TREATING GERD MAY REDUCE NASAL SYMPTOMS

FCAAIA Notes: Lots of things are connected on the inside, so we should not be surprised when one condition (in this case reflux) is associated with another (in this case nasal congestion).  I can speculate a couple of possible mechanisms:  Maybe reflux triggers a neurological reflex that leads to nasal congestion.  Maybe reflux into the back of the nose and upper throat have a direct effect causing some inflammation, irritation, swelling, and obstruction. Maybe it’s a combination or there are other mechanisms.

More research will be needed to identify why the association exists, but let’s not be afraid to address what on the surface seems to be an unlikely cause of nasal congestion when other more common causes have been ruled out.

(Source: For Medscape articles: http://www.medscape.com/viewarticle/877236?nlid=113469_3821&src=WNL_mdplsfeat_170321_mscpedit_aimm&uac=112079PK&spon=38&impID=1312573&faf=1 Mrch 21, 2017. User name: FCAAIA, Password: Allergies)

According to a new study, in patients with gastroesophageal reflux disease (GERD) who have laryngopharyngeal reflux (LPR) and symptoms of nasal obstruction, treatment of the reflux with a proton pump inhibitor (PPI) may also reduce nasal symptoms.

Elif Dagli, MD, from Kecioren Training and Research Hospital, Ankara, Turkey, and colleagues published the results of their study online March 9 in JAMA Otolaryngology–Head & Neck Surgery.

“In this study, laryngopharyngeal reflux had a negative effect on nasal resistance and nasal congestion. Treatment was associated with improved subjective and objective nasal findings,” the authors write.

“To our knowledge, this is the first study investigating the effect of LPR on nasal resistance.”

Although GERD is considered an important cause of LPR, studies have also implicated reflux as a potential exacerbating factor in upper respiratory disease.

However, a definitive relationship between reflux and sinonasal disease has yet to be established. The mechanisms involved in any such relationship also remain poorly understood.

Dr Dagli and colleagues therefore conducted a prospective observational case-control study in adults to investigate whether LPR is associated with nasal resistance, and whether treating LPR improves symptoms of nasal congestion.

They included 50 patients with classic symptoms of GERD who also had evidence of lower esophageal sphincter dysfunction and esophagitis, as well as a diagnosis of LPR (reflux symptom index [RSI] > 13, reflux finding score [RFS] > 7). The researchers also included 50 participants with no history of LPR or nasal disease as a control group.

The patients with LPR took the oral PPI pantoprazole for 12 weeks (40 mg, twice daily). They also received advice about dietary modification and lifestyle changes to help improve their symptoms.

Before treatment, patients with LPR had higher Nasal Obstruction Symptom Evaluation (NOSE) and Total Nasal Resistance (TNR) scores than those in the control group (median NOSE, 8 vs 6; median TNR, 0.29 vs 0.20).

PPI treatment was associated with significant decreases in all parameters of the NOSE (median, 0.19; difference, −3.0), and TNR (median, 0.19; difference, −0.08) values.

“Whereas the TNR scores of the LPR group were higher than those of the control group before treatment (difference, −0.77; 95%[confidence interval], −0.10 to 0.05), they were almost the same after treatment (difference, 0.01; 95%[confidence interval], &minus’0.01 to 0.03),” the authors add.

Although these findings show that LPR had a negative effect on nasal resistance and nasal congestion, the underlying mechanism involved remains unclear. Because the patients in the treatment group had esophagitis, Dr Dagli and colleagues suggest the pathophysiology may involve vagal reflex activation. However, because the researchers did not perform nasopharyngeal pH testing in this study, they note that direct acid exposure could also be an exacerbating factor.

“Additional clinical trials are needed to elucidate the pathophysiological processes that contribute to these respiratory changes,” they conclude.

This study “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,” write Stacey T. Gray, MD, from Harvard Medical School, Boston, Massachusetts, and Ahmad R. Sedaghat, MD, PhD, from Massachusetts Eye and Ear Infirmary, Boston, in an accompanying invited commentary.

They emphasize that these findings have important implications for treatment of patients who present with symptoms of nasal obstruction, especially those without an apparent sinonasal etiology. Clinicians should evaluate these patients for comorbid LPR and, if found, might consider treatment with a PPI to help manage the nasal obstruction, the editorialists say.

However, because this study was nonrandomized, Dr Gray and Dr Sedaghat stress the need for a double-blind randomized clinical trial of PPIs for the treatment of nasal obstruction in patients with LPR.

It will also be important to identify whether the results of this study by Dr Dagli and colleagues are applicable to all patients with LPR, or only to specific subsets of patients with LPR.

“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,” the editorialists conclude.

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