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01.11.2010 | 2010 SSAT Plenary Presentation | Ausgabe 11/2010

Journal of Gastrointestinal Surgery 11/2010

Loss of Alkalization in Proximal Esophagus: a New Diagnostic Paradigm for Patients with Laryngopharyngeal Reflux

Zeitschrift:
Journal of Gastrointestinal Surgery > Ausgabe 11/2010
Autoren:
Shahin Ayazi, Jeffrey A. Hagen, Joerg Zehetner, Matt Lilley, Priyanka Wali, Florian Augustin, Arzu Oezcelik, Helen J. Sohn, John C. Lipham, Steven R. DeMeester, Tom R. DeMeester
Wichtige Hinweise
This manuscript was presented at the plenary session of the Annual Meeting of the Society for Surgery of the Alimentary Tract at Digestive Diseases Week, May 1–5, 2010, New Orleans, LA.

Discussant

Dr. Michael F. Vaezi (Nashville, TN): As you and your group knows, identifying more sensitive and more specific markers in LPR has been a challenge, limiting our ability to adequately diagnose and treat this difficult group of patients. I have a few questions, if you could clarify for us.
One is that you had mentioned that your patient population was mostly those that had concomitant typical symptoms and LPR. Were they patient mix and their chief complaints LPR symptoms, or were they predominantly typical symptoms but they had LPR complaints as well?
Number 2. As you know, when we increase the sensitivity of the test, this often is at the cost of specificity. Can you comment on that for me, whether or not you have increased sensitivity for LPR diagnosis but decreased the specificity for GERD?
Finally, since your cases were patients who responded to your surgical intervention, do you think the choice of using healthy controls was the correct one instead of choosing patients who had fundoplication without response to therapy?

Closing Discussant

Dr. Shahin Ayazi: Your first question referred to the chief complaint of our LPR patients. Eight out of 51 patients in our study had isolated LPR symptoms. The remaining 43 patients had combination of both typical and atypical reflux symptoms. The chief complaint in majority of the 43 patients was LPR symptoms, but there were also patients whose main driving force for treatment was typical reflux symptoms, and the LPR complaints were secondary or tertiary.
Your second question addresses the specificity of pH threshold of 7 in the diagnosis of LPR. This is a fair question since the effort of our study was to improve the sensitivity of the test. The accuracy of a diagnostic test depends on providing the best combination of sensitivity and specificity. We concur that improvement in sensitivity may result in sacrificing specificity. Unfortunately, the design of our study did not allow us to determine specificity. This would require having a true negative and a false positive group in our study population. For obvious reasons, it is difficult to identify such groups. Therefore, I cannot comment on the specificity of our approach. However, as you have correctly pointed out, there is a need to improve the accuracy of LPR diagnostic markers. The shortcomings of the different diagnostic tests vary; some lack sensitivity while others suffer from low specificity. The “achilles heel” of pH monitoring in the diagnosis of LPR is its low sensitivity, reflected by 50–60% sensitivity reported in publications on the subject, including the study from your group. The driving force in the design and conduct of our study was improving the sensitivity of pH monitoring in the diagnosis LPR.
This is in contrast to laryngoscopy that has a low specificity. Improvement in specificity of laryngoscopy requires identifying more specific laryngoscopic signs for reflux-related upper aerodigestive tract complaints. This is a task that needs our ENT colleagues’ attention.
Your last question is focused on our control group. I agree with you that from the methodology point of view, having a control group consisting of patients who did not benefit from a treatment might be a better choice than choosing healthy controls. The problem is identifying patients in whom reflux is the cause of laryngopharyngeal symptoms is challenging. Our goal was to validate our hypothesis in a clean and carefully selected group of patients. While it is reasonable to blame reflux as the cause of LPR symptoms in those who had complete relief of their LPR symptoms after antireflux surgery, the opposite is not as true. This is because the etiology of LPR symptoms is multifactorial and LPR patients may have more than one factor as the cause of their symptoms. Antireflux surgery can stop reflux but has no impact on other factors such as ENT pathologies (sinusitis and etc.). In addition, antireflux surgery’s ability in eliminating atypical reflux symptoms is not as effective as it is with typical reflux symptoms. Consequently, it might not be appropriate to exclude reflux as the cause of LPR symptoms based on unsatisfactory results of antireflux surgery. For these reasons, we selected healthy subjects as controls rather than patients who did not respond to surgical therapy.

Abstract

Introduction

Cervical esophageal pH monitoring using a pH threshold of <4 in the diagnosis of laryngopharyngeal reflux (LPR) is disappointing. We hypothesized that failure to maintain adequate alkalization instead of acidification of the cervical esophagus may be a better indicator of cervical esophageal exposure to gastric juice. The aim of this study was to define normal values for the percent time the cervical esophagus is exposed to a pH ≥7 and to use the inability to maintain this as an indicator for diagnosis of LPR.

Material and Methods

Fifty-nine asymptomatic volunteers had a complete foregut evaluation including pH monitoring of the cervical esophagus. Cervical esophageal exposure to a pH <4 was calculated, and the records were reanalyzed using the threshold pH ≥7. The sensitivity of these two pH thresholds was compared in a group of 51 patients with LPR symptoms that were completely relieved after an antireflux operation.

Results

Compared to normal subjects, patients with LPR were less able to maintain an alkaline pH in the cervical esophagus, as expressed by a lower median percent time pH ≥ 7 (10.4 vs. 38.2, p < 0.0001). In normal subjects, the fifth percentile value for percent time pH ≥ 7 in the cervical esophagus was 19.6%. In 84% of the LPR patients (43/51), the percent time pH ≥ 7 were below the threshold of 19.6%. In contrast, 69% (35/51) had an abnormal test when the pH records were analyzed using the percent time pH < 4. Of the 16 patients with a false negative test using pH < 4, 11 (69%) were identified as having an abnormal study when the threshold of pH ≥ 7 was used.

Conclusion

Normal subjects should have a pH ≥7 in cervical esophagus for at least 19.6% of the monitored period. Failure to maintain this alkaline environment is a more sensitive indicator in the diagnosis of the LPR and identifies two thirds of the patients with a false negative test using pH <4.

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