Background /PurposeLimited data are available for acute cholecystitis after Self‐Expandable Metallic Stent (SEMS) placement in patients with malignant distal biliary obstruction. We aimed to identify risk factors for cholecystitis.MethodsThis was a retrospective, single‐center study of 280 patients (336 stents) who received endoscopic SEMS placement between May 2005 and April 2016. Clinical records were used to perform risk factor analyses.ResultsOf 336 SEMS placement procedures, 25 (7.4%) led to development of cholecystitis. Logistic regression analysis revealed three independent risk factors: covered SEMS (P = .014), tumor involvement to the cystic duct (P = .017), and presence of gallstones (P = .022). Median time to cholecystitis onset was shorter with covered SEMS than with uncovered SEMS (P = .034), and in patients with pancreatic cancer compared to those with other cancers (P = .001). Severe cholecystitis developed within 30 days after covered SEMS placement in three patients with pancreatic cancer without tumor involvement to the cystic duct.ConclusionsUse of covered SEMS might be a risk factor for cholecystitis onset within 30 days after placement. Clinicians should be aware of the risk for severe cholecystitis after covered SEMS placement, even if the tumor does not invade the cystic duct.

Background and Aim: It is imperative to distinguish superficial non-ampullary duodenal carcinomas (NADCs) between intramucosal and submucosal invasive carcinoma for treatment selection. The aim of this study was to evaluate the clinicopathological differences of intramucosal and submucosal carcinoma. Methods: This was a retrospective, single-center study comprising 134 patients with 137 superficial NADCs during May 2005 and March 2018. Clinicopathological characteristics and treatment outcomes data were used to perform a comparative analysis of endoscopic findings, preoperative diagnoses of depth of cancer, and treatment outcomes of histologically diagnosed intramucosal and submucosal carcinoma. Results: Of the 137 NADCs, 125 (91%) were intramucosal, and 12 (9%) were submucosal. The proportion of submucosal carcinoma was significantly higher on the oral side of the papilla than on the anal side (16% vs 1%, P = 0.002). Submucosal tumor-like appearance was more frequent in submucosal than in intramucosal carcinoma (58% vs 13%, P = 0.001). There was no significant difference in tumor diameter between the groups, but 33% of submucosal carcinomas were ≤ 10 mm. Correct preoperative diagnosis of depth was achieved in 33% of submucosal carcinoma. Submucosal carcinoma was frequently underestimated when tumor diameters were ≤ 10 mm. Conversely, intramucosal carcinoma was frequently overestimated when the tumor was ≥ 30 mm and had thickness or giant nodules. Lymph node metastasis was found in one submucosal carcinoma patient. Conclusions:The possibility of submucosal invasion should be considered when NADCs are located on the oral side of the papilla or have submucosal tumor-like appearance even if tumor diameters are ≤ 10 mm.

Two tyrosine kinase inhibitors, lenvatinib and sorafenib, are available systemic therapies for patients with metastatic differentiated thyroid carcinoma. However, the treatment options for carcinoma refractory to both lenvatinib and sorafenib are limited. Here, we present a case of metastatic papillary thyroid carcinoma that showed resensitization to rechallenge with lenvatinib. A 72-year-old woman who had been diagnosed with papillary thyroid carcinoma with multiple lymph node and lung metastases progressed with the emergence of subcutaneous metastasis after 3 years of response to initial lenvatinib. Five months after switching to sorafenib, the tumor was enlarged with increased contrast enhancement on computed tomography, suggesting progressive disease. Three months after the reintroduction of lenvatinib, marked tumor shrinkage and a decrease in its contrast enhancement were seen. Rechallenge with lenvatinib showed tumor resensitization. Therefore, rechallenge with lenvatinib may be a treatment option in patients who have experienced progressive disease after initial response to lenvatinib and subsequent sorafenib.

SummaryBackground Immune-related hepatotoxicity is often regarded as immune-related hepatitis (irHepatitis) despite including immune-related sclerosing cholangitis (irSC). This study examined the clinical differences between irSC and irHepatitis. Methods A single-center retrospective study of 530 consecutive patients who received immunotherapy between August 2014 and April 2020 was performed. IrSC and irHepatitis were respectively defined as the radiological presence and absence of bile duct dilation and wall thickness. Results Forty-one patients (7.7%) developed immune-related hepatotoxicity. A CT scan was performed on 12 patients, including 11 of 12 with ≥ grade 3 aminotransferase elevations. IrSC and irHepatitis were diagnosed in 4 (0.8%) and 8 (1.5%) patients, respectively. All the irSC patients had been treated with anti-PD-1. IrHepatitis was more common among patients receiving anti-CTLA-4 than among those receiving anti-PD-1/PD-L1 inhibitors (14%, 7/50 vs. 0.2%, 1/480, P < 0.001). A ≥ grade 2 alkaline phosphatase (ALP) elevation resulting in a cholestatic pattern was seen in all 4 irSC patients. Among the irSC patients, 3 (3/4, 75%) developed ≥ grade 3 aminotransferases elevation. The median duration from the start of immunotherapy until ≥ grade 2 liver enzymes elevation was 257 and 55.5 days in irSC and irHepatitis patients. The median times for progression from grade 2 to 3 liver enzyme elevation were 17.5 and 0 days, respectively. Conclusions IrSC and irHepatitis have different characteristics in the class of immune checkpoint inhibitor and onset pattern. Radiological examination for the diagnosis of irSC should be considered for patients with ≥ grade 2 ALP elevation resulting in a cholestatic pattern. (Registration number J2020-36, Date of registration June 3, 2020)

A small proportion of intraductal papillary mucinous neoplasms (IPMNs) are accompanied by type 1 autoimmune pancreatitis (AIP); however their clinical courses and image characteristics have not been fully reported. A 65-year-old woman was referred to our hospital for the examination of a pancreatic head cyst that had shown exacerbation for two years. Several images demonstrated a multilocular cyst with a symmetrically thickened, enhanced, cyst wall. Cancerization of IPMN was suspected, and pancreatoduodenectomy was performed. The resected specimens showed a multilocular cyst with solid areas. The solid areas demonstrated pathological findings that corresponded with type 1 AIP. Papillary epithelia suggestive of IPMN was recognized in some parts of the cystic wall.