The evolving pharmacotherapy of pulmonary fibrosis.
Identifieur interne : 000117 ( Main/Exploration ); précédent : 000116; suivant : 000118The evolving pharmacotherapy of pulmonary fibrosis.
Auteurs : Harpreet K. Lota [Royaume-Uni] ; Athol U. WellsSource :
- Expert opinion on pharmacotherapy [ 1744-7666 ] ; 2013.
Descripteurs français
- KwdFr :
- Acétylcystéine (usage thérapeutique), Anti-inflammatoires non stéroïdiens (usage thérapeutique), Essais contrôlés randomisés comme sujet (MeSH), Fibrose pulmonaire (traitement médicamenteux), Fibrose pulmonaire (étiologie), Humains (MeSH), Immunosuppresseurs (usage thérapeutique), Indoles (usage thérapeutique), Pneumopathies interstitielles (complications), Pneumopathies interstitielles (traitement médicamenteux), Pneumopathies interstitielles idiopathiques (complications), Pneumopathies interstitielles idiopathiques (traitement médicamenteux), Pyridones (usage thérapeutique), Résultat thérapeutique (MeSH), Sarcoïdose pulmonaire (complications), Sarcoïdose pulmonaire (traitement médicamenteux), Sclérodermie systémique (complications), Sclérodermie systémique (traitement médicamenteux).
- MESH :
- traitement médicamenteux : Fibrose pulmonaire, Pneumopathies interstitielles, Pneumopathies interstitielles idiopathiques, Sarcoïdose pulmonaire, Sclérodermie systémique.
- usage thérapeutique : Acétylcystéine, Anti-inflammatoires non stéroïdiens, Immunosuppresseurs, Indoles, Pneumopathies interstitielles, Pneumopathies interstitielles idiopathiques, Pyridones, Sarcoïdose pulmonaire, Sclérodermie systémique.
- étiologie : Fibrose pulmonaire.
- Essais contrôlés randomisés comme sujet, Humains, Résultat thérapeutique.
English descriptors
- KwdEn :
- Acetylcysteine (therapeutic use), Anti-Inflammatory Agents, Non-Steroidal (therapeutic use), Humans (MeSH), Idiopathic Interstitial Pneumonias (complications), Idiopathic Interstitial Pneumonias (drug therapy), Immunosuppressive Agents (therapeutic use), Indoles (therapeutic use), Lung Diseases, Interstitial (complications), Lung Diseases, Interstitial (drug therapy), Pulmonary Fibrosis (drug therapy), Pulmonary Fibrosis (etiology), Pyridones (therapeutic use), Randomized Controlled Trials as Topic (MeSH), Sarcoidosis, Pulmonary (complications), Sarcoidosis, Pulmonary (drug therapy), Scleroderma, Systemic (complications), Scleroderma, Systemic (drug therapy), Treatment Outcome (MeSH).
- MESH :
- chemical , therapeutic use : Acetylcysteine, Anti-Inflammatory Agents, Non-Steroidal, Immunosuppressive Agents, Indoles, Pyridones.
- complications : Idiopathic Interstitial Pneumonias, Lung Diseases, Interstitial, Sarcoidosis, Pulmonary, Scleroderma, Systemic.
- drug therapy : Idiopathic Interstitial Pneumonias, Lung Diseases, Interstitial, Pulmonary Fibrosis, Sarcoidosis, Pulmonary, Scleroderma, Systemic.
- etiology : Pulmonary Fibrosis.
- Humans, Randomized Controlled Trials as Topic, Treatment Outcome.
Abstract
INTRODUCTION
Novel compounds targeting various aspects of fibrogenesis have been developed consequent to the increasing knowledge of the pathogenetic mechanisms of the interstitial lung diseases (ILDs). The authors review the evolution of treatment approaches in the ILDs, informed by recent placebo-controlled trials, and discuss current clinical trials in which emerging pathogenetic mechanisms are targeted as novel therapeutic agents.
AREAS COVERED
In idiopathic pulmonary fibrosis (IPF), recent randomised, placebo-controlled trials have tested the efficacy of new therapies, and although primary end points have not been met in most, treatment effects have been observed. The demonstration of harmful effects from widely used IPF therapies has been equally important. Pirfenidone and nintedanib are emerging agents that exert pleiotropic effects, reflective of the multiple mechanistic pathways of IPF. Treatment may necessitate a similarly multifaceted approach using combination regimens of antifibrotic and antioxidant agents in order to be effective. In other ILDs, including systemic sclerosis, other connective tissue diseases and pulmonary sarcoidosis, the inflammatory/fibrotic model remains appropriate. Studies in systemic sclerosis have provided 'proof of concept' data for immunosuppressive therapy in the prevention of disease progression but there is a continuing need for controlled clinical trials in the more prevalent ILDs.
EXPERT OPINION
In IPF, significant treatment effects have been reported with pirfenidone, nintedanib and N-acetylcysteine. Combinations of these pleiotropic agents, along with future monotherapies, in 'oncological regimens' may hold the key to more effective IPF treatment. In disorders other than IPF, there is an ongoing need for the controlled evaluation of traditional anti-inflammatory and immunosuppressive therapies. 'Cohort enrichment' (the selective recruitment of patients most likely to progress) holds the key to the identification of worthwhile treatment benefits.
DOI: 10.1517/14656566.2013.758250
PubMed: 23265249
Affiliations:
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Le document en format XML
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<term>Indoles</term>
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<term>Scleroderma, Systemic</term>
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<term>Pneumopathies interstitielles idiopathiques</term>
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<term>Sclérodermie systémique</term>
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<term>Indoles</term>
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<term>Treatment Outcome</term>
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<front><div type="abstract" xml:lang="en"><p><b>INTRODUCTION</b>
</p>
<p>Novel compounds targeting various aspects of fibrogenesis have been developed consequent to the increasing knowledge of the pathogenetic mechanisms of the interstitial lung diseases (ILDs). The authors review the evolution of treatment approaches in the ILDs, informed by recent placebo-controlled trials, and discuss current clinical trials in which emerging pathogenetic mechanisms are targeted as novel therapeutic agents.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>AREAS COVERED</b>
</p>
<p>In idiopathic pulmonary fibrosis (IPF), recent randomised, placebo-controlled trials have tested the efficacy of new therapies, and although primary end points have not been met in most, treatment effects have been observed. The demonstration of harmful effects from widely used IPF therapies has been equally important. Pirfenidone and nintedanib are emerging agents that exert pleiotropic effects, reflective of the multiple mechanistic pathways of IPF. Treatment may necessitate a similarly multifaceted approach using combination regimens of antifibrotic and antioxidant agents in order to be effective. In other ILDs, including systemic sclerosis, other connective tissue diseases and pulmonary sarcoidosis, the inflammatory/fibrotic model remains appropriate. Studies in systemic sclerosis have provided 'proof of concept' data for immunosuppressive therapy in the prevention of disease progression but there is a continuing need for controlled clinical trials in the more prevalent ILDs.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>EXPERT OPINION</b>
</p>
<p>In IPF, significant treatment effects have been reported with pirfenidone, nintedanib and N-acetylcysteine. Combinations of these pleiotropic agents, along with future monotherapies, in 'oncological regimens' may hold the key to more effective IPF treatment. In disorders other than IPF, there is an ongoing need for the controlled evaluation of traditional anti-inflammatory and immunosuppressive therapies. 'Cohort enrichment' (the selective recruitment of patients most likely to progress) holds the key to the identification of worthwhile treatment benefits.</p>
</div>
</front>
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