Introduction: Distortion of esophagogastric junction (EGJ) architecture, caused by repeated proximal gastric distention, creates susceptibility to GERD; the end result is permanent dilation of the gastric cardia which is directly proportional to disease severity, with the largest circumference present in those with Barrett’s esophagus (BE). Because of their propensity to reflux in the upright position, it is unclear whether cardia dilation with resultant anatomic valve deformation is also present in patients with laryngopharyngeal reflux (LPR) symptoms.
Methods: In a prospective study, 113 patients recruited from ENT (N=87) and Gastroenterology Clinics (N=26) underwent unsedated upper endoscopy in the upright position after completing validated questionnaires for GERD and LPR symptoms. Exclusions were made for a poor endoscopic view of the gastric cardia. Three populations were stratified based on symptom complex: 1) LPR symptoms only (Pure LPR), 2) Typical GERD symptoms only (GERD), and 3) Both LPR and typical GERD symptoms (Mixed). The primary outcome was cardia circumference (mm) as measured by an observer blinded to symptom complex using previously validated software. The secondary outcome was the prevalence of biopsy proven BE within each group as a proxy for disease severity and cancer risk.
Results: The Pure LPR group (N=32) had a mean gastric cardia circumference of 33.6 ± 7.3 mm. Similarly, the values in GERD (N=41) and Mixed (N=40) groups were 36.5 ± 9.6mm and 35.1 ± 8.0 mm, respectively (p=0.347, One Way ANOVA). Hiatal hernia size positively correlated with cardia circumference (r=0.219, p=0.02, Pearson’s). The overall prevalence of BE was 20.4%. BE was present in 15.6%, 34.2%, and 10.0% of Pure LPR, GERD, and Mixed patients, respectively (p<0.02, Chi square test). BE patients had a larger cardia circumference of 39.1 mm compared to 34.2 mm in those without BE (p<0.02, t-test).
Conclusion: Patients with LPR display the same degree of EGJ anatomic degradation as those with typical GERD symptoms which suggests a similar pathophysiology. This finding indicates that although LPR patients may sense reflux differently, they have similar risks as patients with typical symptoms. Further, the identification of BE, accompanied by increased gastric cardia diameter in the complete absence of typical GERD symptoms, suggests the potential for occult disease progression and late discovery of cancer.