Helicobacter pylori infection and the administration of non-steroidal anti-inflammatory drugs (NSAIDs) are implicated as the primary etiopathogenetic contributors to peptic ulcers. Therefore, H. pylori eradication or cessation of NSAID administration is the primary therapeutic strategy against peptic ulcers. Acid suppressants including proton pump inhibitors are also used to treat peptic ulcer disease. An increasing number of patients are being prescribed antithrombotic therapy in Japan in recent times; therefore, it is important to focus on prevention of upper gastrointestinal bleeding in this patient population. The clinical research findings in this field should be used as guidelines in real-world practice. Currently, an increasing number of patients are being diagnosed with idiopathic peptic ulcers; therefore, it is important to focus on the clinical management of this condition.
Tumor genomic profiling using next-generation sequencing (NGS) technology enables precision cancer treatment in clinical practice. To date, EUS-FNA plays a pivotal role in the diagnosis of pancreatic lesions. In the era of precision cancer medicine, more effort has been made for tissue acquisition suitable for NGS analysis in EUS-guided sampling. Although the use of EUS-FNA samples for NGS analysis is still controversial in pancreatic cancer, recent studies have reported the feasibility of their use in molecular profiling, including more advanced approaches such as whole-exome/whole-transcriptome sequencing or establishment of patient-derived organoid models. In this review, we discuss the current status and challenges of genomic profiling of pancreatic cancer using EUS-FNA samples.
An 83-year-old man presented with discomfort during swallowing. Endoscopy revealed a smooth, yellowish, submucosal tumor-like lesion in the right pyriform sinus of the hypopharynx. Computed tomography revealed a well-defined low absorbed mass beside the right pyriform sinus. Magnetic resonance imaging revealed a lesion that showed high signal intensity on T1- and T2-weighted images and low signal intensity on fat-suppressed T1-weighted images. No diffusion abnormality or contrast enhancement was observed. Based on the aforementioned findings, we suspected a lipoma in this patient. Endoscopic submucosal dissection was performed under general anesthesia after direct visualization of the larynx using a curved laryngoscope, following consultation with the Otorhinolaryngology Department. The lesion measured 45×13×15 mm, and histopathological evaluation of the resected specimen confirmed diagnosis of lipoma. The patient was symptom-free postoperatively.
A 61-year-old male was referred to our hospital due to anorexia and further evaluation of his gastric lesions. Esophagogastroduodenoscopy (EGD) revealed an erythematous surface polypoid lesion measuring 13-mm in diameter, with a central depression on the anterior wall of the lower body, and multiple submucosal lesions with or without a central depression on the middle to the upper body. EGD also revealed a corpus-dominant advanced gastric atrophy. Endoscopic biopsy specimens of the gastric polypoid lesions revealed a grade 2 gastric neuroendocrine tumor (G-NET).
The serological examination was negative for anti-gastric parietal cell antibodies and intrinsic factor antibodies, and positive for immunoglobulin G antibodies against Helicobacter pylori (HP). The patient’s serum gastrin levels were elevated at 16,030 pg/mL. A computed tomography and positron emission tomography/computed tomography revealed no abnormal lesions.
The patient was diagnosed to have a type ⅠG-NET. He underwent total gastrectomy and lymphadenectomy. Pathological examination of the tumor specimens revealed NET G2 and lymph node metastasis. Moreover, enterochromaffin-like (ECL) cell hyperplasia and endocrine cell micronests were observed in the gastric mucosa around the tumor.
The patient’s HP infection-induced hypergastrinemia. The onset of which has been explained by the gastric mucosal atrophy resulting in low acid output and the production of antibodies. Additionally, cytokines and inflammatory mediators released during chronic inflammation induced by HP infection promoted ECL proliferation. Therefore, HP infection is a risk factor for G-NET, by inducing hypergastrinemia.
This case is of interest because it reports a patient with multiple G-NETs and extreme hypergastrinemia, following type B chronic gastritis due to HP infection. Further studies are necessary to elucidate how HP infection was implicated in the pathogenesis of G-NET.
An 80-year-old woman presented for further evaluation of a huge gastric tumor. Esophagogastroduodenoscopy revealed a huge tumor at the gastric fundus and upper body. The tumor appeared as a protruding papillary mass surrounded by a flat elevated lesion. Based on the endoscopic findings, we diagnosed the lesion as a pyloric gland adenoma; however, we suspected that the protruding lesion included a concurrent carcinomatous component and therefore performed laparoscopic total gastrectomy. Histopathological evaluation of the protruding lesion showed findings of a pyloric gland adenoma and well-differentiated adenocarcinoma. The adenocarcinoma component showed papillary morphology combined with gastric and intestinal mucin phenotype. The surface layer of the flat elevated lesion showed tumor cell differentiation into foveolar epithelium, and the middle layer showed cells that were differentiated into pyloric glands. We diagnosed the tumor as an adenocarcinoma that originated from a pyloric gland adenoma. We report a rare case of an adenocarcinoma of combined with gastric and intestinal mucin phenotype that originated from a huge pyloric gland adenoma.
A 62-year-old man had been diagnosed two years prior with acquired hemophilia A. Although combination therapy of steroids and rituximab could have induced disease remission, the treatment needed to be reinstated after a recurrence following steroid discontinuation. Colonoscopic examination for bloody stools revealed a laterally spreading tumor in the rectum with a diameter of approximately 60 mm. In spite of the patient’s tendency to bleed, tumor resection with curative intent was indicated, and endoscopic submucosal dissection was performed with coagulation factor replacement. After the procedure, the patient exhibited chronic bloody stools and anemia, with frequent bleeding from the resection site. With repeated blood coagulation factor supplementation and blood transfusions, along with nine endoscopic hemostasis procedures, the patient ultimately achieved complete hemostasis in a period of approximately three weeks.
Non-Helicobacter pylori Helicobacter gastritis (NHPHG) was detected in 14 of 298 patients (4.7％) who underwent gastric tissue biopsy during routine medical checkup. The prevalence of NHPHG observed in this study was higher than that reported by previous studies, which suggests that NHPHG is not uncommon as was previously assumed.
Esophageal achalasia is one of the most common esophageal motility disorders. When peroral endoscopic myotomy (POEM) was invented, it became popular worldwide as a minimally invasive alternative to Heller myotomy. While POEM is an excellent and effective endoscopic treatment, its novelty brings about several problems during starting up in each hospital. In addition to clinical issues, such as the rarity of esophageal achalasia, there are also systemic issues involved, such as institutional standards for medical insurance, which make it difficult to initiate POEM. Neither of these problems are easy to overcome, but POEM is a very rewarding treatment for endoscopists, as symptoms often improve dramatically. In addition, POEM is an excellent procedure that has the potential to develop into a variety of new treatments, so it is important to overcome these problems and start it up.
Barrett’s esophagus (BE) is characterized by replacement of the usual esophageal squamous epithelium with abnormal, intestinal-type columnar epithelium. BE predisposes patients to esophageal adenocarcinoma through a multistep carcinogenic process, which includes intestinal metaplasia, low- to high-grade dysplasia, and adenocarcinoma. Prevention of metachronous cancer recurrence warrants a multipronged therapeutic approach, including endoscopic removal of the dysplastic mucosa and endoscopic ablative therapy for Barrett’s mucosa. Currently, several therapeutic options are available, including radiofrequency ablation, cryotherapy, and argon plasma coagulation. A thorough understanding of device specifications and indications is essential to select the optimal treatment strategy for favorable treatment outcomes. This chapter discusses the indications for endoscopic ablation of BE, device selection, and procedural details.
Objectives: Some patients with gastroesophageal reflux disease (GERD) are refractory to proton pump inhibitor (PPI) therapy. Anti-reflux mucosectomy (ARMS) is a minimally invasive endoscopic procedure for treatment of GERD. In this study, we retrospectively evaluated the outcomes of ARMS performed in patients with PPI-refractory GERD at our institution.
Methods: A total of 109 patients with PPI-refractory GERD who underwent ARMS were retrospectively reviewed. Pre- and post-ARMS questionnaire scores, acid exposure time (AET), DeMeester score, proximal extent, and PPI discontinuation rate were compared.
Results: There was a significant improvement in the symptom score (P < 0.01) and 40-50％ of patients were able to discontinue PPI after ARMS. In patients who were followed up for 3 years, sustained improvement in subjective symptoms was observed. AET and DeMeester score significantly improved after ARMS (P < 0.01); however, there was no significant improvement in proximal extent (P = 0.0846).
Conclusions: Anti-reflux mucosectomy is an effective minimally invasive therapy for patients with PPI-refractory GERD. The therapeutic efficacy is attributable to suppression of acid backflow due to contraction of the scar tissue in cardia.