The prevalence of gastro-esophageal reflux disease and esophageal dysmotility in Chinese patients with idiopathic pulmonary fibrosis.

BACKGROUND: The cause of idiopathic pulmonary fibrosis (IPF) remains unknown, yet gastro-esophageal reflux disease (GERD) is highly prevalent in this population. GERD prevalence was studied, and esophageal function tests (EFT) were assessed in Chinese IPF patients. METHODS: We prospectively studied 69 IPF patients who undertook both stationary High Resolution esophageal Manometry/Impedance (HRiM) and 24-hour esophageal Multi-Channel Intraluminal Impedance with pH Recordings (MII/pH). Patients were divided into GERD+ and GERD- groups according to pH results. Controls were HRiM treated healthy volunteers, and patients without IPF received HRiM and MII/pH diagnosed with GERD. RESULTS: 69 IPF patients, 62 healthy volunteers, and 88 IPF negative GERD patients were selected. GERD prevalence in IPF was 43/69 (62.3%), and 58.1% of patients presented with at least one typical symptom. Symptoms had a sensitivity of 58.1%, a specificity of 61.6%, a positive predictive value of 71.4% and a negative predictive of 47.1%. Compared with healthy volunteers, IPF patients had significantly decreased lower esophageal sphincter pressure (LESP), upper esophageal sphincter pressure (UESP) and complete bolus transit rate (CBTR). By contrast, IPF patients had increased total bolus transit time and prevalence of weak peristalsis. MII/pH showed that one third of IPF patients had abnormal distal and proximal reflux, especially non-acid reflux. Compared with GERD patients without IPF, GERD patients with IPF had significantly decreased CBTR and UESP with increased bolus exposure time. CONCLUSIONS: GERD prevalence in IPF was high, but symptoms alone were an unreliable predictor of reflux. IPF patients had lower LESP and UESP, impaired esophageal peristalsis and bolus clearance function with more proximal reflux events.

Comparisons of Esophageal Function Tests between Chinese and British Patients with Gastroesophageal Reflux Disease.

Objective. To investigate the esophageal function tests in British and Chinese patients with gastroesophageal reflux disease (GERD). Methods. Patients with GERD were selected from the functional gut clinic, London, and digestive department, Beijing Chao-Yang Hospital, after taking the examinations of High-resolution Manometry and Impedance (HRiM) and 24-hour Multi-Channel Intraluminal Impedance and pH Recording (MII/pH) between 2013 and 2014. Chinese healthy volunteers who undertook HRiM were also selected as control group. Results. Fifty-nine British and 82 Chinese patients with GERD and 62 Chinese healthy volunteers were entered. Values for British patients, Chinese patients, and healthy volunteers were as follows: Lower esophageal sphincter pressure (LESP) 16.0 ± 8.6, 16.5 ± 10.0, and 26.4 ± 10.9 mmHg, peristalsis (normal/small break/large break) 24/12/23, 44/10/28, and 57/1/4, total bolus transit time (TBTT) 7.3 ± 1.3, 7.6 ± 1.2, and 6.9 ± 0.9 s, and complete bolus transit rate (CBTR) 66.7 ± 37.8, 61.7 ± 36.4, and 90.3 ± 14.0%, respectively. Stepwise linear regression analysis showed that age, gender, and ethnicity did not have significant effect on LESP, TBTT, esophageal peristalsis, and CBTR in patients with GERD. Conclusions. British and Chinese patients with GERD presented similar values of LESP, TBTT, and impaired esophageal peristalsis and CBTR.

The development and maintenance of human visceral pain hypersensitivity is dependent on the N-methyl-D-aspartate receptor.

BACKGROUND & AIMS: Visceral hypersensitivity is a common feature of functional gastrointestinal disorders. One speculated mechanism is an activity-dependent increase in spinal cord neuronal excitability (central sensitization), which is dependent on activation of the N-methyl-D-aspartate (NMDA) receptor. Our aims were to determine whether the development and maintenance of human visceral hypersensitivity is NMDA receptor mediated. METHODS: Healthy subjects were studied using a randomized, double-blind, placebo-controlled, crossover design. Pain thresholds to electrical stimulation were determined both in the proximal esophagus and in the foot (control) before and after a 30-minute distal esophageal infusion of 0.15 mol/L HCl acid. Ketamine (NMDA receptor antagonist) or saline (vehicle) was given intravenously either prior to or following acid infusion, and pain thresholds were measured for the following 120 minutes. Protocol 1: In 6 subjects, the effect of ketamine in the esophagus was assessed without acid infusion. Protocol 2: In 14 subjects, ketamine was given prior to esophageal acid. Protocol 3: In 12 subjects, ketamine was given after esophageal acid. RESULTS: Protocol 1: In the absence of esophageal acid, ketamine had no effect on either esophageal or foot pain thresholds (area-under-the-curve, [AUC] P = 0.36 esophagus, P = 0.34 foot, ANOVA) within 30 minutes of cessation of the infusion. Protocol 2: Acid-induced esophageal hypersensitivity was prevented by ketamine (AUC, P < 0.0001, ANOVA) without affecting foot pain thresholds (AUC, P = 0.06, ANOVA). Protocol 3: Ketamine delivered after acid reversed the induction of esophageal hypersensitivity induced by acid (AUC, P < 0.0001, ANOVA). CONCLUSIONS: The induction and maintenance of acid-induced esophageal hypersensitivity is prevented and reversed by ketamine. This finding strongly indicates that central sensitization is a mechanism of visceral hypersensitivity.