Idiopathic Pulmonary Fibrosis. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-99975-3.

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Meyer, Keith C., e Steven D. Nathan, eds. Idiopathic Pulmonary Fibrosis. Totowa, NJ: Humana Press, 2014. http://dx.doi.org/10.1007/978-1-62703-682-5.

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Nakamura, Hiroyuki, e Kazutetsu Aoshiba, eds. Idiopathic Pulmonary Fibrosis. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55582-7.

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P, Lynch Joseph, ed. Idiopathic pulmonary fibrosis. New York: Marcel Dekker, 2004.

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Nathan, Steven D., A. Whitney Brown e Christopher S. King. Guide to Clinical Management of Idiopathic Pulmonary Fibrosis. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32794-5.

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He breathes again: A true and amazing narrative of survival from an incurable lung disease. [Sri Lanka}: publisher not identified, 2015.

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Lynch, Joseph, ed. Idiopathic Pulmonary Fibrosis. CRC Press, 2003. http://dx.doi.org/10.1201/b14211.

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Idiopathic Pulmonary Fibrosis. Elsevier, 2019. http://dx.doi.org/10.1016/c2016-0-04562-x.

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Costabel, Ulrich, Bruno Crestani e Athol U. Wells, eds. Idiopathic Pulmonary Fibrosis. European Respiratory Society, 2016. http://dx.doi.org/10.1183/2312508x.erm7116.

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Ross, Clare, e Athol Wells. Idiopathic pulmonary fibrosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199657742.003.0010.

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Interstitial lung diseases are a complex heterogeneous group which are challenging to diagnose and treat. The diagnosis of idiopathic pulmonary fibrosis, as opposed to connective tissue interstitial lung disease, is important, as treatments and prognoses are very different. This chapter focusses on a case where this diagnosis is challenging. The evidence for the treatment of idiopathic pulmonary fibrosis is reviewed, in light of recent trials and new recommendations.

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Capítulos de livros sobre o assunto "Idiopathic pulmonary fibrosi"

Wells, Athol U., e Simon Ward. "Pulmonary Function Tests in Idiopathic Pulmonary Fibrosis". In Idiopathic Pulmonary Fibrosis, 103–21. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-682-5_6.

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Abe, Shinji, e Akihiko Gemma. "Definition of IPF". In Idiopathic Pulmonary Fibrosis, 3–9. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55582-7_1.

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Bando, Masashi. "Pharmacotherapy of IPF (Corticosteroids, Immunosuppressants, Etc.)". In Idiopathic Pulmonary Fibrosis, 161–70. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55582-7_10.

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Umeda, Yukihiro, Tamotsu Ishizuka e Takeshi Ishizaki. "Non-pharmacological Therapy for IPF". In Idiopathic Pulmonary Fibrosis, 171–88. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55582-7_11.

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Itoh, Masayuki. "Pharmacotherapy of Acute Exacerbation of IPF (Corticosteroids, Immunosuppressants, and Direct Hemoperfusion with Polymyxin)". In Idiopathic Pulmonary Fibrosis, 189–201. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55582-7_12.

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Morio, Yoshiteru, e Kazuhisa Takahashi. "Combined Pulmonary Fibrosis and Emphysema (CPFE)". In Idiopathic Pulmonary Fibrosis, 205–15. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55582-7_13.

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Koyama, Nobuyuki. "Common Pathways in IPF and Lung Cancer". In Idiopathic Pulmonary Fibrosis, 217–47. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55582-7_14.

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Date, Hiroshi. "Acute Exacerbation of Interstitial Pneumonia After Pulmonary Resection for Lung Cancer". In Idiopathic Pulmonary Fibrosis, 249–59. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55582-7_15.

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Kuwano, Kazuyoshi, Jun Araya e Hiromichi Hara. "Epidemiology and Risk Factors of IPF". In Idiopathic Pulmonary Fibrosis, 11–25. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55582-7_2.

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Ishii, Yoshiki. "Acute Exacerbation of IPF". In Idiopathic Pulmonary Fibrosis, 27–42. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55582-7_3.

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Trabalhos de conferências sobre o assunto "Idiopathic pulmonary fibrosi"

Hariri, Lida P., David C. Adams, Thomas V. Colby, Andrew M. Tager e Melissa J. Suter. "Assessing idiopathic pulmonary fibrosis (IPF) with bronchoscopic OCT (Conference Presentation)". In Optical Techniques in Pulmonary Medicine III, editado por Melissa J. Suter, Stephen Lam e Matthew Brenner. SPIE, 2016. http://dx.doi.org/10.1117/12.2214663.

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Justet, Aurélien, Mada Ghanem, Madeleine Jaillet, Mouna Hachem, Tiara Boghanim, Aurélie Vadel, Arnaud Mailleux e Bruno Crestani. "FGFR4 has pro fibrotic properties in Idiopathic Pulmonary Fibrosis". In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.3359.

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Mendes de Moraes, F. G., F. Anselmo, L. F. Faria, M. C. Lopes, B. Rangel, E. Bessa, R. Rufino e C. H. Costa. "Comorbidities in Idiopathic Pulmonary Fibrosis". In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3368.

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Juan Samper, Gustavo, Cristina Sabater Abad, Susana Torres Martinez, Estrella Fernández-Fabrellas, Vanessa Jaimes Diaz, Esther Verdejo Mengual e Silvia Calabuig Fariñas. "Angiogenesis in idiopathic pulmonary fibrosis". In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.828.

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Kizhikkilot, Venugopal. "Idiopathic Pulmonary Fibrosis & Curcumin". In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1531.

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Drakopanagiotakis, Fotios, Franziska Rösner, Carlo Vancheri, Philippe Bonniaud, Athol Wells, Jasmin Wagner, Bruno Crestani e Andreas Guenther. "Non-pulmonary comorbidities in idiopathic pulmonary fibrosis". In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2036.

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Hasaneen, Nadia, Tuong Vu, Timothy Fusiak, Hussein Foda, Rany Condos e Gerald Smaldone. "Anti-fibrotic role of inhaled interferon-γ in idiopathic pulmonary fibrosis". In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2034.

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Baba, T., T. Ogura, E. Hagiwara, J. Shiihara, A. Sekine, A. Matsushima, N. Tsuchiya et al. "Comparison of Clinical Features between Familial Idiopathic Pulmonary Fibrosis and Non-Familial Idiopathic Pulmonary Fibrosis." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2980.

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Kang, V., e K. Jordan. "Idiopathic Pulmonary Fibrosis Concealing Lung Adenocarcinoma". In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6347.

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Aouadi, Samira, sabrine majdoub, najla ghrairi, emna brahem, houda gharsalli, sonia maalej e leila douik elgharbi. "Bronchoalveolar lavage in idiopathic pulmonary fibrosis". In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa3811.

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Relatórios de organizações sobre o assunto "Idiopathic pulmonary fibrosi"

Barros-Poblete, Marisol, Rodrigo Torres-Castro, Mauricio Henríquez, Anita Guequen, Isabel Blanco e Carlos Flores. Dysbiosis as a prognostic factor for clinical worsening in chronic respiratory disease: A systematic review and metanalysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, abril de 2022. http://dx.doi.org/10.37766/inplasy2022.4.0089.

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Review question / Objective: Is dysbiosis a prognostic factor for clinical worsening in patients with chronic respiratory diseases?. Condition being studied: Dysbiosis, defined as changes in the quantitative and qualitative composition of the microbiota. Eligibility criteria: Over 18 years old adult patients with chronic respiratory diseases clinical diagnosis (cystic fibrosis, chronic obstructive pulmonary disease, asthma, idiopathic pulmonary fibrosis, interstitial lung disease, sarcoidosis, bronchiectasis, non-CF bronchiectasis, pulmonary hypertension) according to the International Statistical Classification of Diseases and Related Health Problems (ICD) from OMS) and international guidelines of each disease.

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Hu, Yuqi, Chenyang Lv, Xiaonan Wang, Xiaowan Zhao e Ai Cui. The prognosis and its clinical predictors of combined pulmonary fibrosis and emphysema comparison with idiopathic pulmonary fibrosis: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, outubro de 2022. http://dx.doi.org/10.37766/inplasy2022.10.0081.

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Di, Jiaqi, Xuanlin Li, Jingjing Yang, Luguang Li e Xueqing Yu. Critical appraisal of the reporting quality of risk prediction models for idiopathic pulmonary fibrosis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, novembro de 2020. http://dx.doi.org/10.37766/inplasy2020.11.0105.

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Zhang, Haoyang, Lijian Pang, Xiaodong Lv, Weidong Zheng, Ningzi Zang, Quan Yuan e Ling Lv. The effectiveness and safety of Chinese herbal formula for idiopathic pulmonary fibrosis: an overview of systematic reviews. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, fevereiro de 2021. http://dx.doi.org/10.37766/inplasy2021.2.0012.

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Wu, Zenan, Liangji Liu, Siwen Ke e Wei Zhu. The Baduanjin Mind-Body training improve the pulmonary functiont of patients with idiopathic pulmonary fibrosis(IPF): a protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, setembro de 2021. http://dx.doi.org/10.37766/inplasy2021.9.0071.

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Zhang, Haoyang, Lijian Pang, Xiaodong Lv, Chuang Liu e Minghua Nan. Multiple Traditional Chinese Medicine interventions for idiopathic pulmonary fibrosis: a protocol for systematic review and meta analysis of overview. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, agosto de 2020. http://dx.doi.org/10.37766/inplasy2020.8.0110.

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Wang, Liyuan, Baihua Jiang, Tianyang Yu e Yanpeng Xie. Clinical efficacy and safety of Huoxue Huayu method in the treatment of idiopathic pulmonary fibrosis A protocol for systemic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, abril de 2022. http://dx.doi.org/10.37766/inplasy2022.4.0056.

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