Progressively, the patient developed thoracic pain, dysphagia, and regurgitations leading to reduced food intake. Clinical examination evidenced a loss of 10 kg. Treatment with proton pump inhibitors and trimebutine did not improve the symptoms. Laboratory testing, thoracoabdominopelvic CT scanner, esophagogastroduodenoscopy, and colonoscopy with biopsies (including esophageal biopsies) were unremarkable. A high-resolution esophageal manometry uncovered a median 4-second integrated relaxing pressure of 20.2 mmHg, with a minor resting pressure of the low esophageal sphincter of 50.6 mmHg, and 100% normotonic and peristaltic esophageal contractions induced with the wet swallows, a mean Centrinone distal latency of 6 secs, and a mean distal contractile essential of 2262 mmHgcmsec (Body A). Barium esophagogram demonstrated a reasonably distended esophageal body and a postponed esophageal emptying (Body B). Considering the standard (and repeated) endoscopic and scannographic investigations, we regarded the chance of a job from the gabapentin in the esophagogastric junction outflow blockage (EGJOO) and ceased this treatment. 90 days afterwards, the dysphagia got improved, and follow-up manometry and barium swallow had been normal (Statistics C and D). Open in another window Figure High-resolution esophageal manometry and barium esophagogram teaching an esophagogastric junction outflow blockage characterized by a normotonic persistaltic esophageal contraction associated with an elevated median 4-seconds integrated resting pressure ( 15 mmHg) (panel A), and a tight esophagogastric junction with mildly dilated esophagus on esophagogram (panel B). Three months later, after discontinuation of gabapentin, high-resolution manometry (panel C) as well as barium esophagogram (panel D) went back to normal. Gabapentin has a recognized efficacy in the treatment of neuropathic pain,1 and has been proposed as a therapy for pharyngeal pain and pain during chemoradiotherapy2 or functional cervical pain.3 Gabapentin is a gamma-amino butyric acid analogue of which the exact mechanism of action remains to be determined. However, it could act as a gamma-aminobutyric acid B (GABAB) receptor agonist, like baclofen.1 Baclofen, along with other GABAB receptor agonists, has been proposed as a second line treatment of gastro-esophageal reflux disease, since it reduces the rate of transient lower esophageal sphincter relaxations, the rate of gastroesophageal reflux episodes and increases the basal lower Rabbit polyclonal to MEK3 esophageal sphincter pressure.4,5 In our patient case, the symptoms and high-resolution manometry measurements before and after discontinuation of gabapentin are in favor of an increased tonicity of the lower esophageal sphincter, characterized as an esophagogastric junction outflow obstruction according to the Chicago classification of esophageal motility disorders version 3.06 induced by gabapentin. The recurrence of dysphagia and EGJOO after reintroduction of gabapentin would have further supported this hypothesis but Centrinone was however not performed in this patient. EGJOO is usually a manometric entity including a variety of conditions. Usually, the patient workup includes, as in our patient case, repeat endoscopy and CT scanner to rule out esophageal stenosis, hiatal hernia, and tumoral infiltration of the esophagogastric junction; and going through the patient medications, to check for the absence of any opioid-derived treatment capable of inducing such manometric features. Our patient case suggests that gamma-amino butyric acid analogues such as gabapentin should belong to the list. Footnotes Financial support: None. Conflicts of interest: None. Author contributions: Maximilien Barret drafted the manuscript, Marie-Anne Guillaumot, Chlo Landri, Raphael Gaillard, and Stanislas Chaussade analyzed the data and provided critical review to the manuscript. All authors approved the final version of the paper.. with a minimal resting pressure of the lower esophageal sphincter of 50.6 mmHg, and 100% normotonic and peristaltic esophageal contractions induced by the wet swallows, a mean distal latency of 6 seconds, and a mean distal contractile integral of 2262 mmHgcmsec (Determine A). Barium esophagogram showed a moderately distended esophageal body and a delayed esophageal emptying (Physique B). Considering the standard (and repeated) endoscopic and scannographic investigations, we regarded the chance of a job from the gabapentin in the esophagogastric junction outflow blockage (EGJOO) and ended this treatment. 90 days afterwards, the dysphagia acquired improved, and follow-up manometry and barium swallow had been normal (Statistics C and D). Open up in another window Body High-resolution esophageal manometry and barium esophagogram displaying an esophagogastric junction outflow blockage seen as a a normotonic persistaltic esophageal contraction connected with an increased median 4-secs integrated resting pressure ( 15 mmHg) (panel A), and a tight esophagogastric junction with mildly dilated esophagus on esophagogram (panel B). Three months later, after discontinuation of gabapentin, high-resolution manometry (panel C) as well as barium esophagogram (panel D) went back to normal. Gabapentin has a acknowledged efficacy in the treatment of neuropathic pain,1 and has been proposed as a therapy for pharyngeal pain and pain during chemoradiotherapy2 or functional cervical pain.3 Gabapentin is a gamma-amino butyric acid analogue of which the exact mechanism of action remains to be determined. However, it could act as a gamma-aminobutyric acid B (GABAB) receptor agonist, like baclofen.1 Baclofen, along with other GABAB receptor agonists, has been proposed as a second collection treatment of gastro-esophageal reflux disease, since it reduces the rate of transient lower esophageal sphincter relaxations, the rate of gastroesophageal reflux episodes and increases the basal lower esophageal sphincter pressure.4,5 In our individual case, the symptoms and high-resolution manometry measurements before and after discontinuation of gabapentin are and only an elevated tonicity of the low esophageal sphincter, characterized as an esophagogastric junction outflow obstruction based on the Chicago classification of esophageal motility disorders version 3.06 induced by gabapentin. The recurrence of dysphagia and EGJOO after reintroduction of gabapentin could have additional backed this hypothesis but was nevertheless not performed within this affected individual. EGJOO is certainly a manometric entity including a number of Centrinone conditions. Usually, the individual workup contains, as inside our individual case, do it again endoscopy and CT scanning device to eliminate esophageal stenosis, hiatal hernia, and tumoral infiltration from the esophagogastric junction; and going right through the patient medicines, to check on for the lack of any opioid-derived treatment with the capacity of inducing such manometric features. Our affected individual case shows that gamma-amino butyric acidity analogues such as for example gabapentin should participate in the list. Footnotes Financial support: non-e. Conflicts appealing: None. Writer efforts: Maximilien Barret drafted the manuscript, Marie-Anne Guillaumot, Chlo Landri, Raphael Gaillard, and Stanislas Chaussade examined the data and provided crucial review to the manuscript. All authors approved the final version of the paper..