Rahul Kataria

Mirtazapine for symptom control in refractory gastroparesis

Introduction Gastroparesis symptoms can be severe and debilitating. Many patients do not respond to currently available treatments. Mirtazapine has been shown in case reports to reduce symptoms in gastroparesis. Aim To assess the efficacy and safety of mirtazapine in gastroparetic patients. Methods Adults with gastroparesis and poorly controlled symptoms were eligible. Participants were prescribed mirtazapine 15 mg PO qhs. Questionnaires containing the gastrointestinal cardinal symptom index (GCSI) and the clinical patient grading assessment scale (CPGAS) were completed by patients’ pretreatment, at 2 weeks, and at 4 weeks. Primary end point was nausea and vomiting response to mirtazapine using the GCSI. Secondary end point was nausea and vomiting severity assessment using the CPGAS. P-values were calculated using the paired two-tailed Student’s t-test. Intention to treat analysis was used. Results A total of 30 patients aged 19–86 years were enrolled. Of those, 24 patients (80%) completed 4 weeks of therapy. There were statistically significant improvements in nausea, vomiting, retching, and perceived loss of appetite at 2 and 4 weeks (all P-values <0.05) compared with pretreatment. There was a statistically significant improvement in the CPGAS score at week 2 (P=0.003) and week 4 (P<0.001). Of the total patients, 14 (46.7%) experienced adverse effects from mirtazapine and due to this, 6 patients stopped therapy. Conclusion Mirtazapine significantly improved both nausea and vomiting in gastroparetics after 2 and 4 weeks of treatment. Side effects led to treatment self-cessation in a fifth of patients. From these data, we conclude that mirtazapine improves nausea and vomiting, among other symptoms, in patients with gastroparesis and might be useful in select patients.

Post-Fundoplication Dumping Syndrome: A Frequent “Rare” Complication

Gastroparesis, caused by delayed emptying of the stomach, has been shown to be associated with Nissen fundoplication. However, symptomatic rapid emptying of the stomach is rare after Nissen fundoplication, and its treatment is often challenging. We report 2 patients with dumping-like syndrome post-fundoplication with marked improvement of symptoms after dietary management and medical treatment.

Mo1827 Radiofrequency Ablation of Esophageal Gastric Heterotopia Leads to Improvement in Atypical Reflux Symptoms As Well As Eradication of Oxyntic and Metaplastic Mucosa

A gastric inlet patch (GIP), also known as a cervical inlet patch or gastric heterotopia, is a discrete island of columnar mucosa in the cervical esophagus. Its origin may be congenital or acquired. GIPs, seen in up to 10% of patients on upper endoscopy, are usually asymptomatic. In some patients, acid secretion from oxyntic mucosa within a GIP may create symptoms including globus sensation, hoarseness, dysphagia or even reflux. Cases of Barretts esophagus, high grade dysplasia and adenocarcinoma arising from GIPs have been reported. These findings suggest a role for continued acid exposure of the surrounding squamous mucosa generating a metaplasia to dysplasia to neoplasia sequence, similar to what occurs in the distal esophagus in patients with gastroesophageal reflux disease and Barretts metaplasia. Given the potential to both cause symptoms and progress to malignancy, eradication of GIPs using endoscopic ablation has been considered. We present a series of 3 cases from our institution of successful radiofrequency ablation of these lesions. All 3 patients in this series presented for evaluation of upper GI complaints including atypical reflux symptoms such as hoarseness, globus sensation and dysphagia. Each patient underwent upper endoscopy, where a GIP was identified. Biopsies obtained from each patient confirmed the presence of gastric-type mucosa. In two cases, the presence of oxyntic mucosa with parietal cells within the GIP was confirmed. Intestinal metaplasia consistent with non-dysplastic Barretts esophagus was confirmed in one case where oxyntic mucosa was present. This patient had mild reflux esophagitis without Barretts metaplasia on distal esophageal biopsies and only mildly increased distal esophageal acid exposure on 48 hour pH capsule testing. The other 2 patients had negative pH testing off proton pump inhibitors (PPI) with either 24 hour pH/impedance catheter or a 48 hour pH capsule study. Given the presence of symptoms suspected to be related to the GIP, as well as the presence of Barretts esophagus, endoscopic treatment with radiofrequency ablation (RFA) was planned for all 3 patients. Each patient underwent either 1 or 2 ablation sessions using the Barrx-90 device (Covidien GI Solutions, Sunnyvale, CA). Follow-up endoscopy confirmed successful eradication of all GIPs. All three patients reported significant improvement in their upper gastrointestinal symptoms, even after discontinuation of PPI therapy. These cases demonstrate the ability of RFA to eradicate esophageal gastric heterotopia. Concurrent improvement in atypical reflux symptoms, even off PPI therapy, suggests RFA can generate symptomatic improvement as well as reduce the risk of neoplastic progression. With more widespread availability of RFA, we should reconsider the role of endoscopic surveillance and intervention for GIPs.