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Toxicology
Published in Anthony FT Brown, Michael D Cadogan, Emergency Medicine, 2020
Anthony FT Brown, Michael D Cadogan
Paraquat is a highly toxic herbicide. Significant oral ingestion is associated with fulminant multi-organ failure. If patients survive this, they develop progressive pulmonary fibrosis, and may die 4–6 weeks later from hypoxaemia.
Monitoring health status
Published in Claudio F. Donner, Nicolino Ambrosino, Roger S. Goldstein, Pulmonary Rehabilitation, 2020
Claire M. Nolan, William D.-C. Man, Richard L. ZuWallack
Systemic impairments, functional limitations, symptom burdens, comorbid conditions, and maladaptive behaviours, which are potentially amenable to PR, are by no means unique to individuals with COPD. Rather, they are prominent in many patients with chronic respiratory disease (and chronic disease in general). Therefore, it would not be unreasonable to expect that PR would be effective in these patients too. While most scientific inquiry has been in COPD, some attention has been given to the effect of PR in other disease states. What follows are analyses in two non-COPD respiratory diseases: idiopathic pulmonary fibrosis and bronchiectasis. Interestingly, many PR studies in non-COPD respiratory patients have persisted with using health status questionnaires originally designed for use in COPD, partly due to the relative paucity of respiratory disease−specific health status instruments developed outside of COPD.
The respiratory system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
There are many causes of pulmonary fibrosis. These include sarcoidosis, Langerhans’ cell histiocytosis, and collagen vascular diseases, such as rheumatoid disease, systemic lupus erythematosus, systemic sclerosis, and asbestosis. Drugs, such as methotrexate, used for cancer treatment or immunosuppression, or amiodarone, used to treat cardiac disease, are also implicated and there is an increased incidence among metal- or wood-dust workers. In many cases, however, no cause is found. Chronic interstitial lung disease is traditionally classified according to the histological pattern present, which corresponds to fairly well-characterized clinicopathological entities: Usual interstitial pneumoniaNon-specific interstitial pneumoniaDesquamative interstitial pneumonia and respiratory bronchiolitisOrganizing pneumoniaLymphocytic interstitial pneumonia
The Promising Therapeutic Potential of Oligonucleotides for Pulmonary Fibrotic Diseases
Published in Expert Opinion on Drug Discovery, 2023
Divyani Paul, Madelyn H Miller, Josh Born, Shayak Samaddar, Huanzhen Ni, Hugo Avila, Venkata R. Krishnamurthy, Kannan Thirunavukkarasu
Pulmonary fibrosis is observed in several lung diseases such as interstitial lung diseases (ILDs), chronic asthma, chronic obstructive pulmonary disease (COPD), and cystic fibrosis (CF). Per the CDC in 2022, prior to the COVID-19 pandemic, chronic pulmonary diseases were the third leading cause of death in the US behind cardiovascular disease and neoplasms. Additionally, chronic lung disease affects over 500 million people worldwide, and is increasing in prevalence [1]. Particularly, interstitial lung diseases (ILDs) which result in pulmonary fibrosis have significant unmet needs; in 2019, over 600,000 Americans were diagnosed with ILDs. The most extensively studied and aggressive form of ILD, idiopathic pulmonary fibrosis (IPF), has a poor prognosis and a median survival of 3–5 years if left untreated [2]. Thus, fibrotic pulmonary diseases represent a significant global disease burden, and increased efforts should be made to understand the pathogenesis of these diseases and to find novel treatment strategies and drug delivery systems.
The study of metabolism and metabolomics in a mouse model of silica pulmonary fibrosis based on UHPLC-QE-MS
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2022
Min Qiu, Ling Qin, Yonghe Dong, Junbing Ma, Zheng Yang, Zhixiang Gao
At present, there is no specific drug that can effectively treat pulmonary fibrosis. The clinical symptoms of patients with pulmonary fibrosis always include a dry cough and progressive dyspnoea, eventually leading to progressive respiratory failure and death, which seriously threatens the life of patients [6,7]. Due to the lack of animal models that can truly reflect the disease and the exact pathogenesis, as well as the not fully clarified disease mechanism, the development of anti-pulmonary fibrosis drugs is very slow. On this basis, this study established mouse models of pulmonary fibrosis closer to human chronic and progressive pulmonary fibrosis [8]. In addition, combined with histological, cytological and metabolic methods, multiple characteristics of the mice were revealed, so as to provide an ideal animal model for accelerating the development of anti-pulmonary fibrosis drugs and the research on disease mechanism.
Potential therapeutic targets to prevent organ damage in chronic pulmonary sarcoidosis
Published in Expert Opinion on Therapeutic Targets, 2022
In general recruiting patients for treatment studies is challenging and time-consuming. Clinicians therefore again should join forces at national and international level, and prioritize development of clear and inclusive study protocols and pharmaceutical and biotech companies should be encouraged to financially support clinical trials. There is great need to soon find robust answers to many outstanding questions. What are best strategies for screening for triggers? Which molecular pathways are key? Can different antigenic triggers and different key pathways be classified as endotypes? Who and which to screen for in individual patients? Which of the therapeutic targets are most promising? Are the existing antifibrotics (nintedanib and pirfenidone) effective in slowing down progression in the fibrotic sarcoidosis phenotype? Are they protective and preventive against the development of pulmonary fibrosis in certain genetic predisposed subgroups? Etcetera.