Gastroesophageal reflux disease (GERD) is a common chronic condition that not only impairs the quality of life of those who are affected by it but also poses a significant economic burden. It encompasses a wide spectrum of symptoms as a result of gastric content moving into the esophagus. The most common cause of GERD, other than a hiatus hernia, is considered to be transient lower esophageal sphincter relaxation. The lower esophageal sphincter (LES) normally has a higher resting tone than the stomach, thus preventing the reflux of gastric contents into the esophagus. The greater prevalence of GERD and GERD symptoms in obese individuals has generated significant interest in understanding the association between these 2 conditions and the underlying physiological mechanisms. The potential relationship between GERD and obesity and the exact mechanism by which obesity may cause reflux, however, remains uncertain. It has been proposed that patients with GERD have altered autonomic nervous function and, more specifically, have reduced parasympathetic activity. Obese individuals also have shown diminished parasympathetic activity, which may be reversed after weight reduction through exercise, diet control, and bariatric surgery. Given that contraction and relaxation of the LES are vagally mediated, the question that arises is whether the autonomic nervous system is, in fact, the missing link between obesity and GERD. In this article we examine the current evidence and hypothesize that the potential imbalance in sympathovagal stimulation to the LES is a key contributing factor to the increased prevalence of GERD symptoms in obese individuals.

The retrospective study was conducted with IRB approval. Patients who received Y90 treatment within 30 days of immunotherapy were considered to have concurrent therapy. Baseline laboratory values obtained within one month prior to Y90 and at 1 and 3 months after Y90 were evaluated. Hepatobiliary and immunotherapy-related adverse events were characterized according to NCI CTCAE v5.0. Patient survival was estimated using Kaplan-Meier analysis. Results: Between June 2015 and March 2018, 18 patients received concurrent therapy. 14 patients had hepatocellular carcinoma (3 BCLC B, and 11 BCLC C), and 4 had metastatic disease to the liver (3 melanoma, 1 gastric cancer). The median interval between Y90 and immunotherapy was 7 days. Grade 3 hepatobiliary toxicity occurred in 1 patient at 1 month (6%) and in 3 patients at 3 months (17%) after Y90. Grade 3 toxicities occurred only in patients with advanced HCC (BCLC C). No grade 3 immune-associated toxicities occurred at 1 or 3 months in any patients. Median overall survival from first Y90 was 27.4 months for patients with HCC and 13.7 months for patients with metastatic disease to the liver. Conclusions: Concurrent Y90 radioembolization and checkpointinhibitor immunotherapy appears to be safe with a low incidence of toxicity. Toxicities were limited to patients with advanced HCC and may be confounded by disease progression.

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