Abstract
Introduction: Exhaled nitric oxide (eNO) is considered a marker of T-helper cell Type 2 mediated airway inflammation, particularly in asthma. Conflicting data exists regarding chronic lung allograft dysfunction (CLAD) after lung transplantation1,2. This prospective study compares eNO with CLAD phenotypes and outcomes.
Methods: All outpatient eNO measurements performed between 01.07.2009 - 31.01.2016 were reviewed. Patients with ≥3 measurements, including a baseline measurement ≤6 mts, who underwent bilateral-lung / heart-lung transplantation and developed CLAD were included. Individual baseline values acted as controls. Longitudinal comparisons used the Wilcoxon Signed Ranks Test C, with the Mann-Whitney U test or Kruskal-Wallis H test for analysis between groups.
Results: CLAD developed in 80pts, each with 6 [IQR 5-9] eNO measurements. Bronchiolitis obliterans syndrome (BOS) developed in 62pts (78%), with 18pts (22%) exhibiting the restrictive allograft syndrome (RAS). Treatment refractory CLAD developed in 32pts (40%). Significant increases in eNO were evident at CLAD onset, but did not persist. This was independent of CLAD phenotype or treatment response
N | eNO baseline vs CLAD onset | eNO baseline vs. established CLAD | |
BOS | 62 | p=0.001 | p=0.575 |
RAS | 18 | p=0.031 | p=0.586 |
CLAD progress | 32 | p=0.003 | p=0.881 |
CLAD stable | 32 | p=0.079 | p=0.822 |
CLAD improved | 16 | p=0.044 | p=0.532 |
Change in eNO at CLAD-onset and subsequent control.
Conclusions: Individual variation in baseline eNO is considerable. Significant, albeit transient rises nevertheless occurred in 71% of patients at CLAD onset. Similar courses were evident in both phenotypes, arguing against mutually exclusive pathophysiology. eNO does not appear to predict treatment response.
- Copyright ©the authors 2016