OBJECTIVE: To explore whether the airway inflammation marker in exhaled breath condensate is increased in obstructive sleep apnea-hypopnea syndrome (OSAHS). METHODS: Thirty-one patients with OSAHS (15 smokers and 16 non-smokers) and 10 healthy age-matched and weight-matched controls were included in the study. Exhaled breath condensate (EBC) was collected before and after sleep at the same night from both groups. Interleukin-6 (IL-6) in EBC was measured by a specific enzyme immunoassay. RESULTS: (1) There was no difference in the pre-sleep IL-6 level among OSAHS smoker group, OSAHS non-smoker group and the control subjects (F = 0.515, P > 0.05). Compared with the level of pre-sleep [(2.5 +/- 1.0) ng/L in OSAHS smoker, and (2.3 +/- 0.8) ng/L in OSAHS non-smoker], the post-sleep level of IL-6 was elevated significantly in EBC from OSAHS patients of non-smokers [(3.1 +/- 1.2) ng/L] and smokers [(3.7 +/- 1.9) ng/L, P < 0.05]. Nevertheless, IL-6 level from the control group showed a reverse change. IL-6 was decreased significantly [(2.0 +/- 0.8) ng/L in pre-sleep vs (2.7 +/- 1.0) ng/L in post-sleep] after sleep in this group. There was no difference in post-sleep IL-6 level between OSAHS smokers [(3.7 +/- 1.9) ng/L] and non-smokers [(3.1 +/- 1.2) ng/L, P > 0.05]. A significant higher IL-6 level was observed in both OSAHS smokers [(3.7 +/- 1.9) ng/L] and non-smokers [(3.1 +/- 1.2) ng/L] compared with the controlled group [(2.0 +/- 0.8) ng/L, P < 0.05]. IL-6 level in EBC was correlated positively with AHI (r = 0.441, P < 0.05), ODI(4) (r = 0.533, P < 0.05), and negatively with minimal oxygen saturation (r = -0.529, P < 0.05). CONCLUSIONS: These findings suggest that inflammation was characteristic in the airways of OSAHS patients. Nocturnal hypoxia could be responsible for this change. The levels of IL-6 in EBC are associated with the severity of OSAHS and may prove to be useful in monitoring of airway inflammation in OSAHS.
OBJECTIVE: To explore whether the airway inflammation marker in exhaled breath condensate is increased in obstructive sleep apnea-hypopnea syndrome (OSAHS). METHODS: Thirty-one patients with OSAHS (15 smokers and 16 non-smokers) and 10 healthy age-matched and weight-matched controls were included in the study. Exhaled breath condensate (EBC) was collected before and after sleep at the same night from both groups. Interleukin-6 (IL-6) in EBC was measured by a specific enzyme immunoassay. RESULTS: (1) There was no difference in the pre-sleep IL-6 level among OSAHS smoker group, OSAHS non-smoker group and the control subjects (F = 0.515, P > 0.05). Compared with the level of pre-sleep [(2.5 +/- 1.0) ng/L in OSAHS smoker, and (2.3 +/- 0.8) ng/L in OSAHS non-smoker], the post-sleep level of IL-6 was elevated significantly in EBC from OSAHS patients of non-smokers [(3.1 +/- 1.2) ng/L] and smokers [(3.7 +/- 1.9) ng/L, P < 0.05]. Nevertheless, IL-6 level from the control group showed a reverse change. IL-6 was decreased significantly [(2.0 +/- 0.8) ng/L in pre-sleep vs (2.7 +/- 1.0) ng/L in post-sleep] after sleep in this group. There was no difference in post-sleep IL-6 level between OSAHS smokers [(3.7 +/- 1.9) ng/L] and non-smokers [(3.1 +/- 1.2) ng/L, P > 0.05]. A significant higher IL-6 level was observed in both OSAHS smokers [(3.7 +/- 1.9) ng/L] and non-smokers [(3.1 +/- 1.2) ng/L] compared with the controlled group [(2.0 +/- 0.8) ng/L, P < 0.05]. IL-6 level in EBC was correlated positively with AHI (r = 0.441, P < 0.05), ODI(4) (r = 0.533, P < 0.05), and negatively with minimal oxygen saturation (r = -0.529, P < 0.05). CONCLUSIONS: These findings suggest that inflammation was characteristic in the airways of OSAHS patients. Nocturnal hypoxia could be responsible for this change. The levels of IL-6 in EBC are associated with the severity of OSAHS and may prove to be useful in monitoring of airway inflammation in OSAHS.