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Introduction: Non-curative endoscopic resection of T1 colorectal cancer (CRC) carries a substantial risk of recurrence. However, previous studies have reported a significant proportion of cases in which the deep margin of endoscopic resection was positive for cancer due to the technical difficulties of colorectal endoscopic submucosal dissection (ESD). With the advancement of endoscopic technology and techniques resulting in the reduction of positive resection margins, it is important to reassess the long-term prognosis and major risk factors for recurrence in cases of negative deep margins. Methods: We conducted a retrospective cohort study of consecutive patients with T1 CRC who underwent endoscopic resection between January 2006 and December 2021 with negative deep margins. The histological findings of the resected specimens were analyzed to determine the risk factors associated with the primary outcomes of this study, including recurrence and cancer-related deaths. Results: The median age of the 190 patients was 70 years, of which 63% were male, and endoscopic treatment was performed in 64% by endoscopic mucosal resection and 36% by ESD. Eighty-two patients were in the curative resection (CR) group and 108 were in the non-curative resection (NCR) group, wherein the latter comprised 79 patients who underwent additional surgery (AS) and 29 patients who did not receive AS. Five-year recurrence-free survival rates were 98.4% (95% CI: 89.3–99.8) for CR, 98.3% (95% CI: 88.8–99.8) for NCR with AS, and 73.7% (95% CI: 46.5–88.5) for NCR without AS. Lymphatic invasion and budding grade 2/3 were the major risk factors for recurrence, with hazard ratios of 40.7 (p < 0.001) and 23.1 (p = 0.007), respectively. Of the patients in the NCR group without AS, the 5-year recurrence-free rate was 85.6% (95% CI: 52.5–96.3) if there were no major risk factors (i.e., no lymphatic invasion or budding grade 2/3) (n = 21), whereas the prognosis was poor in the presence of one or more of the major risk factors, with a median recurrence-free survival and disease-specific survival of 2.5 and 3.1 years, respectively (n = 8). Discussion: In endoscopically resected T1 CRC with negative deep margins, lymphatic invasion or budding grade 2/3 may indicate a higher risk of recurrence when followed up without AS. [ABSTRACT FROM AUTHOR]

Objectives Methods Results Conclusions Bleeding after endoscopic submucosal dissection (ESD) for gastric tumors in patients taking antithrombotic drugs, in particular direct oral anticoagulants (DOACs), remains unresolved; therefore, we evaluated the risk factors for post‐ESD bleeding and drug differences in patients taking DOACs.We included 278 patients taking antithrombotic drugs who underwent gastric ESD between January 2017 and March 2022. Antithrombotic drugs were withdrawn following the 2017 guidelines (Appendix on anticoagulants including DOACs). To further clarify differences in antithrombotic agents' effects, the peri‐cancerous mucosa in the resected specimen was pathologically evaluated according to the Updated Sydney System. Multivariate analysis was performed to assess the risk of post‐ESD bleeding.The incidence of post‐ESD bleeding in patients taking DOACs was 19.6% (10/51). Among patients taking antithrombotic drugs, DOACs were identified as a possible factor involved in post‐ESD bleeding (odds ratio [OR] 4.92). Among patients taking DOACs, possible factors included resection length diameter ≥30 mm (OR 3.72), presence of neutrophil infiltration (OR 2.71), lesions occurring in the lower third of stomach (OR 2.34), and preoperative antiplatelet use (OR 2.22). Post‐ESD bleeding by DOAC type was 25.0% of patients (4/16) receiving apixaban, in 20.0% (3/15) receiving edoxaban, in 21.4% (3/14) receiving rivaroxaban, and in none of those receiving dabigatran.The administration of DOACs was shown to be a possible factor involved in post‐ESD bleeding, and risk factors for patients taking DOACs included neutrophil infiltration. The pharmacological differences in the effects of DOACs contributing to bleeding in gastric ulcers suggest comparatively less bleeding with dabigatran after ESD. [ABSTRACT FROM AUTHOR]

An 83-year-old Japanese man who underwent cholecystectomy for cholecystolithiasis 17 years ago visited our hospital owing to epigastric pain. He was initially diagnosed with choledocholithiasis and acute cholangitis following white blood cell, C-reactive protein, total bilirubin, alkaline phosphatase, and γ-glutamyltranspeptidase level elevations along with common bile duct stones on computed tomography (CT). Moreover, CT, magnetic resonance imaging, endoscopic retrograde cholangiography (ERC), and endoscopic ultrasonography (EUS) also revealed a 2-cm-diameter mass arising from the remnant cystic duct. The cytology of the bile at the time of ERC was not conclusive. However, EUS-assisted fine needle aspiration (EUS-FNA) of the mass confirmed the diagnosis of adenocarcinoma of the remnant cystic duct. The patient underwent extrahepatic bile duct resection. Cystic duct carcinoma following cholecystectomy is rare. We report a case diagnosed by EUS-FNA.

A 67-year-old man was diagnosed with ulcerative colitis one year ago. Remission was induced via the oral administration of prednisolone and azathioprine;prednisolone was gradually reduced and discontinued. He maintained remission with azathioprine but developed fever and general malaise and visited the Kagawa Prefectural Central Hospital. Chest radiography and a urinary antigen test revealed Legionella pneumonia. His symptoms reduced immediately after the initiation of levofloxacin. Azathioprine suppresses cellular immunity and may increase the risk of Legionella pneumonia.

A 74-year-old male who was receiving endocrine therapy for prostate cancer, with multiple bone and lymph node metastases (T2bN1M1 Stage D2), underwent follow-up computed tomography (CT). The CT revealed multiple liver metastases, a high serum CEA level, and an unchanged PSA level. Upper gastrointestinal endoscopy showed an elevated lesion with mucosal erosion on the lesser curvature of the middle gastric corpus, revealed to be a metastatic prostate cancer lesion following immunohistochemical confirmation. This case demonstrates the potential for gastric metastases in patients with advanced prostate cancer and high serum CEA levels.

A 28-year-old pregnant woman presented with an abdominal mass at 12 weeks' gestation. Magnetic resonance imaging revealed a 7 cm cystic lesion arising extrinsically from the pancreatic head, which was diagnosed as a mucinous cystic neoplasm. Although we recommended surgical excision during the second trimester, the patient refused the procedure and chose to continue her pregnancy. We monitored the lesion and noted that it gradually grew to 13 cm over the course of the pregnancy. Subsequently, we enucleated it after childbirth. Histopathological examination was compatible with high-grade dysplasia and confirmed the diagnosis of mucinous cystadenoma of the pancreas.

Here we report two cases of dabigatran-induced esophageal ulcer. Case 1 was a 67-year-old man who presented with heartburn that developed a month after dabigatran administration. Case 2 was an 81-year-old woman who presented with epigastralgia that developed within a few days of dabigatran administration. Endoscopic findings were similar in both cases, including shallow esophageal ulcers covered with a thin whitish membrane. The patients were advised to consume the drug with plenty of water during meals and to remain in a sitting position for 30 min after consumption. This method successfully decreased their symptoms and ulcers, indicating that drug administration guidance is extremely effective in managing dabigatran-induced esophageal injury.

Non-steroidal anti-inflammatory drugs (NSAIDs) are roughly divided into a low-dose aspirin group used for primary and secondary prevention of cardiovascular events and non-aspirin NSAIDs used for treatment of bone and joint diseases. Both cause gastrointestinal damage directly or indirectly. In the present study, we reviewed gastrointestinal damage due to non-aspirin NSAIDs with respect to the esophagus, stomach/duodenum, small intestine and colon. Damage due to NSAIDs occurs in all digestive tracts and since the analgesic effect of NSIADs hides subjective symptoms, the symptoms are often not treated until they are advanced to a serious state. Further, patients receiving NSAIDs are mostly elderly and have complications so that the onset of the conditions is serious and prevention is important. It is necessary to investigate a method that is effective for preventing damage for all digestive tracts and the mechanisms of damage must be understood for this reason.

Background/aims: Even in Japan where the incidence of H. pylori infection is high, patients with gastroduodenal ulcers caused by NSAIDs are on the increase. A prospective study was conducted to elucidate the characteristics of gastroduodenal ulcers complicated with ulcerous hemorrhage and perforation among Japanese., Methodology: The subjects were 305 consecutive cases with hemorrhaging ulcers and 76 consecutive cases with perforated ulcers basis at Kagawa Prefectural Central Hospital between January 2000 and December 2008. These subjects were divided into 3 groups (lowdose aspirin, non-aspirin NSAIDs and non-NSAIDs) and were further stratified by the presence of an H. pylori infection., Results: The 76 perforating ulcers were composed of 54 non-NSAIDs ulcers and 22 NSAIDs-related ulcers. The 305 hemorrhaging ulcers were composed of 156 non-NSAIDs ulcers, 94 non-aspirin NSAIDs ulcers and 55 on low-dose aspirin. The mortality for the non-aspirin NSAIDs group (12.8%, 12/94) and for the low-dose aspirin group (10.9%, 6/55) was significantly higher (p<0.01 and p<0.05, respectively) than the corresponding figure (2.6%, 4/156) for the non-NSAIDs group. The causes of death were exacerbation of or complications from the background diseases (Charlson Co-morbidity Index 3≤) (Odds ratios (OR) 6.01, 95% CI (1.98-18.89))., Conclusions: Approximately 50% of the gastroduodenal ulcers with complications found in Japanese are NSAIDs-related and may take a fatal turn. It is necessary to take measures to prevent the complicated ulcers corresponding to risk factors such as the severity of background diseases.

A 63-year-old man with Stage IVa pancreas tail cancer was admitted for a distal pancreatectomy and splenectomy; adjuvant chemotherapy with gemcitabine was also administered. The chemotherapy was terminated after 16 courses due to hemolytic anemia, thrombocytopenia and renal dysfunction. Plasma exchange was performed; however the patient's renal function was diminished, requiring chronic hemodialysis. Physicians should be cautious of hemolytic uremic syndrome as a possible adverse reaction to gemcitabine and be aware that tests are needed for its early detection.

Background/aims: When a peptic ulcer is treated with proton pump inhibitors (PPI), protrusion of the ulcer base is sometimes noted during ulcer healing. To clarify the incidence of ulcer base protrusion in ulcers induced by endoscopic submucosal dissection (ESD), and whether the addition of polaprezinc, a cytoprotective agent used for treatment of gastric ulcer, to the PPI regimen helps to suppress it., Methodology: One hundred sixty-three patients on which ESD was performed were randomly allocated to either two groups: one treated with lansoprazole (30mg/day) and the other with lansoprazole (30mg/day) plus polaprezinc (150mg/day) for the treatment of ESD-induced ulcer. The condition of the ESD-induced ulcer was blindly assessed two months after ESD by two physicians., Results: Lansoprazole plus polaprezinc group showed significantly better ulcer healing (p < 0.0001) and protrusion of the ulcer base was recognized in only 1.3% (1/77), an incidence significantly lower than that in lansoprazole group (20.7%, 16/77, p = 0.0001). Polaprezinc was the only significant factor (p = 0.0001) differentiating patients who had ulcer base protrusion (n = 17) from those who did not (n = 137)., Conclusions: Polaprezinc prevents protrusion of the ulcer base during the healing of ESD-induced ulcer with PPI.

Upper gastrointestinal bleeding is a major adverse event of non-steroidal anti-inflammatory drugs (NSAIDs), and co-administration of proton pump inhibitors and H2 receptor antagonists has been established as a means of preventing such an effect. However, the incidence of bleeding associated with NSAID-induced ulcers under conditions where such strong anti-acid agents are used for prevention has yet to be clarified. We aimed to determine the annual incidence of serious upper gastrointestinal ulcer bleeding among Japanese patients in whom NSAIDs were used in our hospital. Before commencing the study, we recommended to all the physicians in our hospital the best method for caring for NSAID users, focusing on the concomitant use of proton pump inhibitors or H2 receptor antagonists. We conducted a cohort study involving 17,270 patients for whom NSAIDs had been newly prescribed. Bleeding from gastric ulcers was observed in 8 of the 17,270 patients using NSAIDs (0.05%). The pooled incidence rate for bleeding was calculated as 2.65 (95% confidence interval, 2.56-2.74) and 1.29 (1.27-1.31) per 1,000 patient years for low-dose aspirin and non-aspirin NSAID users, respectively. None of the bleeding ulcer patients required blood transfusion or were in serious condition. In conclusion, gastric ulcer bleeding occurred in low-dose aspirin or non-aspirin NSAID users, but its incidence was low and outcomes were not serious when adequate preventive measures were taken.

A 48-year-old man was referred to our hospital because of anemia. Upper gastrointestinal endoscopy showed discolored depressive lesion like gastric cancer, 30mm in diameter, in the greater curvature of the upper gastric body. During the endoscopic examination, pulsative bleeding from the lesion was occurred and we performed clipping hemostasis. We diagnosed a gastric arteriovenous malformation by endoscopic ultrasonograph and angiography. A pylorus preserving-gastrectomy was performed and Pathohistological examination revealed arterio-venous connection in the submucosal layer of the gastric wall.