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Postprandial High-Resolution Impedance Manometry Identifies Mechanisms of Nonresponse to Proton Pump Inhibitors.

ABSTRACT: BACKGROUND & AIMS:Recognition of rumination and supragastric belching is often delayed as symptoms may be mistakenly attributed to gastroesophageal reflux disease. However, distinct from gastroesophageal reflux disease, rumination and supragastric belching are more responsive to behavioral interventions than to acid-suppressive and antireflux therapies. Postprandial high-resolution impedance manometry (PP-HRIM) is an efficient method to identify rumination and belches. We investigated the distribution of postprandial profiles determined by PP-HRIM, and identified patient features associated with postprandial profiles among patients with nonresponse to proton pump inhibitors (PPIs). METHODS:We performed a retrospective analysis of PP-HRIM studies performed on 94 adults (mean age, 50.6 y; 62% female) evaluated for PPI nonresponsiveness at an esophageal referral center, from January 2010 through May 2016. Following a standard esophageal manometry protocol, patients ingested a solid refluxogenic test meal (identified by patients as one that induces symptoms) with postprandial monitoring up to 90 minutes (median, 50 min). Patients were assigned to 1 of 4 postprandial profiles: normal; reflux only (>6 transient lower esophageal sphincter relaxations (TLESRs)/h); supragastric belch (>2 supragastric belches/h), with or without TLESR; or rumination (?1 rumination episode/h) with or without TLESR and supragastric belching. The primary outcome was postprandial profile. RESULTS:Of the study participants, 24% had a normal postprandial profile, 14% had a reflux-only profile, 42% had a supragastric belch profile, and 20% had a rumination profile. In multinomial regression analysis, the rumination group most frequently presented with regurgitation, the supragastric belch and rumination groups were younger in age, and the reflux-only group had a lower esophagogastric junction contractile integral. The number of weakly acidic reflux events measured by impedance-pH monitoring in patients receiving PPI therapy was significantly associated with frequency of rumination episodes and supragastric belches. CONCLUSIONS:In a retrospective analysis of 94 nonresponders to PPI therapy evaluated by PP-HRIM, we detected an abnormal postprandial pattern in 76% of cases: 42% of these were characterized as supragastric belching, 20% as rumination, and 14% as reflux only. Age, esophagogastric junction contractility, impedance-pH profiles, and symptom presentation differed significantly among groups. PP-HRIM can be used in the clinic to evaluate mechanisms of PPI nonresponse.

SUBMITTER: Yadlapati R

PROVIDER: S-EPMC5794564 | biostudies-literature | 2018 Feb

REPOSITORIES: biostudies-literature

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Postprandial High-Resolution Impedance Manometry Identifies Mechanisms of Nonresponse to Proton Pump Inhibitors.

Yadlapati Rena R Tye Michael M Roman Sabine S Kahrilas Peter J PJ Ritter Katherine K Pandolfino John E JE

Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association 20170912 2

<h4>Background & aims</h4>Recognition of rumination and supragastric belching is often delayed as symptoms may be mistakenly attributed to gastroesophageal reflux disease. However, distinct from gastroesophageal reflux disease, rumination and supragastric belching are more responsive to behavioral interventions than to acid-suppressive and antireflux therapies. Postprandial high-resolution impedance manometry (PP-HRIM) is an efficient method to identify rumination and belches. We investigated th ...[more]

PMID: 28911949

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Project description:BACKGROUND & AIMS:Esophageal retention is typically evaluated by timed-barium esophagram in patients treated for achalasia. Esophageal bolus clearance can also be evaluated using high-resolution impedance manometry. We evaluated the associations of conventional and novel high-resolution impedance manometry metrics, esophagram, and patient-reported outcomes (PROs) in achalasia. METHODS:We performed a prospective study of 70 patients with achalasia (age, 20-81 y; 30 women) treated by pneumatic dilation or myotomy who underwent follow-up evaluations from April 2013 through December 2015 (median, 12 mo after treatment; range, 3-183 mo). Patients were assessed using timed-barium esophagrams, high-resolution impedance manometry, and PROs, determined from Eckardt scores (the primary outcome) and the brief esophageal dysphagia questionnaire. Barium column height was measured from esophagrams taken 5 minutes after ingestion of barium (200 mL). Impedance-manometry was analyzed for bolus transit (dichotomized) and with a customized MATLAB program (The MathWorks, Inc, Natick, MA) to calculate the esophageal impedance integral (EII) ratio. RESULTS:Optimal cut points to identify a good PRO (defined as Eckardt score of ?3) were esophagram barium column height of 3 cm (identified patients with a good PRO with 63% sensitivity and 75% specificity) and an EII ratio of 0.41 (identified patients with a good PRO with 83% sensitivity and 75% specificity). Complete bolus transit identified patients with a good PRO with 28% sensitivity and 75% specificity. Of the 25 patients who met these cut points for both esophagram barium column height and EII ratio, 23 (92%) had a good PRO. Of the 17 patients who met neither cut point, 14 (82%) had a poor PRO (Eckardt score above 3). CONCLUSIONS:In a prospective study of 70 patients with achalasia, we found EII ratio identified patients with good PROs with higher levels of sensitivity (same specificity) than timed-barium esophagram or impedance-manometry bolus transit assessments. The EII ratio should be added to achalasia outcome evaluations that involve high-resolution impedance manometry as an independent measure and to complement timed-barium esophagram.

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Postprandial High-Resolution Impedance Manometry Identifies Mechanisms of Nonresponse to Proton Pump Inhibitors.

Publications

Postprandial High-Resolution Impedance Manometry Identifies Mechanisms of Nonresponse to Proton Pump Inhibitors.

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