Gotowe bibliografie tematyczne / Acute exacerbation of interstitial lung diseases

Spis treści

  1. Artykuły w czasopismach
  2. Rozprawy doktorskie
  3. Książki
  4. Części książek
  5. Streszczenia konferencji
  6. Raporty organizacyjne

Gotowa bibliografia na temat „Acute exacerbation of interstitial lung diseases”

Autor: Grafiati
Data publikacji: 21 września 2024

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Artykuły w czasopismach na temat "Acute exacerbation of interstitial lung diseases"

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Aritonang, Rachel S., Fanny Fachrucha, Mia Elhidsi i Ginanjar Arum Desianti. "Oxygen Therapy in Exacerbation of Interstitial Lung Disease". Respiratory Science 4, nr 3 (28.06.2024): 221–31. http://dx.doi.org/10.36497/respirsci.v4i3.129.

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Interstitial lung diseases (ILD) are a group of diseases that involve damage in the interstitial tissue, causing diffusion disorders which ultimately lead to hypoxemia. One of the conditions that aggravate hypoxemia in ILD patients is acute exacerbation. Acute exacerbation is a condition of deterioration of ILD that can occur in less than 1 month. During an acute exacerbation, there will be a worsening of the HRCT pattern with increased ground glass opacities and a worsening of the clinical picture including hypoxemia. Acute exacerbations are closely related to increased mortality rates. Oxygen administration is one of the supportive therapies that can be given to acute exacerbations. The provision of oxygen therapy is adjusted to the patient's needs using a high-flow nasal cannula, non-invasive ventilation, invasive mechanical ventilation, and extracorporeal membrane oxygenation.
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Kolb, Martin, Benjamin Bondue, Alberto Pesci, Yasunari Miyazaki, Jin Woo Song, Nitin Y. Bhatt, John T. Huggins i in. "Acute exacerbations of progressive-fibrosing interstitial lung diseases". European Respiratory Review 27, nr 150 (21.12.2018): 180071. http://dx.doi.org/10.1183/16000617.0071-2018.

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Acute exacerbation of interstitial lung disease (ILD) is associated with a poor prognosis and high mortality. Numerous studies have documented acute exacerbation in idiopathic pulmonary fibrosis (IPF), but less is known about these events in other ILDs that may present a progressive-fibrosing phenotype. We propose defining acute exacerbation as an acute, clinically significant respiratory deterioration, typically less than 1 month in duration, together with computerised tomography imaging showing new bilateral glass opacity and/or consolidation superimposed on a background pattern consistent with fibrosing ILDs. Drawing on observations in IPF, it is suspected that epithelial injury or proliferation and autoimmunity are risk factors for acute exacerbation in ILDs that may present a progressive-fibrosing phenotype, but further studies are required. Current acute exacerbation management strategies are based on recommendations in IPF, but no randomised controlled trials of acute exacerbation management have been performed. Although there are no formal strategies to prevent the development of acute exacerbation, possible approaches include antifibrotic drugs (such as nintedanib and pirfenidone), and minimising exposure to infection, airborne irritants and pollutants. This review discusses the current knowledge of acute exacerbation of ILDs that may present a progressive-fibrosing phenotype and acknowledges limitations of the data available.
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Abo Elwafa, GihanS, NaglaaB Ahmed, AmanyA Abou Zeid i MaiA Abo Elhasab. "Noninvasive ventilation in acute exacerbation of interstitial lung diseases". Egyptian Journal of Chest Diseases and Tuberculosis 72, nr 1 (2023): 99. http://dx.doi.org/10.4103/ecdt.ecdt_40_22.

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Drakopanagiotakis, Fotios, Philipp Markart i Paschalis Steiropoulos. "Acute Exacerbations of Interstitial Lung Diseases: Focus on Biomarkers". International Journal of Molecular Sciences 24, nr 12 (15.06.2023): 10196. http://dx.doi.org/10.3390/ijms241210196.

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Interstitial lung diseases (ILDs) are a large group of pulmonary disorders characterized histologically by the cardinal involvement of the pulmonary interstitium. The prototype of ILDs is idiopathic pulmonary fibrosis (IPF), an incurable disease characterized by progressive distortion and loss of normal lung architecture through unchecked collagen deposition. Acute exacerbations are dramatic events during the clinical course of ILDs, associated with high morbidity and mortality. Infections, microaspiration, and advanced lung disease might be involved in the pathogenesis of acute exacerbations. Despite clinical scores, the prediction of the onset and outcome of acute exacerbations is still inaccurate. Biomarkers are necessary to characterize acute exacerbations better. We review the evidence for alveolar epithelial cell, fibropoliferation, and immunity molecules as potential biomarkers for acute exacerbations of interstitial lung disease.
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Drakopanagiotakis, Fotios, Ekaterina Krauss, Ira Michailidou, Vasileios Drosos, Stavros Anevlavis, Andreas Günther i Paschalis Steiropoulos. "Lung Cancer and Interstitial Lung Diseases". Cancers 16, nr 16 (13.08.2024): 2837. http://dx.doi.org/10.3390/cancers16162837.

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Lung cancer continues to be one of the leading causes of cancer-related death worldwide. There is evidence of a complex interplay between lung cancer and interstitial lung disease (ILD), affecting disease progression, management strategies, and patient outcomes. Both conditions develop as the result of common risk factors such as smoking, environmental exposures, and genetic predispositions. The presence of ILD poses diagnostic and therapeutic challenges in lung cancer management, including difficulties in interpreting radiological findings and increased susceptibility to treatment-related toxicities, such as acute exacerbation of ILD after surgery and pneumonitis after radiation therapy and immunotherapy. Moreover, due to the lack of large, phase III randomized controlled trials, the evidence-based therapeutic options for patients with ILDs and lung cancer remain limited. Antifibrotic treatment may help prevent pulmonary toxicity due to lung cancer treatment, but its effect is still unclear. Emerging diagnostic modalities and biomarkers and optimizing personalized treatment strategies are essential to improve outcomes in this patient population.
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Matsunashi, Atsushi, Kazuma Nagata, Takeshi Morimoto i Keisuke Tomii. "Mechanical ventilation for acute exacerbation of fibrosing interstitial lung diseases". Respiratory Investigation 61, nr 3 (maj 2023): 306–13. http://dx.doi.org/10.1016/j.resinv.2023.01.008.

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Papanikolaou, Ilias C., Fotios Drakopanagiotakis i Vlasis S. Polychronopoulos. "Acute exacerbations of interstitial lung diseases". Current Opinion in Pulmonary Medicine 16, nr 5 (wrzesień 2010): 480–86. http://dx.doi.org/10.1097/mcp.0b013e32833ae49d.

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Akulkina, L. A., M. Yu Brovko, A. A. Schepalina, V. I. Sholomova, A. A. Kitbalian, A. S. Moiseev, P. P. Potapov i S. V. Moiseev. "A case of severe COVID-19 in a patient with progressive fibrosing interstitial lung disease". PULMONOLOGIYA 32, nr 5 (21.09.2022): 763–69. http://dx.doi.org/10.18093/0869-0189-2022-32-5-763-769.

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Interstitial lung diseases (ILDs) is a wide group of diffuse parenchymal lung diseases that can lead to interstitial pulmonary fibrosis. Clinical course of all ILDs, in particular with chronic fibrosing phenotype, can be complicated by an acute exacerbation caused by infection. Today, data about clinical course of COVID-19 in patients with progressive interstitial lung diseases is limited. In this case we described the course of COVID-19 infection in a patient with an interstitial pneumonia with autoimmune features (IPAF) and a progressive pulmonary fibrosis (PPF). We also discussed the typical features of COVID-19 in this population and the directions for further research.
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Magdy, Mohammed, Zainab Saaed, Emad Abd El-Aleem i Madyan Mahmoud. "Clinical and radiological signs of acute exacerbation of interstitial lung diseases". Minia Journal of Medical Research 30, nr 3 (1.07.2019): 116–19. http://dx.doi.org/10.21608/mjmr.2022.221906.

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Ito, Yoko, Gen Tazaki, Yusuke Kondo, Genki Takahashi i Fumio Sakamaki. "Therapeutic effect of nintedanib on acute exacerbation of interstitial lung diseases". Respiratory Medicine Case Reports 26 (2019): 317–20. http://dx.doi.org/10.1016/j.rmcr.2019.02.021.

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Rozprawy doktorskie na temat "Acute exacerbation of interstitial lung diseases"

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Berrube, Élise. "Patient self-inflicted lung injury et ventilator induced lung injury : De l'insuffisance respiratoire aiguë de novo à l'exacerbation aiguë de pneumopathie intersititielle diffuse". Electronic Thesis or Diss., Normandie, 2024. http://www.theses.fr/2024NORMR030.

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Introduction Au cours de l’insuffisance respiratoire aiguë (IRA) de novo ou du syndrome de détresse respiratoire aiguë (SDRA), la ventilation invasive (VI) appliquée au patient pour pallier aux altérations sévères de l’hématose, de même que les efforts respiratoires spontanés, peuvent paradoxalement aggraver les lésions alvéolaires initiales et provoquer alors des lésions dénommées ventilator induced lung injury (VILI) ou patient self-inflicted lung injury (P-SILI).L’exacerbation aiguë de pneumopathie interstitielle diffuse (EAPID), bien que proche sémiologiquement, histologiquement et radiologiquement du SDRA et ayant bénéficié de l’amélioration des connaissances du VILI et du P-SILI, reste grevée d’une mortalité bien plus élevée. MéthodeNous nous sommes donc intéressés aux conséquences de la ventilation et des efforts respiratoires spontanés au cours des EAPID.RésultatsNous avons tout d’abord étudié les conséquences des stratégies d’oxygénation non invasives au cours de l’IRA de novo et montré que la ventilation non invasive (VNI) augmentait le volume courant par rapport à l’oxygénothérapie à haut débit (OHD) sans augmentation du recrutement alvéolaire, donc exposant le poumon à un risque de surdistention. Nous avons ensuite mis au point un modèle de poumon artificiel mécanique reproduisant la ventilation spontanée au cours de l’IRA de novo et les mécanismes physiopathologiques impliqués dans le P-SILI.Nous avons ensuite utilisé ces connaissances acquises au cours de l’IRA de novo pour modéliser la ventilation spontanée des patients atteints de PID au repos, au cours d’un exercice maximal et d’une EAPID. Nous avons mis en évidence que l’hétérogénéité de l’atteinte pulmonaire, et donc de la compliance dans les PID, était associée tant à l’effort qu’au cours de l’EAPID à la présence de mécanismes impliqués dans le P-SILI : recrutement/dérecrutement alvéolaires, surdistension, concentration du stress pulmonaire, et phénomène de Pendelluft.Nous avons ensuite soumis ce modèle d’EAPID aux contraintes de la VI. Nous avons ainsi pu montrer que celle-ci, appliquée avec des volumes courants supérieurs à 5 ml/kg de poids prédit sur la taille, des niveaux de pressions expiratoire positive supérieure à 4 cmH2O et une fréquence respiratoire supérieure à 25/min, était potentiellement délétère selon notre modèle. Nous avons parallèlement évalué, au cours d’une étude clinique rétrospective, les conséquences de la stratégie d’oxygénation non invasive appliquée au cours de l’EAPID. A contrario de ce que nous avions pu montrer dans l’IRA de novo, nous n’avons pas retrouvé de différence entre la VNI et l’OHD en termes de mortalité ou de recours à la VI. Grace à notre modèle expérimental d’EAPID, nous devrions pouvoir comprendre les mécanismes physiopathologiques expliquant ce résultat et envisager une stratégie d’oxygénation optimisée et personnalisée pour la prise en charge de l’EAPID. ConclusionNotre travail de recherche, à la fois expérimental et clinique, a donc permis de mettre en évidence la possibilité de P-SILI et de VILI au cours des EAPID, de montrer que le risque de surdistension est majeur dans cette pathologie au cours de la VI. La stratégie d’oxygénation non invasive optimale reste encore à déterminer
IntroductionIn the course of de novo acute respiratory failure (ARF) or acute respiratory distress syndrome (ARDS), invasive mechanical ventilation (IMV) and spontaneous respiratory efforts, may paradoxically worsen initial alveolar lesions and cause ventilator induced lung injury (VILI) or patient self-inflicted lung injury (P-SILI). Acute exacerbation of diffuse interstitial lung disease (AE-ILD) presents similar characteristics to ARDS in semiology, histology and radiology. However, the risk of mortality remains higher in AE-ILD despite improved knowledge of VILI and P-SILI. MethodsWe were interested in the effects of ventilation and spontaneous respiratory effort during AE-ILD.ResultsWe first studied the effects of non-invasive oxygenation strategies during de novo ARF, and showed that non-invasive ventilation (NIV) increased tidal volume compared to high flow nasal canulae oxygen therapy (HFNC) without increasing alveolar recruitment, thus exposing the lung to the risk of overdistention. We then developed a mechanical artificial lung model reproducing spontaneous ventilation during de novo ARF and studied the pathophysiological mechanisms involved in P-SILI.We then used this knowledge learned from de novo ARF to model spontaneous ventilation in patients with ILD at rest, during maximal exercise and AE-ILD. We demonstrated that the inhomogeneity of lung injury and of compliance in ILD was associated during exercise and AE-ILD, with the presence of mechanisms involved in P-SILI: recruitment/derecruitment, overdistension, stress concentration and Pendelluft phenomenon.We then exposed this AE-ILD model to the challenges of IMV. We showed that IMV applied with tidal volumes of more than 5 ml/kg PBW, positive expiratory pressure levels of more than 4 cmH2O and respiratory rates of more than 25 cpm were deleterious in our model. At the same time, we evaluated the effects of non-invasive oxygenation strategies during AE-ILD in a retrospective clinical study. We found no difference between NIV and HFNC in mortality or use of invasive ventilation. ConclusionOur research has highlighted the occurence of P-SILI and VILI during AE-ILD and has shown a major risk of overdistension in AE-ILD during IMV. Our model of AE-ILD could help us to develop optimized and personalized oxygenation strategies for AE-ILD patients
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Książki na temat "Acute exacerbation of interstitial lung diseases"

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Millar, Professor Ann B., Dr Richard Leach, Dr Rebecca Preston, Dr Richard Leach, Dr Richard Leach, Dr Wei Shen Lim, Dr Richard Leach i in. Respiratory diseases and respiratory failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199565979.003.0005.

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Chapter 5 covers respiratory diseases and respiratory failure, including clinical presentations of respiratory disease, assessment of diffuse lung disease, hypoxaemia, respiratory failure, and oxygen therapy, pneumonia, mycobacterial infection, asthma, chronic obstructive pulmonary disease (COPD), lung cancer, mediastinal lesions, pneumothorax, pleural disease, asbestos-related lung disease, diffuse parenchymal (interstitial) lung disease, sarcoidosis, pulmonary hypertension, acute respiratory distress syndrome, bronchiectasis and cystic fibrosis, bronchiolitis, eosinophilic lung disease, airways obstruction, aspiration syndromes, and near-drowning, pulmonary vasculitis, the immunocompromised host, sleep apnoea, and rare pulmonary diseases.
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Części książek na temat "Acute exacerbation of interstitial lung diseases"

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Lazor, Romain, i Marie-Eve Müller. "Organizing Pneumonias and Acute Interstitial Pneumonia". W Orphan Lung Diseases, 605–26. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-12950-6_35.

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Ntiamoah, Prince, Russell Purpura, Susan Vehar, Curtis J. Coley, Jennifer Hasvold, Lindsay A. Schmidt, Kevin R. Flaherty i Leslie B. Tolle. "Nonspecific, Unclassifiable, and Rare Idiopathic Interstitial Pneumonia: Acute Interstitial Pneumonia, Respiratory Bronchiolitis Interstitial Pneumonia, Desquamative Interstitial Pneumonia, Nonspecific Interstitial Pneumonia". W Orphan Lung Diseases, 589–603. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-12950-6_34.

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Coley, Curtis J., Leslie B. Tolle, Jennifer Hasvold, Lindsay A. Schmidt i Kevin R. Flaherty. "Non-specific, Unclassifiable, and Rare Idiopathic Interstitial Pneumonia: Acute Interstitial Pneumonia, Respiratory Bronchiolitis Interstitial Pneumonia, Desquamative Interstitial Pneumonia, Nonspecific Interstitial Pneumonia". W Orphan Lung Diseases, 349–62. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-2401-6_23.

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Date, Hiroshi. "Acute Exacerbation of Interstitial Pneumonia After Pulmonary Resection for Lung Cancer". W 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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Lichtenstein, Daniel A. "BLUE-Protocol and Bronchial Diseases: Acute Exacerbation of COPD (AECOPD) and Severe Asthma". W Lung Ultrasound in the Critically Ill, 187–88. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-15371-1_25.

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"Acute Exacerbation of Interstitial Lung Disease". W Specialty Imaging: HRCT of the Lung, 266–69. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-323-52477-3.50082-2.

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Simonds, Anita K. "Long-term oxygen therapy/ventilation and cardiovascular outcomes in chronic lung and respiratory diseases". W ESC CardioMed, 1047–50. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0252.

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There is a well-established evidence base for prescribing long-term oxygen therapy in chronic obstructive pulmonary disease, and this has been extrapolated to management of hypoxaemia in other conditions such as interstitial lung disease and chronic pulmonary hypertension. Non-invasive ventilation reduces mortality in chronic stable hypercapnic patients with chronic obstructive pulmonary disease and those who remain persistently hypercapnic following an acute infective exacerbation. In patients with some neuromuscular disorders, non-invasive ventilation may increase survival and quality of life significantly. Few cardiovascular endpoints have been monitored systematically in these populations.
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Kim, Dong Soon. "Acute Exacerbations in Patients With Idiopathic Pulmonary Fibrosis". W Interstitial Lung Disease, 131–39. Elsevier, 2018. http://dx.doi.org/10.1016/b978-0-323-48024-6.00011-2.

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Sinharay, Rudy. "Chest Medicine". W Oxford Assess and Progress: Clinical Medicine. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198812968.003.0009.

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Respiratory conditions are common, and the burden of morbidity on the general population is high. You only have to take part in a few general medical takes as a junior doctor to realize this. As the on- call bleep goes off again, you are referred another exacerbation of chronic obstructive pulmonary disease (COPD) or asthma, a breathless patient (is it a pul­monary embolism, pneumothorax, or something less common?), or a patient with haemoptysis and weight loss [is it lung cancer or tuberculosis (TB)?] or productive cough (pneumonia or bronchiectasis?). The number of different respiratory conditions can be bewildering, and it is essential for the developing physician to be able to manage ‘common presenta­tions’, as well as potentially life- threatening situations such as an asthma attack or an acute pulmonary embolism. The nuances of history taking is often key to successfully clinching a diagnosis: ● What chronic conditions, respiratory or otherwise, do your patients have? ● What is the onset of symptoms? Sudden breathlessness may indicate a pneumothorax or pulmonary embolus. A chronic productive cough may indicate COPD or bronchiectasis. ● Social history— do they smoke, what are their living conditions, what is their occupation? Luckily, we have other tools to help us. The age- old art of inspec­tion, palpation, percussion, and auscultation during an examination is essential when assessing the patient. Combined with imaging techniques, including chest radiography, CT scanning, and bedside thoracic ultra­sound, the answer is often easily obtained. Keeping an open mind to the less common causes of breathlessness, cough, and haemoptysis is important. Combined with lung function testing, autoimmune blood tests, and bronchoscopy, subtler diagnoses such as interstitial lung dis­ease, fungal lung disease, and autoantibody- induced haemoptysis may be revealed. And a word to the wise— not all breathlessness originates from the lungs! For instance, an increased body mass index will cause a physical restriction on the mechanics of breathing and a compensated metabolic acidosis may cause tachypnoea. As with all chronic diseases, the management of chronic respira­tory disease is becoming increasingly complicated with the advent of biologics, immunotherapy, antifibrotic therapy, and a genuinely confusing array of inhalers.
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Bhalla, Ashu, i Manisha Jana. "Acute Diffuse Lung Diseases: Imaging". W Clinico Radiological Series: Imaging of Interstitial Lung Diseases, 279. Jaypee Brothers Medical Publishers (P) Ltd., 2018. http://dx.doi.org/10.5005/jp/books/13047_22.

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Streszczenia konferencji na temat "Acute exacerbation of interstitial lung diseases"

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Silva Guerra, Sónia Isabel, Mariana Conceição, Ângela Cunha, Joana Correia, Jorge Vale, Carla António i António Simões Torres. "Acute exacerbation admissions of fibrosing interstitial lung diseases – 3 years study". W ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa4739.

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Artaud Macari, Elise, Emeline Fresnel, Adrien Kerfourn, Christian Caillard, Robin Thévenin, Clemence Roussel, David Debeaumont i in. "Modeling lung ventilation in acute exacerbation of interstitial lung diseases: a bench study". W ERS International Congress 2023 abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/13993003.congress-2023.pa1219.

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Suzuki, A., Y. Kondoh, K. K. Brown, T. Kimura, K. Kataoka, T. Matsuda, T. Yokoyama i in. "Recurrent Acute Exacerbations of Fibrotic Interstitial Lung Diseases". W 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.a5621.

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Trachalaki, Athina, Eliza Tsitoura, Eirini Vasarmidi, Eleni Bibaki, Nikolaos Tzanakis i Katerina Antoniou. "Inflammasomes activation in alveolar macrophages and peripheral blood mononuclear cells in fibrotic Interstitial Lung Diseases". W Abstracts from the 17th ERS Lung Science Conference: ‘Mechanisms of Acute Exacerbation of Respiratory Disease’. European Respiratory Society, 2019. http://dx.doi.org/10.1183/23120541.lungscienceconference-2019.pp127.

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Ohshimo, Shinichiro, Yoshiko Kida, Michihito Kyo, Yasushi Horimasu, Hiroshi Iwamoto, Kazunori Fujitaka, Hironobu Hamada i in. "Extracorporeal membrane oxygenation for the treatment of acute exacerbation of interstitial lung diseases". W ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.oa3396.

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Mochizuka, Y., M. Kono, K. Miyashita, R. Hirama, K. Takeda, M. Katsumata, A. Tsutsumi i in. "Recurrence of Acute Exacerbation in Patients with Interstitial Lung Disease". W 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.a3063.

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Hosoki, Keisuke, Yu Mikami, Taisuke Jo, Kunihiko Soma, Hirokazu Urushiyama i Takahide Nagase. "Risk factors for postoperative acute exacerbation of interstitial lung diseases: a matched case-control study". W ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.oa5327.

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Ramos Martins, M., D. Barros-Coelho, P. Ribeirinho-Soares, A. Terras-Alexandre, N. Melo, P. Caetano-Mota, H. Novais-Bastos i A. Morais. "Clinical outcomes of patients with acute exacerbations in interstitial lung diseases". W ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.4266.

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Avera, S., I. Ogbuka, S. El-Chemeitelli i R. G. Karunakara. "Acute Exacerbation of Interstitial Lung Disease in the Setting of COVID-19". W American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a1456.

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Furuta, Katsuyuki, Daichi Fujimoto, Atsushi Matsunashi, Masanori Tanaka, Ryota Shibaki, Yuri Shimada, Kazuma Nagata, Keisuke Tomii i Nobuyuki Yamamoto. "Clinical course and outcomes of acute exacerbation of fibrosing interstitial lung disease". W ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa2241.

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Raporty organizacyjne na temat "Acute exacerbation of interstitial lung diseases"

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Kuroda, Hiroaki. Presurgical heterogeneity of lung 18FDG-PET uptake predicts acute exacerbation of interstitial lung disease following pulmonary resection in patients with smoke exposures. Science Repository OU, lipiec 2019. http://dx.doi.org/10.31487/j.jso.2019.02.08.

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He, Xing, Jiaqi Ji, Dan Zheng, Zeli Luo, Linjie Luo i Lu Guo. Serum surfactant protein D as a significant biomarker for predicting occurrence, progression, acute exacerbation and mortality in patients with interstitial lung disease. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, maj 2024. http://dx.doi.org/10.37766/inplasy2024.5.0050.

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Zheng, Dan, Xing He, Jiaqi Ji, Zeli Luo, Linjie Luo i Lu Guo. Surface protein A as an important biomarker for interstitial lung disease in the assessment of occurrence, progression, acute exacerbation and mortality: a systemic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, maj 2024. http://dx.doi.org/10.37766/inplasy2024.5.0092.

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