Digestive Endoscopy最新文献

A 52-year-old woman suffering the migration of abdominal pain to right lower quadrant, nausea, and diarrhea sought medical attention in the emergency department. Laboratory investigations revealed a white blood cell count of 12.7 × 10⁹/L, and ultrasound imaging demonstrated an appendiceal diameter of 12 mm without evidence of perforation and tumor (Fig. 1). Acute uncomplicated appendicitis (AUA), the primary indication for endoscopic retrograde appendicitis therapy (ERAT),¹ was diagnosed. Therefore, she was referred to our department following informed consent.

During the ERAT, purulent material emanated from the appendix (Fig. 2a). Repeated attempts to place a contrast catheter (5.5F) through the guidewire failed (Video S1). The stenosis of the appendiceal orifice was considered. We skillfully used a Soehendra stent retriever (Wilson-Cook Medical, Inc., Winston-Salem, NC, USA) (Fig. 2b) to gradually dilate the orifice, facilitating the smooth passage of the contrast catheter into the appendiceal lumen (Fig. 2c, Video S1). After flushing, no significant stenosis was visualized by iohexol radiography (Fig. 2d). A 5F × 5 cm stent was then placed (Fig. 2e). Follow-up coloscopy on 2-month postoperative showed the stent was dislodged, and no abnormality was seen in the appendiceal opening (Fig. 2f).

Appendiceal lumen obstruction stands as the predominant etiology of acute appendicitis.² The constriction of the appendiceal orifice may contribute to this obstruction. However, the successful treatment of appendicitis attributed to appendiceal orifice stenosis by ERAT has been rarely reported, because stenosis is less likely to occur in AUA,³ and surgery is an alternative remedy in instances where ERAT encounters challenges in placing guidewires and contrast catheters.⁴ The electrosurgical incision of the appendiceal orifice to alleviate stenosis has been reported,⁵ albeit with a heightened risk of perforation. The Soehendra stent retriever not only advanced along the guidewire but also functioned as a dilator by means of rotation, offering a safer alternative to mitigate the risk of perforation associated with electrosurgical incision.

Authors declare no conflict of interest for this article.

Crosswise Project of West China Fourth Hospital, Sichuan University (No. 01-186) and Crosswise Project of Sichuan University (No. 22H0415).

Endoscopic full-thickness resection (EFTR) is a less invasive and a potentially effective treatment for gastrointestinal stromal tumors (GISTs).^{1, 2} Although various devices and suture methods have been reported for defect closure after EFTR,³ the current options are cumbersome. Recently, a new closure device (MANTIS Clip; Boston Scientific, Natick, MA, USA) has become available that can be rotated and reopened with a strong grasping force owing to the clip anchors. Its use has been reported in closing ulcers after endoscopic submucosal dissection and esophageal rupture.^{4, 5} We report a case in which combining this closure device and conventional endoclips (SureClip; Micro-Tech, Nanjing, China) was useful for closing a defect after EFTR.

A 64-year-old woman presented with a submucosal tumor in the lesser curvature of the middle gastric body on upper gastrointestinal endoscopy (Fig. 1a). Endoscopic ultrasound (EUS) revealed an 18 mm hypoechoic mass arising from the muscularis propria, which was histologically diagnosed as a GIST by EUS-guided fine needle aspiration biopsy. Subsequently, we performed EFTR for the GIST using an endoknife (ITknife 2; Olympus Medical, Tokyo, Japan) with traction devices under general anesthesia. Immediately after tumor removal (Fig. 1b), we employed the closure device (Fig. 1c, Video S1). The marginal mucosa of the defect was grasped, pulled toward the contralateral mucosa, and closed (Fig. 1d). The defect was closed with three closure devices (Fig. 1e), and the gap between the devices was closed using conventional endoclips placed close to the mucosa (Fig. 1f). Oral intake was initiated on postoperative day 2. She was discharged on postoperative day 6 without adverse events, such as delayed perforation or bleeding. The final histological diagnosis was a very low-risk GIST based on Fletcher's classification. This technique is simple, has a short closure time, and serves as an option for the closure of full-thickness defects after EFTR.

Authors declare no conflict of interest for this article.

Gastroesophageal reflux disease (GERD), including nonerosive reflux disease (NERD) and reflux esophagitis, is defined as the presence of reflux-associated symptoms and/or esophageal mucosal damage caused by the reflux of gastric content into the esophagus.¹ In general, the main therapeutic strategy for GERD is potent acid inhibition for a 24 h period. This is because esophageal mucosal breaks and reflux-related symptoms are closely related to not only intraesophageal and intragastric pH values but also to the number of episodes of reflux and to reflux duration. Cure rates with acid inhibition are generally influenced by a number of factors, including CYP2C19 genotype in treatment with proton pump inhibitors (PPIs), vonoprazan/PPI dose, presence of functional heartburn and reflux hypersensitivity, Helicobacter pylori infection, sliding hernia, eosinophilic esophagitis and major motility disorders (achalasia, esophagogastric junction outflow obstruction, distal esophageal spasm, jackhammer esophagus, and absent contractility).² Of GERD-related diseases refractory to acid inhibition, reflux hypersensitivity is defined as retrosternal symptoms, including heartburn or chest pain triggered by physiological reflux in the absence of abnormally increased gastroesophageal reflux on pH or ambulatory pH-impedance monitoring, and functional heartburn is defined as retrosternal burning discomfort or pain refractory to potent acid inhibition in the absence of GERD.¹ Recently, these diseases have been increasing among GERD patients in Japan, and it is considered important to take measures to cure them.

Although response to potent acid inhibition by PPI/vonoprazan does not exclude diagnosis of reflux hypersensitivity, most reflux hypersensitivity is refractory to PPI/vonoprazan therapy, and reflux hypersensitivity related to bile acid reflux to the esophagus has been the focus of much recent attention. The prevalence of bile acid reflux among all GERD patients ranges from 10% to 97%, in NERD 10–63%, in erosive esophagitis 22–80%, and in Barrett's esophagus 50–100%.³ Although bile acid reflux is most commonly caused by surgery (e.g., gastric surgery, gallbladder removal surgery), esophageal mucosal inflammation and tissue damage also often result from sliding hernia, impaired gastrointestinal motility and kyphosis, and chronic and frequent bile acid reflux. In ex vivo/in vitro studies, bile acids including cholic acid, chenodeoxycholic acid, and deoxycholic acid stimulate squamous cells and Barrett's epithelium cells, resulting in the infiltration of activated inflammatory cells and the increase of proinflammatory cytokines (e.g., interleukin [IL]-6, IL-8) and inflammation-related mediators (e.g., prostaglandin E2, cyclo-oxygenase-2) into the esophageal mucosa.⁴ In fact, esophageal refluxates in patients with GERD and Barrett's ep

Since the development of lumen-apposing metal stents (LAMS), biliary drainage by endoscopic ultrasound guided choledochoduodenostomy (EUS-CDS) has become increasingly popular, thanks especially to its relative simplicity. Initially used as rescue therapy after endoscopic retrograde cholangiopancreatography (ERCP) failure, it is now accepted as first-line treatment in inoperable patients and by expert centers in the latest European guidelines.¹

Indeed, the reported technical success of 88.5–100%, with few adverse effects, has popularized EUS biliary drainage as a more efficient alternative to repeat ERCP or percutaneous transhepatic biliary drainage after failure of a first ERCP.^{2, 3} Initial retrospective observational data have recently been confirmed by two randomized controlled trials (RCTs) that compared EUS-CDS with ERCP, with technical success rates of 90.4% and 96.2% vs. 76.3% and 83.1%, respectively, for ERCP. Although the primary objective of stent patency in those studies did not differ, the contribution of these two publications is essential, as the high technical success rates were obtained by operators who are sometimes nonexperts in EUS-CDS, whereas ERCP, although performed by experts, required an alternative catheterization method, such as a precut, in 40% of cases.^{4, 5}

In view of these results, teams such as ours are considering biliary drainage by EUS-CDS as a first-line procedure for distal tumor obstructions that are operable from the outset in selected patients (with a bile duct greater than 15 mm in diameter) and with no risk factors for stent dysfunction (such as stenosis or duodenal invasion). This alternative, which is just as safe as ERCP and quicker, avoids the risk of acute pancreatitis, which can sometimes delay or even contraindicate curative surgical resection.

Higher costs are currently one of the main factors limiting the already impressive expansion of this technique. However, the development of a competitive market, with the multiplication of devices enabling LAMS EUS-CDS, should logically lead to a reduction in procedure costs.

In view of these factors, it is clear that the number of patients fitted with this type of device will increase, as will the number of patients with LAMS dysfunction. While self-expandable metal stent (SEMS) obstruction and its endoscopic management is now part of the daily routine for interventional endoscopists, LAMS obstructions are a relatively recent problem for which the publication by Vanella et al.⁶ in this issue of Digestive Endoscopy is particularly relevant.

Data on stent patency during follow-up are fairly heterogeneous. The Leuven–Amsterdam–Milan Study Group reported a dysfunction rate of 31.8%.³ A meta-analysis of 201 patients reported a dysfunction rate of 11.5%.⁷ Recently, Fritzsche