P-values <0.05 were taken as statistically significant. Values in impedance–pH monitoring are presented as medians and in the 25th–75th percentiles. An analysis using a generalized linear mixed model was done for comparisons between patients Selleck Pritelivir with pathological acid exposure and patients with pathological bolus exposure.

The characteristics of the patients are shown in Table 1. Typical esophageal symptoms, such as heartburn or acid regurgitation, were observed in 41 patients (54.6%). Sixteen patients (21.3%) had reflux esophagitis, as determined by UGI endoscopy. Esophageal manometry identified 37 patients (49.3%) with esophageal dysmotility. This included nutcracker esophagus in 17 patients, ineffective esophageal motility in 12, non-specific esophageal motility disorder in five, and other findings in three patients. PPI medication improved the symptoms in 50 selleck inhibitor of 54 patients (92.6%), regardless of the presence of GERD. The results of MII–pH metering in patients with NCCP are summarized in Table 2. The impedance test determined a longer bolus exposure in the postprandial period than in the fasting period (P = 0.003). In addition, reflux episodes predominantly involved the distal esophagus. The composition of GERD-related NCCP changed in the postprandial period (Fig. 1). A total

of 48 patients (64%) were compatible with a diagnosis of GERD-related NCCP in the postprandial period. Sixteen patients (21.3%) had GERD-related NCCP upon pH metering.

In contrast, 40 patients (53.3%) also proved to have GERD-related NCCP, according to the impedance test; this included 13 patients (17.3%) who showed pathological bolus exposure and pathological acid exposure at the same acetylcholine time. In this study, pathological bolus exposure upon MII was increased during meals, because more patients in the postprandial period had pathological bolus exposure than in the fasting period (40 patients [53.3%]vs 18 patients [24.0%], respectively). Patients with NCCP were classified as having pathological acid exposure or pathological bolus exposure, according to the results of MII–pH metering. 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, respectively (Table 3). There was no significant difference in age, sex, typical esophageal symptoms, presence of esophageal erosion, esophageal dysmotility, improvement with PPI 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. Although the median values of both patients with pathological acid exposure and patients with pathological bolus exposure were within normal limits, the DeMeester score of patients with pathological acid exposure was higher than that of patients with pathological bolus exposure (P = 0.002). The patients were divided into two groups, according to the presence of GERD (Table 4).