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There has been interest in the use of pyloric therapies for the treatment of refractory gastroparesis. However, data on endoscopic pyloric dilation are scarce. We aimed to assess the efficacy and safety of this procedure in refractory gastroparesis.We performed a retrospective analysis of 47 patients referred for refractory gastroparesis, confirmed by gastric emptying scintigraphy, and treated with endoscopic pyloric through-the-scope balloon dilation. The primary endpoint was the effectiveness of the procedure, evaluated with the Gastric Cardinal Symptom Index (GCSI) at 2 and 6 months.A clinical response, defined by a 1.0 point decrease in the GCSI score, was observed in 25 patients at 2 months (53%) and in 19 patients at 6 months (40%). The mean GCSI score decreased significantly at 2 and 6 months compared to the preoperative score (3.9 ± 0.87 vs 2.3 ± 1.37 and 3.9 ± 0.87 vs 2.9 ± 1.27, respectively; p 0.0001). No complication was observed. Nine patients had a delayed relapse at 1 year. A second dilation was performed for eight patients and it was effective in five of them (63%). The mean follow-up time of the patients was 27.0 ± 10.4 months. At 2 years, 15 patients still experienced improvement following this treatment (32%). No predictive factor of clinical response was identified.The efficacy of pyloric dilation is 53% at 2 months, with sustained improvement in one third of patients at 2 years. This treatment should be considered as an alternative option to pyloromyotomy.

International audience; Background: Predictive factors of evolution or appearance of gastroesophageal reflux disease (GERD) after sleeve gastrectomy (SG) have not been identified to date. We aimed to assess the evolution of GERD symptoms 1 year after SG and to determine preoperative predictive factors using high-resolution manometry (HRM) and ambulatory 24-h esophageal pH monitoring (APM).Methods: We included 160 patients who underwent SG between 2013 and 2017 and performed preoperative APM and HRM. Positive APM was defined according to the Lyon consensus. Symptoms of GERD, proton pump inhibitors (PPI) use, weight loss (WL), and diet were recorded in all patients before and 1 year after surgery.Results: One year after surgery, 58 patients (36.3%) complained of GERD symptoms compared to 52 patients (32.5%) preoperatively (p=0.48). Among patients with preoperative GERD symptoms, only 26/52 patients (50%) still had symptoms, whereas 32/108 (29.6%) asymptomatic patients developed de novo GERD symptoms after surgery. PPI use increased after surgery reaching 36.9% of patients against 15.0% before (p

Evolution of gastroesophageal reflux disease (GERD) after sleeve gastrectomy (SG) is controversial. Some authors report worsening or improvement of preoperative GERD, others the occurrence of de novo GERD between 5 and 69%.The aims of this study are to evaluate the evolution of GERD after SG by ambulatory 24-h pH monitoring (APM) and to determine pre- and postoperative clinical and manometric factors associated with its evolution.Between 2013 and 2015, 47 patients operated in our center performed APM before and 1 year (14.8 ± 4.9 months) after SG. GERD was defined as a percentage of time with esophageal pH 4 (TpH 4) 4.2. Among them, 30 had pre- and postoperative high-resolution esophageal manometry (HRM).Thirty-one patients (66%) had no preoperative GERD (group 1), and 16 had preoperative GERD (group 2). One year after SG, mean TpH 4 increased significantly in group 1 (5.8 ± 4.6 vs. 1.8 ± 1.1%, p 0.01) whereas it was not modified in group 2 (7.4 ± 6.6 vs. 6.6 ± 2.6%). In group 1, 16 patients (52%) had de novo GERD whereas in group 2, 7 had no more GERD, 3 improved, and 6 worsened. Maximal intragastric pressure after swallows increased significantly at postoperative HRM only in patients with de novo GERD (49.2 ± 22.0 vs. 25.4 ± 9.4 mmHg, p = 0.03). No preoperative clinical or manometric parameters were predictive of postoperative GERD.One year after SG, esophageal acid exposure globally worsened, mostly because of de novo GERD, whereas 63% patients with preoperative GERD improved, without preoperative predictive clinical or manometric factor.

Background The effects of bacterial fermentation on human colonic motor activity could be explained by colonic acidification or short-chain fatty acid (SCFA) production. We compared in healthy volunteers the colonic motor effects of intracolonic infusion of neutral or acidic saline solutions and then of neutral or acidic solutions containing an SCFA mixture. Methods 20 healthy volunteers swallowed a probe (with an infusion catheter, 6 perfused catheters and a balloon connected to a barostat) that migrated into the colon. Colonic motor activity was recorded in fasting basal state (1 h), during (3 h) and after (2 h) intracolonic infusion in a random order on two consecutive days of 750 mL of NaCl at pH 7.0 (neutral saline) or 4.5 (acidic saline) in 10 volunteers (first experiment) and of an SCFA mixture (acetic acid 66%, propionic acid 24% and butyric acid 10%; 100 mM) at pH 7.0 or 4.5 in 10 other volunteers (second experiment). We determined for each hour a global motility index (reflecting phasic activity recorded by all catheters), the mean balloon volume (reflecting tonic activity), and the mean number of high-amplitude-propagated contractions (HAPCs). Key Results Intracolonic infusion of neutral or acidic solutions containing saline or an SCFA mixture did not change the global motility index, the barostat balloon volume, or the HAPC number compared with basal values. Conclusions & Inferences Under our experimental conditions, these findings suggest that the stimulation of colonic motor activity induced by carbohydrate fermentation is not explained by the acidification of the colonic contents or the resulting production of SCFAs.

Hypersensitivity during rectal distension has been demonstrated in irritable bowel syndrome (IBS). Studies performed in animals and indirect data in humans suggest that cholecystokinin (CCK) could modulate visceral sensations. The aim of this study was to assess the effects of i.v. infused sulphated cholecystokinin octapeptide (CCK-OP) on rectal sensitivity in response to distension. In eight healthy subjects, rectal sensitivity and compliance were determined during a randomized double-blind study, with four sessions each separated by 7 days. Sensory thresholds and rectal compliance were assessed during slow-ramp (40 mL min-1) and rapid-phasic distensions (40 mL s-1, 5 mmHg stepwise, 1-min duration), and were compared before and during continuous infusion of either saline or CCK-OP at 5, or 20 or 40 ng kg-1 h-1. During rapid phasic distension but not during slow ramp distension, CCK-OP at 40 ng kg-1 h-1 produced a significant decrease in sensory thresholds compared with the basal period. Rectal compliance was not modified by any infusion. At pharmacological doses, CCK-OP decreases sensory thresholds during rapid phasic distension that may preferentially stimulate serosal mechanoreceptors, but has no effect on mucosal mechanoreceptors stimulated during slow ramp distensions. Modulation of rectal sensitivity by CCK could be implicated in the pathogenesis of the rectal hypersensitivity observed in IBS.

In healthy humans, meals stimulate phasic and tonic motor activity in the unprepared distal colon. The response of the proximal colon remains unknown. In this study, we assessed the effect of a liquid meal on proximal and distal colonic motor activity. In 12 healthy volunteers, colonic tone and phasic motility were simultaneously recorded by using an electronic barostat and perfused catheters in the fasting state and in response to a 1,000-kcal meal. The meal significantly increased the phasic activity in the distal colon (230 ± 46% of the basal value; P = 0.02) but not in the proximal colon (138 ± 25% of the basal value; P = 0.2). The intrabag volume of the barostat was significantly more reduced in the distal than in the proximal colon (74 ± 11 vs. 50 ± 9% of the basal values, respectively; P = 0.04). We conclude that the postprandial response of the unprepared proximal colon is an immediate tonic contraction that is less pronounced than in the distal colon.