Predictors of technical difficulty during endoscopic submucosal dissection of superficial esophageal cancer.

BACKGROUND: Endoscopic submucosal dissection (ESD) is the standard treatment for superficial esophageal cancer (SEC); however, it is sometimes technically difficult. Our aim was to identify the predictors of technical difficulty during ESD for SEC. METHODS: We reviewed the records of patients who underwent ESD for superficial esophageal squamous cell carcinomas at a tertiary cancer center between April 2008 and March 2016. Patients undergoing ESD after esophagectomy or for residual/recurrent lesions were excluded. Preoperative factors such as tumor subsite, localization, preoperative size, macroscopic type, endoscopic depth of invasion, and treatment for synchronous multiple SECs or previous history of radiation therapy were analyzed. Logistic regression analysis was performed to identify the predictors of technical difficulty, defined as (1) long procedure time (≥ 120 min), (2) adverse events (perforation, pneumomediastinum), or (3) incomplete resection (piecemeal resection, positive or indeterminate vertical margin). RESULTS: A total of 679 lesions in 511 patients were analyzed. Difficultly was experienced in 60 cases. The procedure time was > 120 min in 43 (6.3%) patients, adverse events occurred in 16 (2.8%), and incomplete resection occurred in 17 (2.5%). Multivariate logistic regression revealed that tumors in the left esophageal wall (OR 2.15; 95% CI 1.17-3.91; p = 0.014) and those encompassing ≥ 1/2 its circumference (OR 5.06; 95% CI 2.40-11.34; p < 0.001) were independently associated with difficulty. CONCLUSIONS: Tumors in the left esophageal wall and tumors measuring > 1/2 of the esophageal circumference are predictors of difficult esophageal ESD. These results may contribute to better patient selection according to each endoscopist's skill.

A Hepatitis B Virus Reactivation Case Potentially Triggered by the Onset of Diffuse Large B Cell Lymphoma.

An 81-year-old man underwent rituximab-containing chemotherapy for chronic lymphocytic leukemia (CLL). Thirteen years after his last chemotherapy, he was diagnosed with hepatitis B virus (HBV) reactivation. He was then treated with entecavir, and improvement was seen in his liver injury. He developed diffuse large B cell lymphoma (DLBCL) after improvement in his hepatitis. Despite chemotherapy, he contracted the coronavirus disease 2019 (COVID-19) and died of COVID-19. We suspect that HBV reactivation was triggered by DLBCL. When HBV reactivation occurs a long time after chemotherapy has concluded, the onset of DLBCL should be considered.

Intraductal Tubulopapillary Epithelial Proliferation Associated with Type 1 Autoimmune Pancreatitis.

A 70-year-old man was referred to our hospital with exacerbation of diabetes. His blood tests showed elevated levels of serum IgG4 and HbA1c. Computed tomography of the pancreatic body demonstrated a weakly enhanced mass, 2 cm in size, with indistinct borders. Magnetic resonance cholangiopancreatography revealed a narrowing of the main pancreatic duct (MPD) at the pancreatic body, a markedly dilated upstream duct, and a slightly dilated downstream duct. Endoscopic ultrasonography demonstrated an iso-hypoechoic heterogeneous mass, protruding and spreading in the pancreatic duct. The histology of a fine needle aspiration sample demonstrated fibrous tissue containing abundant IgG4-positive plasma cells and atypical epithelial cells. The imaging findings and histology were not typical for either pancreatic ductal adenocarcinoma or type 1 autoimmune pancreatitis (AIP), but these were not completely excluded, and a distal pancreatectomy was performed. Histological examination showed an intraductal tubulopapillary epithelial proliferation, which contained cytoplasmic mucin (MUC5AC and MUC6), and severe IgG4-positive lymphoplasmacytic infiltration in the interstitium around the MPD. Next-generation sequencing using DNA extracted from the tumor revealed no mutation of K-ras, GNAS, or TP53. The entire lesion was ultimately diagnosed as AIP with an intraductal tubular and papillary epithelial hyperplasia producing gastric-type mucin. Some recent reports have described AIP development in the background of intraductal papillary mucinous neoplasms, and some have hypothesized a paraneoplastic occurrence of IgG4-related disease. The current case indicates issues in the clinical diagnosis of rare variants of AIP, and raises questions about the relationship between AIP and pancreatic epithelial lesions.