Evaluation of the widths of the mucosal strips in pathological examination of specimens of endoscopic submucosal dissection for early gastric cancer.

BACKGROUND: Endoscopic submucosal dissection (ESD) is the standard treatment for early gastric cancer in Japan. Pathological evaluation of ESD specimens is considered essential to determine if additional gastrectomy is necessary. Usually, specimens resected by ESD are sliced into 2-3 mm wide sections, and each section is examined for depth of tumor and lymphovascular invasion. Nevertheless, in most cases of additional gastrectomy, lymph node metastasis is not present. Given that there are few-studies on how clinical-decisions based on the pathologic-evaluation-method, in particular the specimen cut-width, influence patient outcomes, we retrospectively evaluated whether reducing the number of cuts to one-half or one-third would result in underestimation of the real need for additional surgery. The effect of the actual cut-width on recommended treatment (referral to operation) and patient-outcomes was also assessed. METHODS: Pathological records of 498 lesions from 439 patients were reviewed and re-evaluated. All pathological descriptions are based on the gastric cancer classification system of the Japanese Gastric Cancer Association, 15th edition. RESULTS: In 5.8% and 8.5% of the total specimens, underdiagnosis of tumor-depth and lymphovascular invasion occurred when the number of sections was reduced to one-half and one-third, respectively. Significantly more submucosal invasions were found in the group in which the cut-with was between 3 and 4 mm than in the group in which the cut width was less than 3 mm. CONCLUSION: Evaluation of the appropriate cut-width is important and should be discussed from the standpoint of labor costs and lost opportunities to search for molecular markers in ESD materials.

[Sarcoidosis diagnosed by a tiny esophageal lesion:a case report].

A woman in her 60s was referred to the Department of Gastroenterology with anemia. She had a recurrent transient loss of consciousness 11 years ago, and she was examinated at the cardiology and neurology departments, but the cause was not identified. Epileptic seizures were suspected. Sodium valproate medication was started, and the patient's condition progressed with no recurrence. Esophagogastroduodenoscopy showed a tiny submucosal tumor-like lesion with mild depression in a 21cm thoracic esophagus. Biopsy revealed epithelioid granulomas with multinucleated giant cells in the subepithelial stroma. Computed tomography (CT), positron emission tomography-computed tomography (PET-CT), and magnetic resonance imaging (MRI) showed multiple lesions in the hilar lymph nodes, spleen, and heart that are typical of sarcoidosis. These findings led to the diagnosis of esophageal lesion associated with sarcoidosis. The patient had no subjective symptoms;however, treatment with prednisolone 30mg was started because cardiac sarcoidosis is a risk of death. Gastrointestinal tract involvement in sarcoidosis is rare;esophageal sarcoidosis is particularly rare, and there are few reports on superficial lesions. Here, we report a case of sarcoidosis that was diagnosed from a tiny esophageal lesion.

Factors associated with healing of artificial ulcer after endoscopic submucosal dissection with reference to Helicobacter pylori infection, CYP2C19 genotype, and tumor location: Multicenter randomized trial.

BACKGROUND AND AIM: Healing speed of peptic ulcer is affected by a number of factors, including Helicobacter pylori (H. pylori) infection and intragastric pH. Acid inhibition exerted by proton pump inhibitors differs by CYP2C19 genotype. Herein, we investigated whether healing speed of artificial ulcers formed after endoscopic submucosal dissection (ESD) was influenced by H. pylori infection, CYP2C19 genotype, or other factors. METHODS: A total of 96 H. pylori-positive patients with gastric tumors scheduled for ESD were randomly assigned to receive eradication therapy for H. pylori before ESD (pre-ESD eradication) (n = 44) or after (post-ESD eradication) (n = 52). Patients received eradication therapy consisting of lansoprazole 30 mg, amoxicillin 750 mg, and clarithromycin 200 mg twice daily for 1 week. After ESD, lansoprazole 30 mg was given once daily for 8 weeks. Ulcer size was endoscopically measured on the next day and at 4 and 8 weeks after ESD. RESULTS: Mean reduction rate of artificial ulcer area in the pre-ESD eradication group was 94.7% ± 5.5% at 4 weeks, which was similar to that in the post-ESD eradication group (94.7% ± 6.7%, P = 0.987), irrespective of CYP2C19 genotype. In multivariate analyses, location of gastric tumor (middle and upper, odds ratio: 4.05, 95% CI: 1.620-10.230, P = 0.003) was a factor for 97% reduction of artificial ulcer area at 4 weeks post-ESD, but CYP2C19 genotype and H. pylori infection were not. CONCLUSION: Healing speed of ESD-induced artificial ulcer was affected by tumor location, but not by time of H. pylori eradication, resected size, or CYP2C19 genotype.