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their baseline No when they gave up for one week. In the ten who were able to continue, their
level of exhaled NO had increased to normal non-smoking levels when re-measured at eight
weeks, while in those that were unable to sustain quitting, the No had dropped to the previous
low levels (Hogman, Holmkvist et al. 2OO2). This effect of smoking is unfortunate as it
renders the measurement of No unhelpful, particularly in the asthmatic population where it
could be a helpful longitudinal indicator of airway inflammation and treatment effects.
9.15 Nitric oxide levels in interstitial lung diseases
Interstitial lung diseases have been particularly helpful in proving the value of using differing
flows to measure NO from different areas within the lung (see Section 9.3.1 (i))' In 20
patienrs with scleroderma including five with additional pulmonary hypertension (Girgis,
Gugnani et a:.2002) and in 24 patients with scleroderma including twelve with and twelve
without clinical or radiological evidence of lung disease (Moodley and Lalloo 2001)'
significant differences in exhaled NO levels from control subjects were only seen when the
alveolar rather than airway concentrations were measured. There was also a negative
correlation demonstrated between the alveolar concentration of NO and the diffusion
coefficient in the parient groups (Moodley and Lalloo 2001; Girgis, Gugnani et al' 2002)' In
active fibrosing alveolitis, an alveolar NO increase was associated with increasing
lymphocyte cell counts and an alveolar decrease was associated with corticosteroid treatment
(paredi, Kharitonov et al. 1999). This is in contrast to studies using one standard expiratory
flow for measurement, where no difference was found in 34 patients with systemic sclerosis
(Sud, Khullar et al. 2000), or in 52 patients with sarcoidosis (Wilsher, Fergusson et al' 2005)'
One study did find higher exhaled NO levels using the standard flow in 47 patients with
systemic sclerosis, particularly those with interstitial lung disease, and demonstrated an
inverse correlation with pulmonary artery pressure but no correlation to age, disease duration,
current therapy or the type of disease be it limited or diffuse (Rolla, Colagrande et al' 2000)'
One early paper also measured exhaled NO continuously in expired air at baseline and during
an exercise test and calculated the output of NO, which was low in six subjects with
pulmonary fibrosis compared to normal subjects. The authors suggested that that this patient
group may fail to increase NO output by failing to recruit the capillary bed during exercise
(Riley, Porszasz et al. lgg|). Nasal NO was 887o lower than normals in diffuse
panbronchiolitis, a pulmonary disease of unknown origin confined usually to individuals of
Japanese, Korean or chinese descent (Nakano, Ide et al. 2000). All current and future work in
this area of interstitial lung disease should use the ability to measure NO in the alveolar
compartment for meaningful results.
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