OBJECTIVES/HYPOTHESIS: Laryngopharyngeal reflux (LPR) originates from regurgitation of gastric contents, a mechanism seemingly identical to gastroesophageal reflux disease (GERD). Some researchers postulate a connection between LPR and GERD, whereas some assert LPR is a disease apart from GERD. We examined symptoms of GERD from LPR patients, and performed gastrointestinal endoscopy and transmission electron microscopy (TEM) to evaluate GERD findings from these patients. STUDY DESIGN: Prospective study at an academic tertiary care center. METHODS: Control subjects had no symptoms or signs of LPR/GERD. LPR was diagnosed with a Reflux Symptom Index >13 and Reflux Finding Score >7, and were questioned for GERD-related symptoms and examined with esophagogastroduodenoscopy, then allocated into either an LPR without GERD or LPR with GERD group. Esophageal tissues were obtained from the squamocolumnar junction and managed for TEM, and the intercellular space (IS) was measured to find dilatation, a characteristic GERD finding. RESULTS: About 30% (8/26) of LPR patients showed GERD-related symptoms, connecting LPR with the GERD group. Most of the LPR patients showed grossly normal endoscopic findings. On TEM, IS of control group (n = 15) was measured as 0.35 +/- 0.27 microm, whereas the LPR without GERD group (n = 18) and LPR with GERD group (n = 8) revealed a dilated IS of 0.61 +/- 0.47 microm and 0.95 +/- 0.44 microm, respectively. This difference was statistically significant compared to the control group (P < .05). CONCLUSIONS: The mean IS of LPR was significantly increased, suggesting common pathogenesis between LPR and GERD.
OBJECTIVES/HYPOTHESIS: Laryngopharyngeal reflux (LPR) originates from regurgitation of gastric contents, a mechanism seemingly identical to gastroesophageal reflux disease (GERD). Some researchers postulate a connection between LPR and GERD, whereas some assert LPR is a disease apart from GERD. We examined symptoms of GERD from LPR patients, and performed gastrointestinal endoscopy and transmission electron microscopy (TEM) to evaluate GERD findings from these patients. STUDY DESIGN: Prospective study at an academic tertiary care center. METHODS: Control subjects had no symptoms or signs of LPR/GERD. LPR was diagnosed with a Reflux Symptom Index >13 and Reflux Finding Score >7, and were questioned for GERD-related symptoms and examined with esophagogastroduodenoscopy, then allocated into either an LPR without GERD or LPR with GERD group. Esophageal tissues were obtained from the squamocolumnar junction and managed for TEM, and the intercellular space (IS) was measured to find dilatation, a characteristic GERD finding. RESULTS: About 30% (8/26) of LPR patients showed GERD-related symptoms, connecting LPR with the GERD group. Most of the LPR patients showed grossly normal endoscopic findings. On TEM, IS of control group (n = 15) was measured as 0.35 +/- 0.27 microm, whereas the LPR without GERD group (n = 18) and LPR with GERD group (n = 8) revealed a dilated IS of 0.61 +/- 0.47 microm and 0.95 +/- 0.44 microm, respectively. This difference was statistically significant compared to the control group (P < .05). CONCLUSIONS: The mean IS of LPR was significantly increased, suggesting common pathogenesis between LPR and GERD.