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Talmadge E. King

Bio: Talmadge E. King is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Idiopathic pulmonary fibrosis & Interstitial lung disease. The author has an hindex of 88, co-authored 214 publications receiving 43290 citations. Previous affiliations of Talmadge E. King include National Jewish Health & University of California.


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Journal ArticleDOI
TL;DR: This document represents the current state of knowledge regarding idiopathic pulmonary fibrosis, and contains sections on definition and epidemiology, risk factors, diagnosis, natural history, staging and prognosis, treatment, and monitoring disease course.
Abstract: This document is an international evidence-based guideline on the diagnosis and management of idiopathic pulmonary fibrosis, and is a collaborative effort of the American Thoracic Society, the European Respiratory Society, the Japanese Respiratory Society, and the Latin American Thoracic Association. It represents the current state of knowledge regarding idiopathic pulmonary fibrosis (IPF), and contains sections on definition and epidemiology, risk factors, diagnosis, natural history, staging and prognosis, treatment, and monitoring disease course. For the diagnosis and treatment sections, pragmatic GRADE evidence-based methodology was applied in a question-based format. For each diagnosis and treatment question, the committee graded the quality of the evidence available (high, moderate, low, or very low), and made a recommendation (yes or no, strong or weak). Recommendations were based on majority vote. It is emphasized that clinicians must spend adequate time with patients to discuss patients' values and preferences and decide on the appropriate course of action.

5,834 citations

Journal ArticleDOI
William D. Travis, Talmadge E. King, Eric D. Bateman, David A. Lynch, Frédrique Capron, Thomas V. Colby, Jean-François Cordier, Roland M. Dubois, Jeffrey R. Galvin, Philippe Grenier, David M. Hansell, Gary W. Hunninghake, Masanori Kitaichi, Nestor L. Müller, Jeffrey L. Myers, Sonoko Nagai, Andrew G. Nicholson, Ganesh Raghu, Benoit Wallaert, Christian Brambilla, Kevin K. Brown, Andrew L. Cherniaev, Ulrich Costabel, David B. Coultas, Gerald S. Davis, Maurits G. Demedts, William W. Douglas, Jim J. Egan, Anders Eklund, Leonarda M. Fabbri, Craig A. Henke, Richard Hubbard, Y. Inoue, Takateru Izumi, H. M. Jansen, Ian Johnston, Dong Soon Kim, Nasreen Khalil, Fiona R. Lake, Giuseppe Lungarella, Joseph P. Lynch, Douglas W. Mapel, Fernando J. Martinez, Richard A. Matthay, Lee S. Newman, Paul W. Noble, Ken Ohta, Dario Olivieri, Luis A. Ortiz, Venerino Poletti, Robert Rodriguez-Roisin, William N. Rom, Jay Hoon Ryu, Paulo Hilário Nascimento Saldiva, Raúl H Sansores, Marvin L. Schwarz, Moisés Selman, Cecelia M. Smith, Zhaohui Tong, Zarir F Udwadia, Dominique Valeyre, Athol U. Wells, Robert A. Wise, Antonio Xaubet, Emilio Alvarez Fernandez, Elisabeth Brambilla, Vera Luiza Capelozzi, Andrew Cherniaev, Peter Dalquen, Gerhard Dekan, Philip S. Hasleton, James C. Hogg, N. A. Jambhekar, Anna Luise A Katzenstein, Michael Koss, Osamu Matsubara, Klaus Michael Müller, F. B.J.M. Thunnissen, James A. Waldron, Wei Hua Li, Paul J. Friedman, Martin Remy-Jardin, Theresa C. McLoud 
TL;DR: The Diagnostic Process Is Dynamic Clinical Evaluation Radiological Evaluation Role of Surgical Lung Biopsy Unclassifiable Interstitial Pneumonia Bronchoalveolar Lavage Fluid Evaluation Idiopathic Pulmonary Fibrosis.
Abstract: Executive Summary Objectives Participants Evidence Validation Key Messages Introduction Rationale for a Change in the Approach to Classification of Idiopathic Interstitial Pneumonias Development of a New Classification of Idiopathic Interstitial Pneumonia Current Classification of IIP New ATS/ERS Classification Principles Guiding the Assessment of Patients with Idiopathic Interstitial Pneumonias The Diagnostic Process Is Dynamic Clinical Evaluation Radiological Evaluation Role of Surgical Lung Biopsy Unclassifiable Interstitial Pneumonia Bronchoalveolar Lavage Fluid Evaluation Idiopathic Pulmonary Fibrosis Clinical Features Radiologic Features Histologic Features IPF: Areas of Uncertainty Nonspecific Interstitial Pneumonia Clinical Features Radiologic Features Histologic Features NSIP: Areas of Uncertainty Cryptogenic Organizing Pneumonia Clinical Features Radiologic Features Histologic Features COP: Areas of Uncertainty Acute Interstitial Pneumonia Clinical Features Radiologic Features Histologic Features AIP: Areas of Uncertainty Respiratory Bronchiolitis-Associated Interstitial Lung Disease Clinical Features Radiologic Features Histologic Features RB-ILD: Areas of Uncertainty Desquamative Interstitial Pneumonia Clinical Features Radiologic Features Histologic Features DIP: Areas of Uncertainty Lymphoid Interstitial Pneumonia Clinical Features Radiologic Features Histologic Features LIP: Areas of Uncertainty References Appendix

3,591 citations

Journal ArticleDOI
TL;DR: This update is a supplement to the previous 2002 IIP classification document and outlines advances in the past decade and potential areas for future investigation.
Abstract: Background: In 2002 the American Thoracic Society/European Respiratory Society (ATS/ERS) classification of idiopathic interstitial pneumonias (IIPs) defined seven specific entities, and provided standardized terminology and diagnostic criteria. In addition, the historical “gold standard” of histologic diagnosis was replaced by a multidisciplinary approach. Since 2002 many publications have provided new information about IIPs.Purpose: The objective of this statement is to update the 2002 ATS/ERS classification of IIPs.Methods: An international multidisciplinary panel was formed and developed key questions that were addressed through a review of the literature published between 2000 and 2011.Results: Substantial progress has been made in IIPs since the previous classification. Nonspecific interstitial pneumonia is now better defined. Respiratory bronchiolitis–interstitial lung disease is now commonly diagnosed without surgical biopsy. The clinical course of idiopathic pulmonary fibrosis and nonspecific inte...

2,931 citations

Journal ArticleDOI
TL;DR: Pirfenidone, as compared with placebo, reduced disease progression, as reflected by lung function, exercise tolerance, and progression-free survival, in patients with idiopathic pulmonary fibrosis.
Abstract: Background In two of three phase 3 trials, pirfenidone, an oral antifibrotic therapy, reduced disease progression, as measured by the decline in forced vital capacity (FVC) or vital capacity, in patients with idiopathic pulmonary fibrosis; in the third trial, this end point was not achieved. We sought to confirm the beneficial effect of pirfenidone on disease progression in such patients. Methods In this phase 3 study, we randomly assigned 555 patients with idiopathic pulmonary fibrosis to receive either oral pirfenidone (2403 mg per day) or placebo for 52 weeks. The primary end point was the change in FVC or death at week 52. Secondary end points were the 6-minute walk distance, progression-free survival, dyspnea, and death from any cause or from idiopathic pulmonary fibrosis. Results In the pirfenidone group, as compared with the placebo group, there was a relative reduction of 47.9% in the proportion of patients who had an absolute decline of 10 percentage points or more in the percentage of the predicted FVC or who died; there was also a relative increase of 132.5% in the proportion of patients with no decline in FVC (P<0.001). Pirfenidone reduced the decline in the 6-minute walk distance (P = 0.04) and improved progression-free survival (P<0.001). There was no significant between-group difference in dyspnea scores (P = 0.16) or in rates of death from any cause (P = 0.10) or from idiopathic pulmonary fibrosis (P = 0.23). However, in a prespecified pooled analysis incorporating results from two previous phase 3 trials, the between-group difference favoring pirfenidone was significant for death from any cause (P = 0.01) and from idiopathic pulmonary fibrosis (P = 0.006). Gastrointestinal and skin-related adverse events were more common in the pirfenidone group than in the placebo group but rarely led to treatment discontinuation. Conclusions Pirfenidone, as compared with placebo, reduced disease progression, as reflected by lung function, exercise tolerance, and progression-free survival, in patients with idiopathic pulmonary fibrosis. Treatment was associated with an acceptable sideeffect profile and fewer deaths. (Funded by InterMune; ASCEND ClinicalTrials.gov number, NCT01366209.)

2,289 citations

Journal ArticleDOI
TL;DR: The hypothesis that idiopathic pulmonary fibrosis is a fibrotic rather than an inflammatory disease is examined, and the therapeutic implications of these findings are discussed.
Abstract: Idiopathic pulmonary fibrosis is a progressive and usually fatal lung disease characterized by fibroblast proliferation and extracellular matrix remodeling, which result in irreversible distortion of the lung's architecture. Although the pathogenetic mechanisms remain to be determined, the prevailing hypothesis holds that fibrosis is preceded and provoked by a chronic inflammatory process that injures the lung and modulates lung fibrogenesis, leading to the end-stage fibrotic scar. However, there is little evidence that inflammation is prominent in early disease, and it is unclear whether inflammation is relevant to the development of the fibrotic process. Evidence suggests that inflammation does not play a pivotal role. Inflammation is not a prominent histopathologic finding, and epithelial injury in the absence of ongoing inflammation is sufficient to stimulate the development of fibrosis. In addition, the inflammatory response to a lung fibrogenic insult is not necessarily related to the fibrotic response. Clinical measurements of inflammation fail to correlate with stage or outcome, and potent anti-inflammatory therapy does not improve outcome. This review presents a growing body of evidence suggesting that idiopathic pulmonary fibrosis involves abnormal wound healing in response to multiple, microscopic sites of ongoing alveolar epithelial injury and activation associated with the formation of patchy fibroblast-myofibroblast foci, which evolve to fibrosis. Progress in understanding the fibrogenic mechanisms in the lung is likely to yield more effective therapies.

1,696 citations


Cited by
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Journal ArticleDOI
TL;DR: Atherosclerosis is an inflammatory disease as discussed by the authors, and it is a major cause of death in the United States, Europe, and much of Asia, despite changes in lifestyle and use of new pharmacologic approaches to lower plasma cholesterol concentrations.
Abstract: Atherosclerosis is an inflammatory disease. Because high plasma concentrations of cholesterol, in particular those of low-density lipoprotein (LDL) cholesterol, are one of the principal risk factors for atherosclerosis,1 the process of atherogenesis has been considered by many to consist largely of the accumulation of lipids within the artery wall; however, it is much more than that. Despite changes in lifestyle and the use of new pharmacologic approaches to lower plasma cholesterol concentrations,2,3 cardiovascular disease continues to be the principal cause of death in the United States, Europe, and much of Asia.4,5 In fact, the lesions of atherosclerosis represent . . .

19,881 citations

Journal Article
TL;DR: Despite changes in lifestyle and the use of new pharmacologic approaches to lower plasma cholesterol concentrations, cardiovascular disease continues to be the principal cause of death in the United States, Europe, and much of Asia.

9,749 citations

Journal ArticleDOI
TL;DR: This document represents the current state of knowledge regarding idiopathic pulmonary fibrosis, and contains sections on definition and epidemiology, risk factors, diagnosis, natural history, staging and prognosis, treatment, and monitoring disease course.
Abstract: This document is an international evidence-based guideline on the diagnosis and management of idiopathic pulmonary fibrosis, and is a collaborative effort of the American Thoracic Society, the European Respiratory Society, the Japanese Respiratory Society, and the Latin American Thoracic Association. It represents the current state of knowledge regarding idiopathic pulmonary fibrosis (IPF), and contains sections on definition and epidemiology, risk factors, diagnosis, natural history, staging and prognosis, treatment, and monitoring disease course. For the diagnosis and treatment sections, pragmatic GRADE evidence-based methodology was applied in a question-based format. For each diagnosis and treatment question, the committee graded the quality of the evidence available (high, moderate, low, or very low), and made a recommendation (yes or no, strong or weak). Recommendations were based on majority vote. It is emphasized that clinicians must spend adequate time with patients to discuss patients' values and preferences and decide on the appropriate course of action.

5,834 citations

Journal ArticleDOI
TL;DR: This section is written to provide guidance in interpreting pulmonary function tests (PFTs) to medical directors of hospital-based laboratories that perform PFTs, and physicians who are responsible for interpreting the results of PFTS most commonly ordered for clinical purposes.
Abstract: SERIES “ATS/ERS TASK FORCE: STANDARDISATION OF LUNG FUNCTION TESTING” Edited by V. Brusasco, R. Crapo and G. Viegi Number 5 in this Series This section is written to provide guidance in interpreting pulmonary function tests (PFTs) to medical directors of hospital-based laboratories that perform PFTs, and physicians who are responsible for interpreting the results of PFTs most commonly ordered for clinical purposes. Specifically, this section addresses the interpretation of spirometry, bronchodilator response, carbon monoxide diffusing capacity ( D L,CO) and lung volumes. The sources of variation in lung function testing and technical aspects of spirometry, lung volume measurements and D L,CO measurement have been considered in other documents published in this series of Task Force reports 1–4 and in the American Thoracic Society (ATS) interpretative strategies document 5. An interpretation begins with a review and comment on test quality. Tests that are less than optimal may still contain useful information, but interpreters should identify the problems and the direction and magnitude of the potential errors. Omitting the quality review and relying only on numerical results for clinical decision making is a common mistake, which is more easily made by those who are dependent upon computer interpretations. Once quality has been assured, the next steps involve a series of comparisons 6 that include comparisons of test results with reference values based on healthy subjects 5, comparisons with known disease or abnormal physiological patterns ( i.e. obstruction and restriction), and comparisons with self, a rather formal term for evaluating change in an individual patient. A final step in the lung function report is to answer the clinical question that prompted the test. Poor choices made during these preparatory steps increase the risk of misclassification, i.e. a falsely negative or falsely positive interpretation for a lung function abnormality or a change …

5,078 citations

Journal ArticleDOI
William D. Travis, Talmadge E. King, Eric D. Bateman, David A. Lynch, Frédrique Capron, Thomas V. Colby, Jean-François Cordier, Roland M. Dubois, Jeffrey R. Galvin, Philippe Grenier, David M. Hansell, Gary W. Hunninghake, Masanori Kitaichi, Nestor L. Müller, Jeffrey L. Myers, Sonoko Nagai, Andrew G. Nicholson, Ganesh Raghu, Benoit Wallaert, Christian Brambilla, Kevin K. Brown, Andrew L. Cherniaev, Ulrich Costabel, David B. Coultas, Gerald S. Davis, Maurits G. Demedts, William W. Douglas, Jim J. Egan, Anders Eklund, Leonarda M. Fabbri, Craig A. Henke, Richard Hubbard, Y. Inoue, Takateru Izumi, H. M. Jansen, Ian Johnston, Dong Soon Kim, Nasreen Khalil, Fiona R. Lake, Giuseppe Lungarella, Joseph P. Lynch, Douglas W. Mapel, Fernando J. Martinez, Richard A. Matthay, Lee S. Newman, Paul W. Noble, Ken Ohta, Dario Olivieri, Luis A. Ortiz, Venerino Poletti, Robert Rodriguez-Roisin, William N. Rom, Jay Hoon Ryu, Paulo Hilário Nascimento Saldiva, Raúl H Sansores, Marvin L. Schwarz, Moisés Selman, Cecelia M. Smith, Zhaohui Tong, Zarir F Udwadia, Dominique Valeyre, Athol U. Wells, Robert A. Wise, Antonio Xaubet, Emilio Alvarez Fernandez, Elisabeth Brambilla, Vera Luiza Capelozzi, Andrew Cherniaev, Peter Dalquen, Gerhard Dekan, Philip S. Hasleton, James C. Hogg, N. A. Jambhekar, Anna Luise A Katzenstein, Michael Koss, Osamu Matsubara, Klaus Michael Müller, F. B.J.M. Thunnissen, James A. Waldron, Wei Hua Li, Paul J. Friedman, Martin Remy-Jardin, Theresa C. McLoud 
TL;DR: The Diagnostic Process Is Dynamic Clinical Evaluation Radiological Evaluation Role of Surgical Lung Biopsy Unclassifiable Interstitial Pneumonia Bronchoalveolar Lavage Fluid Evaluation Idiopathic Pulmonary Fibrosis.
Abstract: Executive Summary Objectives Participants Evidence Validation Key Messages Introduction Rationale for a Change in the Approach to Classification of Idiopathic Interstitial Pneumonias Development of a New Classification of Idiopathic Interstitial Pneumonia Current Classification of IIP New ATS/ERS Classification Principles Guiding the Assessment of Patients with Idiopathic Interstitial Pneumonias The Diagnostic Process Is Dynamic Clinical Evaluation Radiological Evaluation Role of Surgical Lung Biopsy Unclassifiable Interstitial Pneumonia Bronchoalveolar Lavage Fluid Evaluation Idiopathic Pulmonary Fibrosis Clinical Features Radiologic Features Histologic Features IPF: Areas of Uncertainty Nonspecific Interstitial Pneumonia Clinical Features Radiologic Features Histologic Features NSIP: Areas of Uncertainty Cryptogenic Organizing Pneumonia Clinical Features Radiologic Features Histologic Features COP: Areas of Uncertainty Acute Interstitial Pneumonia Clinical Features Radiologic Features Histologic Features AIP: Areas of Uncertainty Respiratory Bronchiolitis-Associated Interstitial Lung Disease Clinical Features Radiologic Features Histologic Features RB-ILD: Areas of Uncertainty Desquamative Interstitial Pneumonia Clinical Features Radiologic Features Histologic Features DIP: Areas of Uncertainty Lymphoid Interstitial Pneumonia Clinical Features Radiologic Features Histologic Features LIP: Areas of Uncertainty References Appendix

3,591 citations