Renske A.B. Oude Nijhuis | Jurjaan A. Snelleman | Jac M. Oors|
Boudewijn F. Kessing | Derrek A. Heuveling| Jeroen M. Schuitenmaker |Liesbeth ten Cate | Andreas J.P.M. Smout | Albert J. Bredenoord
Introduction: Although inability to belch has previously been linked to dysfunction of the upper esophageal sphincter (UES), its underlying pathogenesis remains unclear.
Our aim was to study mechanisms underlying inability to belch and the effect of UES botulinum toxin (botox) injections in these patients.
Methods: We prospectively enrolled consecutive patients with symptoms of inability to belch. Patients underwent stationary high-resolution impedance manometry (HRIM) with belch provocation and ambulatory 24-h pH-impedance monitoring before and 3 months after UES botox injection.
Results: Eight patients (four males, age 18–37 years) were included. Complete and normal UES relaxation occurred in response to deglutition in all patients. A median number of 33(15–64) gastroesophageal gas reflux episodes were observed. Despite the subsequent increase in esophageal pressure (from −4.0 [−7.7–4.2] to 8 [3.3–16.1] mmHg; p < 0.012), none of the gastroesophageal gas reflux events resulted in UES relaxation. Periods of continuous high impedance levels, indicating air entrapment (median air presence time 10.5% [0–43]), were observed during 24-h impedance monitoring. UES botox reduced UES basal pressure (from 95.7[41.2–154.0]to 29.2[16.7–45.6] mmHg; p < 0.02) and restored belching capacity in all patients. As a result, esophageal air presence time decreased from 10.5% (0–43.4) to 0.7% (0.1–18.6; p < 0.02) and esophageal symptoms improved in all patients (VAS 6.0 [1.0–7.9] to 1.0 [0.0–2.5];p < 0.012).
Conclusion: The results of this study underpin the existence of a syndrome characterized by an inability to belch and support the hypothesis that ineffective UES relaxation, with subsequent esophageal air entrapment, may lead to esophageal symptoms.