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In reference to An electron microscopic study—Correlation of gastroesophageal reflux disease and laryngopharyngeal reflux
Author(s) -
Toohill Robert J.
Publication year - 2011
Publication title -
the laryngoscope
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.181
H-Index - 148
eISSN - 1531-4995
pISSN - 0023-852X
DOI - 10.1002/lary.21444
Subject(s) - laryngopharyngeal reflux , reflux , citation , otorhinolaryngology , medicine , library science , disease , computer science , surgery
In the July 2010 issue of Laryngoscope, authors Park et al. published their study titled ‘‘An Electron Microscopic Study—Correlation of Gastroesophageal Reflux Disease and Laryngopharyngeal Reflux.’’ Although it is well known that both gastroesophageal reflux disease (GERD) and laryngopharyngeal reflux (LPR) occur because of tissue reactions in the lower esophagus (GERD) and the pharyngeal and laryngeal (LPR) areas from regurgitated gastric fluids, the similarities of these two disorders are otherwise quite different and do not correlate well. The authors have not related that the majority of GERD patients do not have LPR or other extraesophageal reflux (EER) disorders, and that only 20% to 30% of LPR patients have associated GERD. Also not mentioned is the fact that LPR patients are invariably upright refluxers as opposed to GERD patients who are more inclined to reflux in the supine position. GERD is a time-honored well-described clinical entity of heartburn and regurgitation, and LPR is a significant but much different EER disorder both in diagnostic and treatment modalities. Transmission electron microscopy of biopsies of the distal esophagus demonstrating dilated intercellular spaces (DIS) has been well established to confirm the diagnosis of GERD. Studies at both the basic and clinical level show the acid component of refluxate will cause DIS to occur. Pharyngeal and laryngeal biopsies of patients with LPR have also shown DIS. Basic studies of pepsin and bile have also shown DIS to occur in epithelial tissues affected by reflux. Thus, DIS is also a likely non–acid-mediated mechanism in some patients. To select out a few patients with LPR who have associated GERD and demonstrate DIS in esophageal biopsies is of interest, and the authors should be commended for their study. The implications and conclusions seem to indicate a lot of commonality in these two disorders, and this in most cases is not the true picture. Such a correlation, it is feared, will leave readers with the wrong conclusions. Those interested in DIS of the esophagus might want to read the study by Orlando and Orlando.