Airway inflammation in subjects with gastro-oesophageal reflux and gastro-oesophageal reflux-related asthma.
OBJECTIVE
Asthma and gastro-oesophageal reflux (GER) are both characterized by airway inflammation.


METHODS
The purposes of this work were (i) to study airway inflammation in patients troubled by gastro-oesophageal reflux (GER) and GER associated with asthma, (ii) to ascertain whether GER can aggravate asthma by exacerbating the pre-existing airway inflammation and oxidative stress and (iii) to establish the validity of analysing breath condensate and induced sputum when studying the airways of subjects affected by GER. PATIENT S AND METHODS: We enrolled 14 patients affected by mild asthma associated with GER (40 +/-12 years), nine with mild but persistent asthma (39 +/- 13 years), eight with GER (35 +/- 11 years) and 17 healthy subjects (37 +/- 9 years). Sputum cell counts and concentrations of interleukin-4 (IL-4), IL-6 and 8-isoprostane were measured in breath condensate and supernatant.


RESULTS
GER-related asthma is characterized by an eosinophilic inflammation, as determined by elevated concentrations of IL-4 in breath condensate and sputum supernatant, and by sputum cell analysis. GER alone presents a neutrophilic pattern of inflammation when determined by elevated concentrations of IL-6 in sputum cell analysis. A concomitant increase has been found in 8-isoprostane in GER associated (or not associated) with asthma.


CONCLUSIONS
We conclude that GER is characterized by a neutrophilic airway inflammation and by increased oxidative stress. GER does not however aggravate pre-existing airway inflammation in asthma patients. Determinations of inflammatory and oxidant markers in the breath condensate of subjects with GER reflect these measured in the induced sputum.
Institute of Respiratory Diseases, University of Foggia, Foggia, Italy. ge.carpagnano@unifg.it
G E
GE
Carpagnano
O
O
Resta
M T
MT
Ventura
A C
AC
Amoruso
G
G
Di Gioia
T
T
Giliberti
L
L
Refolo
M P
MP
Foschino-Barbaro
D000328:Adult; D001249:Asthma / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D015415:Biomarkers / Q000032:analysis; D001944:Breath Tests; D003430:Cross-Sectional Studies; D015237:Dinoprost / Q000031:analogs & derivatives / Q000032:analysis; D005260:Female; D005541:Forced Expiratory Volume; D005764:Gastroesophageal Reflux / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D006863:Hydrogen-Ion Concentration; D018836:Inflammation Mediators / Q000032:analysis; D015847:Interleukin-4 / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D013183:Sputum / Q000737:chemistry / Q000166:cytology; D014797:Vital Capacity
D015415:Biomarkers; D018836:Inflammation Mediators; D015850:Interleukin-6; D015847:Interleukin-4; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost