Chronic obstructive pulmonary disease in HIV
- PMID: 33167728
- PMCID: PMC7856058
- DOI: 10.1080/17476348.2021.1848556
Chronic obstructive pulmonary disease in HIV
Abstract
Introduction: Chronic obstructive pulmonary disease (COPD) is more prevalent in people with HIV (PWH) than in the general population and leads to an increased burden of morbidity and mortality in this population. The mechanisms behind COPD development and progression in PWH are not fully elucidated, and there are no PWH-specific guidelines for COPD management. Areas covered: The goal of this broad narrative review is to review the epidemiology of COPD in PWH globally, highlight proposed pathways contributing to increased COPD prevalence and progression in PWH, discuss structural and functional changes in the lungs in this population, assesses the excess mortality and comorbidities in PWH with COPD, and address management practices for this unique population. Expert opinion: Understanding how a chronic viral infection leads to COPD, independent of cigarette smoking, is of critical scientific importance. Further research should focus on the pathophysiology of the interaction between HIV and COPD, and determine the role of disease-modifying risk factors such as opportunistic pneumonia and air pollution, as well as generate data from randomized clinical trials on the safety and efficacy of specific therapies for this vulnerable patient population.
Keywords: Air pollution; COPD; HIV; inflammation; lung function; lung structure; management; smoking.
Conflict of interest statement
Declaration of interest
KM Kunisaki reports personal fees from GlaxoSmithKline for consulting and from Nuvaira for independent Data Monitoring Committee services; contracted clinical research support from Sanofi; and government grants from NIH R01 HL140971, Department of Defense, and Department of Veterans Affairs. J Vasquez is supported by NIH K01 HL140804 and the Robert Wood Johnson Foundation Harold Amos Medical Faculty Development Program; P30 AI027763; U19 AI096109; and R01 AI141003. L Huang is partly supported by NIH R01 HL128156 and R01 HL143998. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
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