The Experts below are selected from a list of 72285 Experts worldwide ranked by ideXlab platform
Katherine E. Zychowski - One of the best experts on this subject based on the ideXlab platform.
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Metal-Induced Pulmonary Fibrosis
Current Environmental Health Reports, 2018Co-Authors: Nour Assad, Matthew J. Campen, Akshay Sood, Katherine E. ZychowskiAbstract:Purpose of Review The incidence of Pulmonary Fibrosis is increasing worldwide and may, in part, be due to occupational and environmental exposures. Secondary fibrotic interstitial lung diseases may be mistaken for idiopathic Pulmonary Fibrosis with important implications for both disease management and prognosis. The purposes of this review are to shed light on possible underlying causes of interstitial Pulmonary Fibrosis and to encourage dialogue on the importance of acquiring a thorough patient history of occupational and environmental exposures. Recent Findings A recent appreciation for various occupational and environmental metals inducing both antigen-specific immune reactions in the lung and nonspecific “innate” immune system responses has emerged and with it a growing awareness of the potential hazards to the lung caused by low-level metal exposures. Advancements in the contrast and quality of high-resolution CT scans and identification of histopathological patterns of interstitial Pulmonary Fibrosis have improved clinical diagnostics. Moreover, recent findings indicate specific hotspots of Pulmonary Fibrosis within the USA. Increased prevalence of lung disease in these areas appears to be linked to occupational/environmental metal exposure and ethnic susceptibility/vulnerability. Summary A systematic overview of possible occupational and environmental metals causing interstitial Pulmonary Fibrosis and a detailed evaluation of vulnerable/susceptible populations may facilitate a broader understanding of potential underlying causes and highlight risks of disease predisposition.
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Metal-Induced Pulmonary Fibrosis
Current Environmental Health Reports, 2018Co-Authors: Nour Assad, Matthew J. Campen, Akshay Sood, Katherine E. ZychowskiAbstract:The incidence of Pulmonary Fibrosis is increasing worldwide and may, in part, be due to occupational and environmental exposures. Secondary fibrotic interstitial lung diseases may be mistaken for idiopathic Pulmonary Fibrosis with important implications for both disease management and prognosis. The purposes of this review are to shed light on possible underlying causes of interstitial Pulmonary Fibrosis and to encourage dialogue on the importance of acquiring a thorough patient history of occupational and environmental exposures. A recent appreciation for various occupational and environmental metals inducing both antigen-specific immune reactions in the lung and nonspecific “innate” immune system responses has emerged and with it a growing awareness of the potential hazards to the lung caused by low-level metal exposures. Advancements in the contrast and quality of high-resolution CT scans and identification of histopathological patterns of interstitial Pulmonary Fibrosis have improved clinical diagnostics. Moreover, recent findings indicate specific hotspots of Pulmonary Fibrosis within the USA. Increased prevalence of lung disease in these areas appears to be linked to occupational/environmental metal exposure and ethnic susceptibility/vulnerability. A systematic overview of possible occupational and environmental metals causing interstitial Pulmonary Fibrosis and a detailed evaluation of vulnerable/susceptible populations may facilitate a broader understanding of potential underlying causes and highlight risks of disease predisposition.
Nour Assad - One of the best experts on this subject based on the ideXlab platform.
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Metal-Induced Pulmonary Fibrosis
Current Environmental Health Reports, 2018Co-Authors: Nour Assad, Matthew J. Campen, Akshay Sood, Katherine E. ZychowskiAbstract:Purpose of Review The incidence of Pulmonary Fibrosis is increasing worldwide and may, in part, be due to occupational and environmental exposures. Secondary fibrotic interstitial lung diseases may be mistaken for idiopathic Pulmonary Fibrosis with important implications for both disease management and prognosis. The purposes of this review are to shed light on possible underlying causes of interstitial Pulmonary Fibrosis and to encourage dialogue on the importance of acquiring a thorough patient history of occupational and environmental exposures. Recent Findings A recent appreciation for various occupational and environmental metals inducing both antigen-specific immune reactions in the lung and nonspecific “innate” immune system responses has emerged and with it a growing awareness of the potential hazards to the lung caused by low-level metal exposures. Advancements in the contrast and quality of high-resolution CT scans and identification of histopathological patterns of interstitial Pulmonary Fibrosis have improved clinical diagnostics. Moreover, recent findings indicate specific hotspots of Pulmonary Fibrosis within the USA. Increased prevalence of lung disease in these areas appears to be linked to occupational/environmental metal exposure and ethnic susceptibility/vulnerability. Summary A systematic overview of possible occupational and environmental metals causing interstitial Pulmonary Fibrosis and a detailed evaluation of vulnerable/susceptible populations may facilitate a broader understanding of potential underlying causes and highlight risks of disease predisposition.
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Metal-Induced Pulmonary Fibrosis
Current Environmental Health Reports, 2018Co-Authors: Nour Assad, Matthew J. Campen, Akshay Sood, Katherine E. ZychowskiAbstract:The incidence of Pulmonary Fibrosis is increasing worldwide and may, in part, be due to occupational and environmental exposures. Secondary fibrotic interstitial lung diseases may be mistaken for idiopathic Pulmonary Fibrosis with important implications for both disease management and prognosis. The purposes of this review are to shed light on possible underlying causes of interstitial Pulmonary Fibrosis and to encourage dialogue on the importance of acquiring a thorough patient history of occupational and environmental exposures. A recent appreciation for various occupational and environmental metals inducing both antigen-specific immune reactions in the lung and nonspecific “innate” immune system responses has emerged and with it a growing awareness of the potential hazards to the lung caused by low-level metal exposures. Advancements in the contrast and quality of high-resolution CT scans and identification of histopathological patterns of interstitial Pulmonary Fibrosis have improved clinical diagnostics. Moreover, recent findings indicate specific hotspots of Pulmonary Fibrosis within the USA. Increased prevalence of lung disease in these areas appears to be linked to occupational/environmental metal exposure and ethnic susceptibility/vulnerability. A systematic overview of possible occupational and environmental metals causing interstitial Pulmonary Fibrosis and a detailed evaluation of vulnerable/susceptible populations may facilitate a broader understanding of potential underlying causes and highlight risks of disease predisposition.
Ganesh Raghu - One of the best experts on this subject based on the ideXlab platform.
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Does Chronic Microaspiration Cause Idiopathic Pulmonary Fibrosis
The American Journal of Medicine, 2010Co-Authors: Harold R Collard, Matthew P. Sweet, Steven R Hays, Jeffrey A. Golden, Ganesh Raghu, Guilherme M. Campos, Talmadge E KingAbstract:Idiopathic Pulmonary Fibrosis is a diffuse fibrotic lung disease of unknown etiology with no effective treatment. Emerging data support a role for chronic microaspiration (ie, subclinical aspiration of small droplets) in the pathogenesis and natural history of idiopathic Pulmonary Fibrosis. However, the precise relationship between chronic microaspiration and idiopathic Pulmonary Fibrosis remains unknown. Gastroesophageal reflux, a presumed risk factor for microaspiration, has been strongly associated with idiopathic Pulmonary Fibrosis with an estimated prevalence of up to 90%. This review aims to describe the relationship between chronic microaspiration and idiopathic Pulmonary Fibrosis by laying out the clinical and biologic rationale for this relationship and exploring the scientific evidence available. The gaps in our current understanding of the diagnosis of chronic microaspiration and idiopathic Pulmonary Fibrosis and the ongoing uncertainties in management and treatment will be highlighted. Defining the role of chronic microaspiration in idiopathic Pulmonary Fibrosis is essential as it has potential clinical, pathobiological, and treatment implications for this deadly disease.
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Genetics of Pulmonary Fibrosis
Seminars in Respiratory and Critical Care Medicine, 2002Co-Authors: Mark Matsuo Wurfel, Ganesh RaghuAbstract:: Pulmonary Fibrosis is a devastating disease that occurs in association with environmental exposures, several inherited diseases, collagen vascular disease, as well as in an idiopathic form. Epithelial cell damage, excessive fibroblast proliferation, upregulation of extracellular matrix production, and attenuated matrix degradation are shared pathophysiological features of these different forms of Pulmonary Fibrosis. Several observations suggest that genetic predisposition plays an important role in the pathophysiology of Pulmonary Fibrosis. There is significant inter-individual variation in the degree of Pulmonary Fibrosis resulting from exposure to similar levels of an inhaled fibrogenic agent. There are several inherited diseases with known genetic mutations that have high rates of Pulmonary Fibrosis. Idiopathic Pulmonary Fibrosis can occur in multiple first-degree relatives, including those separated at an early age. Finally, recent studies have identified polymorphisms within genes for cytokines, histocompatability antigens, and extracellular matrix components that are associated with the development of Pulmonary Fibrosis. Identification of putative Pulmonary Fibrosis gene/s (PF gene/s) may result in novel diagnostic and therapeutic interventions for those at risk for development of Pulmonary Fibrosis.
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Genetic predisposition of idiopathic Pulmonary Fibrosis.
Current Opinion in Pulmonary Medicine, 1997Co-Authors: Yolanda N. Mageto, Ganesh RaghuAbstract:: The Pulmonary parenchyma in interstitial Fibrosis responds stereotypically to a variety of insults. The observation that only a small subset of persons exposed to known fibrogenic agents develop Fibrosis and the induction of Pulmonary Fibrosis in genetically susceptible mice support a genetic predisposition. The description of familial idiopathic Pulmonary Fibrosis is the strongest evidence available supporting this hypothesis. Unfortunately, despite all the recent advances in molecular genetic techniques there have been few human studies to date. Given the poor prognosis and the lack of a cure for Pulmonary Fibrosis, future genetic studies will, it is hoped, clarify the pathogenesis of Pulmonary Fibrosis and lead to preventive measures and new therapeutic interventions. Idiopathic Pulmonary Fibrosis typically occurs in patients who are older than 50. The etiology is unknown.
Fernando J. Martinez - One of the best experts on this subject based on the ideXlab platform.
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idiopathic Pulmonary Fibrosis
The New England Journal of Medicine, 2018Co-Authors: David J Lederer, Fernando J. MartinezAbstract:Idiopathic Pulmonary Fibrosis Idiopathic Pulmonary Fibrosis appears to be increasing in incidence. It requires early recognition and intervention with supportive care and pharmacologic agents to forestall its progression. Lung transplantation may be curative, but the disease may recur in transplanted lungs.
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mechanisms of Pulmonary Fibrosis
Annual Review of Medicine, 2004Co-Authors: Victor J Thannickal, Joseph P Lynch, Eric S. White, Galen B Toews, Fernando J. MartinezAbstract:Tissue injury evokes highly conserved, tightly regulated inflammatory responses and less well-understood host repair responses. Both inflammation and repair involve the recruitment, activation, apoptosis, and eventual clearance of key effector cells. In this review, we propose the concept of Pulmonary Fibrosis as a dysregulated repair process that is perpetually "turned on" even though classical inflammatory pathways may be dampened or "switched off." Significant regional heterogeneity, with varied histopathological patterns of inflammation and Fibrosis, has been observed in individual patients with idiopathic Pulmonary Fibrosis. We discuss environmental factors and host response factors, such as genetic susceptibility and age, that may influence these varied manifestations. Better understanding of the mechanisms of lung repair, which include alveolar reepithelialization, myofibroblast differentiation/activation, and apoptosis, should offer more effective therapeutic options for progressive Pulmonary Fibrosis.
Roland M. Du Bois - One of the best experts on this subject based on the ideXlab platform.
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Genetics of Pulmonary Fibrosis.
Seminars in respiratory and critical care medicine, 2003Co-Authors: Roland M. Du Bois, I Kangesan, S VeeraraghavanAbstract:Identifying genetic determinants of Pulmonary Fibrosis is at an early stage of evolution. It is now well recognized that "Pulmonary Fibrosis" covers a broad range of lung diseases including most topically the idiopathic interstitial pneumonias that have been classified recently. Additionally, it is recognized that the diffuse lung diseases of children that may progress to Fibrosis are quite different from those of adults. Defining clinical phenotype is an absolute prerequisite to precise identification of genetic determinants, and this is at least part of the reason why we understand relatively little of these genetic determinants to date. In children, a number of mutations have been identified, particularly with regard to surfactant protein. In adults, families with idiopathic Pulmonary Fibrosis are being collected but there are no genetic data on these at this point. In sporadic disease, associations have been reported in early phase genes with disease predisposition and also, importantly, with disease severity: future studies will inevitably incorporate issues of severity of disease in analyses.
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Idiopathic Pulmonary Fibrosis.
Annual Review of Medicine, 1993Co-Authors: Roland M. Du BoisAbstract:: Idiopathic Pulmonary Fibrosis kills half of its victims within five years of diagnosis. Currently available treatment regimens are disappointing, and the incidence of the disease appears to be increasing. Newer techniques of imaging coupled with laboratory advances in molecular and cellular biology may produce new strategies for modulating the disease process. This article explores new approaches to the diagnosis and management of idiopathic Pulmonary Fibrosis.
