Gastroesophageal reflux disease (GERD) is highly prevalent, and its most common symptoms, including heartburn and regurgitation, may be present in up to 45% of the population.1 Laryngopharyngeal reflux (LPR) is an extraesophageal manifestation of GERD that may be present in up to 10% of patients presenting for ambulatory otolaryngology visits.2 Typical symptoms that have been attributed to LPR include globus sensation, laryngospasm, throat clearing, and hoarseness. Moreover, it has been postulated that mucosal inflammation due to LPR may extend beyond the larynx and oropharynx to the nasopharynx and nasal cavity, contributing to the pathogenesis of sinonasal diseases. For example, an association between chronic rhinosinusitis (CRS) and GERD has been shown through epidemiologic studies that have found high rates of pharyngeal reflux in CRS,3 as well as the finding of digestive enzymes in the nasal secretions of patients with CRS.4 Despite this, few studies have objectively examined the effect of treatment of LPR on sinonasal symptoms.
In this issue of JAMA Otolaryngology–Head & Neck Surgery, Dagli and colleagues5 report their experience with the symptom of nasal obstruction in patients with LPR and report how the use of a proton pump inhibitor (PPI) to treat these patients’ LPR affects concomitant nasal obstruction. The authors conducted a prospective observational clinical study in which 50 patients with confirmed esophagitis and symptoms of LPR, making up the study group, were treated with a PPI for 12 consecutive weeks and no other treatment for nasal obstruction, such as intranasal corticosteroids, was given. The study group had no other evidence of sinonasal disease, such as CRS or allergic rhinitis, and was compared with a control group, consisting of 50 patients with no evidence of LPR or other sinonasal diseases who had no symptoms of nasal obstruction. Pretreatment assessment of the LPR group included a subjective measurement of nasal congestion with the Nasal Obstruction Symptom Evaluation (NOSE) instrument and an objective measurement of total nasal resistance (TNR) using rhinomanometry. Compared with the control group, the LPR group had a significantly higher median NOSE score and TNR before treatment with a PPI. After 12 weeks of treatment with a PPI, not only did the study group demonstrate significantly lower NOSE scores and TNR, but the posttreatment NOSE scores and TNR of the study group also normalized to be no different than what was found in the control group.
This is the first study to prospectively study the impact of LPR treatment on subjective and objective measures of nasal obstruction, and the results provide novel evidence for the relationship of LPR to sinonasal symptoms. The finding that treatment of LPR with a PPI alone—and no treatment directed at nasal symptoms—was sufficient to reduce nasal obstruction in patients with LPR suggests that LPR at the very least has the ability to contribute to nasal symptoms. Moreover, the findings of this study have important implications for the treatment of patients presenting with nasal obstruction. Dagli and colleagues5 show that in patients with nasal obstruction, LPR may have a causative role and that in these patients, comorbid LPR should be investigated for and treated with a PPI as a component of management for nasal obstruction.
This prospective study by Dagli and colleagues5 provides the strongest evidence to date for a causative role for LPR in nasal obstruction symptoms and thus provides novel insights for the clinical investigation and potential treatment of patients presenting with nasal obstruction. These findings should also motivate further studies in the form of a double-blind randomized clinical trial of PPIs for the treatment of nasal obstruction in patients with LPR given the lack of randomization in this study. Because the study patients were recruited on the basis of LPR rather than complaints of nasal obstructive symptoms, an interventional study designed for the specific treatment of nasal obstruction in patients with LPR may best determine the efficacy of PPIs. Moreover, the authors excluded patients from this study who might have any sinonasal etiology—such as chronic rhinosinusitis, allergic rhinitis, inferior turbinate hypertrophy, or septal deviation—for nasal obstruction. Future investigation will need to identify whether the results of this study are generally applicable to all patients with LPR or whether there are particular subsets of patients with LPR who experience the greatest reduction in nasal obstructive symptoms after treatment with a PPI. For example, how would comorbid allergy affect the efficacy of LPR treatment in reducing nasal obstruction, and for those with seasonal allergies, does the time of the year affect the efficacy of PPIs in reducing nasal obstruction? Along the same line of reasoning, it will also be interesting to investigate whether the addition of treatment that specifically targets nasal obstruction, such as intranasal corticosteroids or antihistamines (in patients with allergies or CRS), to PPIs provides additional benefits for improving nasal obstructive symptoms in patients with comorbid LPR. For now, however, Dagli and colleagues5have provided evidence that LPR should be considered as a potential contributing factor in patients presenting with nasal obstruction, in particular those patients without an apparent sinonasal etiology for nasal obstruction. It is not yet clear whether treatment of LPR for nasal obstruction in patients with other comorbid nasal conditions would be beneficial. Given the recent concerns about potential adverse effects of long-term PPI use, these issues need to be further studied before treatment recommendations are made.