Pathological bolus exposure plays a significant role in eliciting non-cardiac chest pain
Article first published online: 15 JUN 2010
© 2010 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd
Journal of Gastroenterology and Hepatology
Volume 25, Issue 12, pages 1855–1860, December 2010
How to Cite
Kim, B. J., Choi, S. C., Kim, J. J., Rhee, J. C. and Rhee, P.-L. (2010), Pathological bolus exposure plays a significant role in eliciting non-cardiac chest pain. Journal of Gastroenterology and Hepatology, 25: 1855–1860. doi: 10.1111/j.1440-1746.2010.06415.x
- Issue published online: 23 NOV 2010
- Article first published online: 15 JUN 2010
- Accepted manuscript online: 15 JUN 2010 12:00AM EST
- Accepted for publication 3 June 2010.
- combined impedance–pH monitoring;
- non-cardiac chest pain;
- pathological bolus exposure
Background and Aim: Pathological bolus exposure is defined in the present study as cases in which all reflux percentage times are above 1.4% of the total reflux number, as revealed by impedance–pH monitoring. The role of pathological bolus exposure in the pathogenesis of non-cardiac chest pain (NCCP) is poorly known. We aimed to classify and characterize NCCP using combined impedance–pH monitoring.
Methods: Seventy-five consecutive patients with NCCP were prospectively enrolled from January 2006 to October 2008. All the patients underwent upper endoscopy, esophageal manometry, and 24-h multichannel intraluminal impedance (MII)–pH metering.
Results: Sixteen patients (21.3%) had esophageal erosion upon endoscopy. Upon esophageal manometry, 37 patients (49.3%) had esophageal dysmotility. When the patients were classified based on MII–pH metering, 16 (21.3%) showed pathological acid exposure, and 40 (53.3%) showed pathological bolus exposure. The DeMeester score of patients with pathological acid exposure was higher than that of patients with pathological bolus exposure (P = 0.002). There was no significant difference in age, sex, typical esophageal symptoms, presence of esophageal erosion, esophageal dysmotility, improvement with proton pump inhibitor medication, symptom index ≥50%, percentage of time clearance pH below 4 ≥4%, and all reflux time ≥1.4% in the fasting period between the two groups. When the patients were divided into gastroesophageal reflux disease (GERD)-related NCCP and non-GERD-related NCCP groups based on MII–pH metering and upper endoscopy, there was no difference between the two groups.
Conclusions: Combined impedance–pH monitoring improves the detection and characterization of NCCP. This study suggests that pathological bolus exposure plays a major role in eliciting NCCP.