Related Experiment Video
Updated: Jul 12, 2026
Simultaneous Laryngopharyngeal and Conventional Esophageal pH Monitoring
Published on: December 14, 2020
Gene expression changes of inflammatory mediators in posterior laryngitis due to laryngopharyngeal reflux and
Susan L Thibeault1, Marshall E Smith, Kathryn Peterson
1Division of Otolaryngology-Head and Neck Surgery, Department of Surgery, University of Wisconsin-Madison, Madison, WI 53792-7375, USA. thibeault@surgery.wisc.edu
Hypothesis:
Standard of care in laryngopharyngeal reflux (LPR) is acid suppression therapy. Its treatment efficacy and mechanism of action are not well documented. No objective study investigating the molecular patterns of inflammation in LPR or in response to proton pump inhibitor (PPI) treatment has been accomplished. We hypothesized that gene expression levels of mediators of inflammation -- interleukin 6 (IL6), interleukin 8 (IL8), interleukin 1a (IL1a), interleukin 1b (IL1b), transforming growth factor beta 1 (TGFbeta1), vascular endothelial growth factor (VEGF), fibroblast growth factor-2 (FGF2), and tumor necrosis factor alpha (TNFalpha) -- in posterior larynx tissue would be increased in those with diagnosed LPR and would be then reduced with PPI treatment.
Study Design:
Prospective uncontrolled trial.
Methods:
Biopsies from the posterior larynx were taken from 25 participants with LPR before and after a 10-week period with rabeprazole (40 mg). RNA isolation and real-time PCR was used to measure gene expression levels.
Results:
No significant differences were measured for any of the cytokines, either for the entire participant group (n = 25) or for the subset of participants who did not have a previous history of PPI usage (n = 15). In those participants who had a history of PPI usage (n = 10), a significant increase in gene expression levels post medication was measured for TGFbeta1 (P = .0396), VEGF (P = .0216), IL8 (P = .0297), after adjusting for compliance, subjective improvement, and reflux severity.
Conclusions:
Our findings are provocative and speak to the unresolved understanding of the pathophysiology of LPR, its diagnosis, and its differences from gastroesophageal reflux disease.
Related Concept Videos
01:25Gastroesophageal Reflux Disease
01:29Gastroesophageal Reflux Disease II: Clinical Features and Management
Clinical Manifestations
GERD presents itself in a multitude of ways, with symptoms varying from person to person. The hallmark symptoms are...
01:29Gastroesophageal Reflux Disease I: Meaning and Pathophysiology
01:23Chronic Pharyngitis
Etiology
It often arises from persistent viral or bacterial infections affecting sinuses and tonsils.
Additional contributing factors include inadequate dental hygiene, mouth breathing, recurring tonsillitis, allergic rhinitis, laryngopharyngeal reflux, and exposure to smoke, chemicals, and other environmental pollutants. Allergic reactions to pollen, mold, and pet dander, chronic cough, excessive voice usage,...
01:24Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features
01:30Peptic Ulcer Disease I: Introduction
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...