Pathological bolus exposure plays a significant role in eliciting non-cardiac chest pain
- Authors
- Kim, Beom Jin; Choi, Sung Chul; Kim, Jae J.; Rhee, Jong Chul; Rhee, Poong-Lyul
- Issue Date
- Dec-2010
- Publisher
- WILEY
- Keywords
- combined impedance-pH monitoring; non-cardiac chest pain; pathological bolus exposure
- Citation
- JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, v.25, no.12, pp 1855 - 1860
- Pages
- 6
- Journal Title
- JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
- Volume
- 25
- Number
- 12
- Start Page
- 1855
- End Page
- 1860
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/22040
- DOI
- 10.1111/j.1440-1746.2010.06415.x
- ISSN
- 0815-9319
1440-1746
- Abstract
- 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.
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