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Will expanded ART use reduce the burden of HIV-associated chronic lung disease?

ABSTRACT: The pulmonary complications of chronic HIV infection have shifted from infectious complications toward noninfectious pulmonary complications, predominantly chronic obstructive pulmonary disease (COPD). Although the best-established COPD risk factor is cigarette smoking, emerging data suggest that HIV infection also independently increases COPD risk. The purpose of this article is to review these data and the conflicting data regarding the role of antiretroviral therapy (ART) in modifying COPD risk.Observational studies favor HIV as an independent risk factor for COPD, particularly when viral load is high. The mechanisms underlying these associations are unclear, but untreated HIV infection is associated with pulmonary inflammatory responses similar to those seen in non-HIV COPD. ART reduces this pulmonary inflammation, but the clinical benefit of such reduction is unknown. Some observational studies suggest that ART users are at lower risk of COPD, whereas other studies suggest the opposite scenario.The effect of ART in causing COPD or reducing COPD risk is unknown, but is currently being tested in a randomized trial. Smoking cessation should remain of high priority.

SUBMITTER: Kunisaki KM

PROVIDER: S-EPMC4068344 | biostudies-literature | 2014 Jan

REPOSITORIES: biostudies-literature

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Will expanded ART use reduce the burden of HIV-associated chronic lung disease?

Kunisaki Ken M KM

Current opinion in HIV and AIDS 20140101 1

<h4>Purpose of review</h4>The pulmonary complications of chronic HIV infection have shifted from infectious complications toward noninfectious pulmonary complications, predominantly chronic obstructive pulmonary disease (COPD). Although the best-established COPD risk factor is cigarette smoking, emerging data suggest that HIV infection also independently increases COPD risk. The purpose of this article is to review these data and the conflicting data regarding the role of antiretroviral therapy ...[more]

PMID: 24247667

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Project description:Chronic cough (CC; ≥8 weeks in duration) is a common and burdensome feature of respiratory diseases. The understanding of cough has progressed significantly in recent years, albeit largely in refractory (unexplained) chronic cough (RCC) in the absence of other respiratory conditions. The prevalence of CC in respiratory diseases is poorly described, but estimates have been reported: asthma (8-58%), chronic obstructive pulmonary disease (COPD; 10-74%), bronchiectasis (82-98%), interstitial lung disease (ILD; 50-89%) and sarcoidosis (3-64%). CC in respiratory conditions generally predicts impaired health status and more severe disease. It is associated with increased symptom burden and disease severity in asthma, COPD, bronchiectasis and ILD, higher exacerbation frequency in asthma and bronchiectasis, and increased mortality and lung transplantation in idiopathic pulmonary fibrosis (IPF). Physiologically, heightened cough reflex sensitivity (CRS) has been reported and postulated to be mechanistic in isolated RCC. Cough reflex hypersensitivity (CRH) has also been reported in asthma, COPD, bronchiectasis, ILD and sarcoidosis. Unlike recent advances in isolated RCC, there are limited studies and understanding of central cough neuropathways in other respiratory conditions. Of note, dysfunctional central voluntary cough suppression neuropathways and physiology were observed in isolation in RCC; cough suppression is preserved in COPD. Understanding in the mechanism of RCC cannot be simply extrapolated to other respiratory conditions. The restricted understanding of cough mechanisms in these conditions has limited cough-specific therapeutic options in this context. There is currently an unmet need to expand our understanding of cough in chronic respiratory conditions, both in order to improve the quality of life of patients, and to improve knowledge of cough in general. This review aims to describe the prevalence, impact, pathophysiology and management of CC in asthma, COPD, bronchiectasis, ILD and sarcoidosis.

Dataset Information

Will expanded ART use reduce the burden of HIV-associated chronic lung disease?

Publications

Will expanded ART use reduce the burden of HIV-associated chronic lung disease?

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