BACKGROUND: Patients with gastroesophageal reflux disease (GERD) are commonly instructed to reduce coffee intake. However, prior studies evaluating the effects of coffee on GERD yielded conflicting results. We aimed to perform a comprehensive systematic review and meta-analysis to assess the association between coffee use and risk of GERD and its complications.

METHODS: A protocolized search strategy was developed for PubMed, EMBASE, and Web of Science databases in accordance with PRISMA and MOOSE guidelines. Measured outcomes for GERD were compared between coffee drinkers and non-drinkers. Dichotomous events between unmatched groups were used to calculate pooled proportions with rates estimated using random effects models and effect size. Heterogeneity was assessed with I2 statistics and publication bias by funnel plot asymmetry and Egger regression.

RESULTS: A total of 40 studies encompassing 122,074 patients were included (85,400 coffee drinkers vs 36,674 non-drinkers). GERD was more common among coffee users than non-users [34.9% (CI:28.5-41.8) vs 30.7% (CI:25.2-36.7); OR:1.18 (CI:1.03-1.36; I2=89.38)]. There was no significant association between coffee intake and Barrett's esophagus [22.1% (CI:12.8-35.4) users vs 17.6% (CI:5.5-43.8) non-users; OR:1.13 (CI:0.79-1.61; I2=55.5)]. There was no evidence of publication bias based on funnel plot and Egger regression testing (p>0.05 for all analyses).

CONCLUSION: Coffee use was associated with a small, statistically significant increased rate of GERD, but not Barrett's. The magnitude of this effect, however, is of unclear clinical significance. The role of routine avoidance/reduction of coffee intake as universal lifestyle modification for GERD needs further evaluation.

BACKGROUND: The value of esophageal baseline impedance (BI) in assessing proximal reflux and laryngopharyngeal symptoms (LPS) is unclear.

METHODS: 208 patients with LPS underwent 24-hour combined hypopharyngeal-esophageal impedance-pH monitoring. Proximal/distal BI were obtained and a slope-and-intercept model of proximal BI contour was constructed.

RESULTS: Proximal BI correlated with proximal/pharyngeal reflux (r=-0.21, p<0.01) and reflux symptom index (r=-0.14, p=0.08). Proximal BI contour model incorporating both BI change (slope) and BI just below upper esophageal sphincter (intercept) outperformed models using individual BI measures in predicting proximal (AIC: 110 vs 251-253) or pharyngeal (AIC: 32 vs 141-148) reflux.

CONCLUSION: Proximal esophageal impedance contour predicts proximal reflux n patients with LPS.

BACKGROUND & AIMS: The impact of the esophageal eosinophilic distribution pattern on treatment outcomes in eosinophilic esophagitis (EoE) is unclear. We aimed to determine if the eosinophil distribution at index endoscopy predicts proton pump inhibitor (PPI) response in EoE.

METHODS: This was a cohort study of newly diagnosed adult patients with EoE from 3 hospitals. All included patients received ≥8-week PPI trial and underwent repeat biopsies to assess response. Primary analyses compared PPI response between isolated distal disease (≥15 eosinophils/hpf on distal but not proximal biopsies) and proximal/diffuse eosinophilia (≥15 eosinophils/hpf on proximal ± distal biopsies). Secondary analyses categorized patients as distal-predominant (distal >proximal eosinophils by ≥10/hpf), proximal predominant (proximal >distal eosinophils by ≥10/hpf), or even distribution pattern. Multivariable analyses were performed using logistic regression, adjusting for potential confounders.

RESULTS: A total of 266 patients (50.8% male; 89.1% White) met inclusion criteria, including 66 with isolated distal and 200 with proximal/diffuse disease. PPI response was higher among patients with isolated distal disease (histologic remission [<15 eosinophils/hpf post-PPI]: 63.6% vs 44.5%; P = .01; deep remission [<6 eosinophils/hpf]: 54.5% vs 31.0%; P = .001; symptom improvement: 92.4% vs 81.0%; P = .03). On multivariable analyses, isolated distal disease remained independently associated with histologic response (adjusted odds ratio [aOR], 2.04; 95% confidence interval [CI], 1.10-3.77; P = .02), deep remission (aOR, 2.46; 95% CI, 1.33-4.54; P = .02), and symptom improvement (aOR, 4.1; 95% CI, 1.4-12.01; P = .01). On secondary analyses, proximal-predominant eosinophilia independently predicted PPI histologic nonresponse compared with distal-predominant (aOR, 0.52; 95% CI, 0.28-0.99; P = .04) or any nonproximal (aOR, 0.54; 95% CI, 0.3-0.97; P = .04) pattern.

CONCLUSIONS: Isolated distal eosinophilia at index endoscopy independently predicted PPI response in patients with EoE, whereas proximal-predominant pattern predicted nonresponse. Patterns of esophageal eosinophilic distribution may reflect different disease phenotypes and help guide management.

INTRODUCTION: The term laryngopharyngeal reflux (LPR) is frequently applied to aerodigestive symptoms despite lack of objective reflux evidence. The aim of this initiative was to develop a modern care paradigm for LPR supported by otolaryngology and gastroenterology disciplines.

METHODS: A 28-member international interdisciplinary working group developed practical statements within the following domains: definition/terminology, initial diagnostic evaluation, reflux monitoring, therapeutic trials, behavioral factors and therapy, and risk stratification. Literature reviews guided statement development and were presented at virtual/in-person meetings. Each statement underwent 2 or more rounds of voting per the RAND Appropriateness Method; statements reaching appropriateness with ≥80% agreement are included as recommendations.

RESULTS: The term laryngopharyngeal symptoms (LPS) applies to aerodigestive symptoms with potential to be induced by reflux and include cough, voice change, throat clearing, excess throat phlegm, and throat pain. Laryngopharyngeal reflux disease (LPRD) refers to patients with LPS and objective evidence of reflux. Importantly, the presence of LPS does not equate to LPRD. Laryngoscopy has value in assessing for nonreflux laryngopharyngeal processes, but laryngoscopic findings alone cannot diagnose LPRD. LPS patients should be categorized as with or without concurrent esophageal reflux symptoms. While lifestyle modification and empiric trials of acid suppression ± alginates are appropriate when esophageal reflux symptoms coexist, upper endoscopy and ambulatory reflux monitoring are required for LPRD diagnosis when symptoms persist, when LPS is isolated, or when management needs to be escalated to include invasive antireflux management. The two recommended ambulatory reflux monitoring modalities, 24-hour pH-impedance and 96-hour wireless pH monitoring, are not mutually exclusive with distinct roles for the evaluation of LPS. Laryngeal hyperresponsiveness and hypervigilance commonly contribute to both LPS and LPRD presentations and are responsive to laryngeal recalibration therapy and neuromodulators.

DISCUSSION: The San Diego Consensus represents the formal modern-day interdisciplinary care paradigm to evaluate and manage LPS and LPRD.