Clinical Practice Update: Extraesophageal Symptoms Attribute to Gastroesophageal Reflux Disease

A recent practice update (MF Vaezi, D Katzka, F Zerbib. Clin Gastroenterol Hepatol 2018; 16: 1018-29) reviews the data and provides up-to-date recommendations for extraesophageal symptoms attributed to gastroesophageal reflux disease (GERD) in adults.

Extraesophageal symptoms attributed to GERD could include cough, asthma, hoarseness, sore throat, sinusitis, dental erosions, and ear pain.

Key recommendations:

  • Non-GI evaluations by ENT, pulmonary and/or allergy are essential and often should be performed initially in most patients.
  • “Abnormalities seen on endoscopy have poor predictive value for determination of GERD as the cause of extraesophageal symptoms”
  • “Ambulatory pH/impedance monitoring…have limited ability to establish GERD as the cause of an extraesophageal symptom.  The main role of testing is to document the absence of GERD.”
  • Empiric therapy with ‘aggressive’ acid suppression for 6-8 weeks can help in assessing association between reflux and extraesophageal symptoms.
  • Testing for reflux on therapy should be considered mainly in those with high probability of baseline reflux (eg. previous esophagitis, Barrett’s esophagus, or prior abnormal pH study).
  • Surgical treatment is discouraged in those with extraesophageal reflux symptoms unresponsive to aggressive PPI therapy

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Salivary Pepsin Doesn’t Pass Muster for Evaluation of Reflux

For quite a long time, I thought the expression was “Pass Mustard”.

A recent study (F Dy et al. J Pediatr 2016; 177: 53-8) shows that testing salivary pepsin is probably a waste of time in assessing for extraesophageal reflux disease. The authors prospectively recruited 50 children who underwent multiple studies including 24-hour pH-MII testing. The idea of pepsin as a biomarker has some plausibility since it is produced in the stomach and its presence in the oropharynx (or airway) would be unexpected.  Since salivary pepsin does not require invasive diagnostic testing, it would be useful if it had adequate sensitivity and specificity.

Key findings:

  • 21 of 50 (42%) were salivary pepsin-positive with a median concentration of 10 ng/mL.  Pepsin was detected in 6 of 21 with abnormal impedance testing and 8 of 21 with abnormal pH results (per Table 1 –the discussion used a denominator of 11 for each of these results)
  • There was no significant correlation between salivary pepsin-positivity compared with salivary pepsin-negative for reflux episodes, acid reflux, nonacid reflux or any other reflux variable.

  • The authors also reiterate in the discussion that clinical trials, evaluating reflux and chronic cough, “have failed to find a consistent relationship between measure dreflux and clinical response.”
  • The authors note that bronchoscopy pepsin correlation with esophageal reflux monitoring was similarly low in sensitivity
  • The authors note that “one-third of healthy asymptomatic adults have pepsin detected in their saliva.”  In this study, 38% (15 of 39) of children had pepsin detected despite normal impedance results.

My take:  While this study mainly shows that pepsin detected in the saliva has no practical use in correlation with reflux, the bigger picture is the uncertain relationship of reflux as a causal association with chronic cough.

Any of the reflux-esophageal gurus care to comment?

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