Y M Fouad1, P O Katz, D O Castell. 1. Oesophageal Research Laboratory, Department of Medicine, Graduate Hospital, Philadelphia, Pennsylvania 19146, USA.
Abstract
BACKGROUND: Recent studies from our laboratory reveal that 70% of patients with gastro-oesophageal reflux disease (GERD) on proton pump inhibitors twice daily (b.d.) have nocturnal gastric acid breakthrough (gastric pH < 4 > 1 h) which is often accompanied by oesophageal acid exposure. The pathogenesis of GER during gastric acid breakthrough is not clear. AIM: To determine the prevalence of oesophageal motility abnormalities in patients with nocturnal GER associated with nocturnal acid breakthrough on proton pump inhibitor b.d. METHODS: We reviewed the pH-metry and manometric studies of 100 consecutive patients with GERD who were on proton pump inhibitor b.d. pH tracings were analysed for the nocturnal period (10.00 hours until 06.00 hours). Nocturnal GER was defined as> 0.5% time distal oesophageal pH < 4. Manometric tracings were reviewed for lower oesophageal sphincter (LES) pressure and oesophageal body motility. Chi-squared and Fischer's test were used for statistical analysis. RESULTS: Of the 100 patients, 74 (74%) had nocturnal gastric acid breakthrough. Thirty-one (42%) had concurrent abnormal nocturnal GER (refluxers) and 43 out of 74 (58%) had no GER (non-refluxers). The prevalence of ineffective oesophageal motility, and low LES pressure was significantly higher in refluxers than in non-refluxers (P < 0. 05, P < 0.001, respectively). Ineffective-oesophageal motility has a high specificity (91%), but low sensitivity (45%) as a diagnostic predictor for patients who are more likely to develop nocturnal GER on proton pump inhibitor b.d. CONCLUSION: Ineffective oesophageal motility is a risk factor for proton pump inhibitor refractory GER.
BACKGROUND: Recent studies from our laboratory reveal that 70% of patients with gastro-oesophageal reflux disease (GERD) on proton pump inhibitors twice daily (b.d.) have nocturnal gastric acid breakthrough (gastric pH < 4 > 1 h) which is often accompanied by oesophageal acid exposure. The pathogenesis of GER during gastric acid breakthrough is not clear. AIM: To determine the prevalence of oesophageal motility abnormalities in patients with nocturnal GER associated with nocturnal acid breakthrough on proton pump inhibitor b.d. METHODS: We reviewed the pH-metry and manometric studies of 100 consecutive patients with GERD who were on proton pump inhibitor b.d. pH tracings were analysed for the nocturnal period (10.00 hours until 06.00 hours). Nocturnal GER was defined as> 0.5% time distal oesophageal pH < 4. Manometric tracings were reviewed for lower oesophageal sphincter (LES) pressure and oesophageal body motility. Chi-squared and Fischer's test were used for statistical analysis. RESULTS: Of the 100 patients, 74 (74%) had nocturnal gastric acid breakthrough. Thirty-one (42%) had concurrent abnormal nocturnal GER (refluxers) and 43 out of 74 (58%) had no GER (non-refluxers). The prevalence of ineffective oesophageal motility, and low LES pressure was significantly higher in refluxers than in non-refluxers (P < 0. 05, P < 0.001, respectively). Ineffective-oesophageal motility has a high specificity (91%), but low sensitivity (45%) as a diagnostic predictor for patients who are more likely to develop nocturnal GER on proton pump inhibitor b.d. CONCLUSION: Ineffective oesophageal motility is a risk factor for proton pump inhibitor refractory GER.