Background: Obesity is associated with restrictive ventilatory defects and a faster rate of decline in FVC. This association is not exclusively mediated by mechanical factors and may reflect direct pulmonary injury by adipose-derived mediators.
Research question: Is adipose tissue involved in the pathogenesis of interstitial lung disease (ILD)?
Study design and methods: We evaluated the association of CT measures of pericardial, abdominal visceral, and abdominal subcutaneous adipose tissue with high-attenuation areas (HAAs) and interstitial lung abnormalities (ILAs) in a large multicenter cohort study of community-dwelling adults, using multivariable-adjusted models. We secondarily evaluated the association of adipose depot size with FVC and biomarkers of obesity and inflammation.
Results: In fully adjusted models, every doubling in pericardial adipose tissue volume was associated with a 63.4-unit increase in HAA (95% CI, 55.5-71.3), 20% increased odds of ILA (95% CI, -2% to 50%), and a 5.5% decrease in percent predicted FVC (95% CI, -6.8% to -4.3%). IL-6 levels accounted for 8% of the association between pericardial adipose tissue and HAA. Every doubling in visceral adipose tissue area was associated with a 41.5-unit increase in HAA (95% CI, 28.3-54.7), 30% increased odds of ILA (95% CI, -10% to 80%), and a 5.4% decrease in percent predicted FVC (95% CI, -6.6% to -4.3%). IL-6 and leptin accounted for 17% and 18%, respectively, of the association between visceral adipose tissue and HAA.
Interpretation: Greater amounts of pericardial and abdominal visceral adipose tissue were associated with CT measures of early lung injury and lower FVC in a cohort of community-dwelling adults. Adipose tissue may represent a modifiable risk factor for ILD.
Keywords: IL-6; high-attenuation areas; interstitial lung abnormalities; interstitial lung disease; leptin; obesity.
Copyright © 2021 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.