
Value of lung diffusing capacity for nitric oxide in systemic sclerosis
Author(s) -
Barisione Giovanni,
Garlaschi Alessandro,
Occhipinti Mariaelena,
Baroffio Michele,
Pistolesi Massimo,
Brusasco Vito
Publication year - 2019
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.14149
Subject(s) - dlco , diffusing capacity , interstitial lung disease , cardiology , lung , medicine , lung volumes , pathology , lung function
A decreased lung diffusing capacity for carbon monoxide ( DL CO ) in systemic sclerosis ( SS c) is considered to reflect losses of alveolar membrane diffusive conductance for CO ( DM CO ), due to interstitial lung disease, and/or pulmonary capillary blood volume ( V C ), due to vasculopathy. However, standard DL CO does not allow separate DM CO from V C . Lung diffusing capacity for nitric oxide ( DL NO ) is considered to be more sensitive to decrement of alveolar membrane diffusive conductance than DL CO . Standard DL CO and DL NO were compared in 96 SS c subjects with or without lung restriction. Data showed that DL NO was reduced in 22% of subjects with normal lung volumes and DL CO , whereas DL CO was normal in 30% of those with decreased DL NO . In 30 subjects with available computed tomography of the chest, both DL CO and DL NO were negatively correlated with the extent of pulmonary fibrosis. However, DL NO but not DL CO was always reduced in subjects with ≥ 5% fibrosis, and also decreased in some subjects with < 5% fibrosis. DM CO and V C partitioning and Doppler ultrasound‐determined systolic pulmonary artery pressure could not explain individual differences in DL CO and DL NO . DL NO may be of clinical value in SS c because it is more sensitive to DM CO loss than standard DL CO , even in nonrestricted subjects without fibrosis, whereas DL CO partitioning into its subcomponents does not provide information on whether diffusion limitation is primarily due to vascular or interstitial lung disease in individual subjects. Moreover, decreased DL CO in the absence of lung restriction does not allow to suspect pulmonary arterial hypertension without fibrosis.