Peristaltic dysfunction in asthma is secondary to increased Gastro-Oesophageal Reflux

Abstract

BACKGROUND: Vagal dysfunction and prolonged intra-oesophageal acidification cause oesophageal hypomotility. Asthmatics have ineffective oesophageal motility, but demonstrate increased vagal activity. Whether oesophageal hypomotility in asthmatics is a primary abnormality or secondary to pathological gastro-oesophageal reflux is unclear. Our aim was to investigate the relationship of oesophageal motility and gastro-oesophageal reflux (GOR)to vagal function in asthmatics. METHODS: Thirty consecutive mild, stable asthmatics (ATS criteria) and 30 healthy volunteers underwent 24-hour ambulatory dual-sensor oesophageal monitoring, stationary oesophageal manometry and autonomic function testing. They also underwent gastro-oesophageal reflux disease (GORD) symptom assessment. Twenty seven of the thirty asthmatics underwent gastroscopy. A parasympathetic autonomic function score was calculated from vagal function tests (valsalva manouvre, heart rate variation to deep breathing, heart rate and blood pressure response to standing from a supine position) and correlated with gastro-oesophageal function parameters. RESULTS: Age and sex of asthmatics (mean age(SD), 34.8 years (8.4); 60% female) and controls (mean age(SD), 30.9 years (7.7); 50% female) were comparable. Asthmatics had a higher frequency and severity of GORD symptoms and 10/27 (39%) had oesophageal mucosal damage. Twenty two (69%) asthmatics showed a hypervagal response and none had a hyperadrenergic response. Manometrically, LOS and UOS parameters were similar in the two groups, but 14 asthmatics had ineffective oesophageal motility. Asthmatics with higher GORD symptom scores had a significantly lower percentage of peristaltic contractions and a higher percentage of simultaneous contractions than controls. They also had higher total and upright oesophageal acid contact times in the proximal oesophagus than those with low symptom scores. All reflux parameters were significantly higher in asthmatics. Twenty (66.7%) asthmatics had abnormal distal acid reflux and 22 (73.3%) had abnormal proximal acid reflux. Asthmatics also had significantly prolonged proximal and distal acid clearance times than controls. There was no association between parasympathetic function and either oesophageal motility or reflux parameters. CONCLUSIONS: Asthmatics with mild, stable asthma have abnormal oesophageal motility and pathological GOR. The asthmatics did not show any evidence of vagal dysfunction nor did the vagal function score correlate with oesophageal motility parameters. It seems likely that the peristaltic dysfunction is secondary to damage due to GOR and not primary vagal dysfunction.