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Background & Aims Endoscopic ultrasound-guided transmural gallbladder drainage (EUS-GBD) is an alternative to percutaneous transhepatic gallbladder drainage (PTGBD) for patients with acute, high-risk, or advanced-stage cholecystitis who do not respond to initial medical treatment and cannot undergo emergency cholecystectomy. However, the technical feasibility, efficacy, and safety of EUS-GBD and PTGBD have not been compared. Methods Fifty-nine patients with acute cholecystitis, who did not respond to initial medical treatment and were unsuitable for an emergency cholecystectomy, were chosen randomly to undergo EUS-GBD (n = 30) or PTGBD (n = 29). The technical feasibility, efficacy, and safety of EUS-GBD and PTGBD were compared. Results EUS-GBD and PTGBD showed similar technical (97% [29 of 30] vs 97% [28 of 29]; 95% 1-sided confidence interval lower limit, −7%; P = .001 for noninferiority margin of 15%) and clinical (100% [29 of 29] vs 96% [27 of 28]; 95% 1-sided confidence interval lower limit, −2%; P = .0001 for noninferiority margin of 15%) success rates, and similar rates of complications (7% [2 of 30] vs 3% [1 of 29]; P = .492 in the Fisher exact test) and conversions to open cholecystectomy (9% [2 of 23] vs 12% [3 of 26]; P = .999 in the Fisher exact test). The median post-procedure pain score was significantly lower after EUS-GBD than after PTGBD (1 vs 5; P Conclusions EUS-GBD is comparable with PTGBD in terms of the technical feasibility and efficacy; there were no statistical differences in the safety. EUS-GBD is a good alternative for high-risk patients with acute cholecystitis who cannot undergo an emergency cholecystectomy.

Background & Aims Endoscopic ultrasonography (EUS)-guided interventions have been used to treat patients with cystic lesions of the pancreas (CLPs). We used EUS to guide injection and lavage of ethanol, followed by injection of paclitaxel, into cysts, and investigated treatment response and predictors. Methods Fifty-two patients were enrolled in the study using the following inclusion criteria: unilocular or oligolocular cysts, indeterminate cystic lesions that required EUS fine-needle aspiration, and cystic lesions that grew during the observation period. Forty-seven patients were followed up for more than 12 months and their outcomes were analyzed. Results The mean diameter of the CLPs was 31.8 mm (range, 17–68 mm) and the estimated volume was 14.09 mL (range, 1.16–68.74 mL). Twenty CLPs were oligolocular. The mean level of carcinoembryonic antigen was 463 ng/mL (range, 1–8190 ng/mL). The median follow-up period was 21.7 months. A complete response was observed in 29 patients, a partial response in 6 patients, and persistent cysts in 12 patients. Four of 12 patients with persistent cysts underwent surgery. The histopathologic degree of epithelial ablation varied from 0% to 100%. Based on univariate analysis, EUS diameter and original volume predicted cyst resolution; in multivariate analysis, only original volume predicted resolution. Mild pancreatitis and splenic vein obliteration each occurred in 1 patient. Conclusions EUS-guided injection and lavage of ethanol, followed by injection of paclitaxel, appears to be a safe method for treating pancreatic cysts; 62% of patients had complete resolution. Small cyst volume predicted complete resolution.

Background & Aims: Although autoimmune pancreatitis (AIP) responds well to corticosteroid therapy, relapse during maintenance corticosteroid therapy or after the withdrawal of corticosteroid treatment is not uncommon. To date, the factors related to relapse of AIP have not been fully explored. Methods: To determine the clinical and genetic predictors relating to the relapse of AIP, we evaluated clinical factors, HLA polymorphisms, and the amino acid sequences in 40 patients with AIP. Results: At a median follow-up period of 40 months (range, 12–67 months), relapse developed in 13 of 40 patients with AIP (33%), in whom complete remission was achieved with oral corticosteroid therapy. Among demographics, clinical characteristics in the initial diagnosis of AIP, we could not find any clinical predictor for relapse of AIP; however, in amino acid sequence analysis for relapse of AIP, the substitution of aspartic acid to nonaspartic acid at residue 57 of DQβ1 showed a significant association with relapse of AIP (nonrelapse group, 29.6%; relapse group, 100%; P = .00003; odds ratio, 3.38; 95% confidence interval, 1.9–6.0). There was a significant difference in the timing of relapse of AIP, according to density of the nonaspartic acid residue at DQβ1 57 (nonaspartic acid homozygosity: mean ± SD, 6.7 ± 4.2 months; nonaspartic acid heterozygosity: mean ± SD, 33 ± 11 months; P Conclusions: Substitution of aspartic acid to nonaspartic acid at DQβ1 57 appears to represent a key genetic factor for relapse of AIP (ClinicalTrials.gov number, NCT00444444).

Background: Branch duct-type intraductal papillary mucinous neoplasm (BD-IPMN) is a risk factor for pancreatic ductal adenocarcinoma (PDAC), but the groups at high risk for developing PDAC during the follow-up period of BD-IPMN are not clear. Objectives: To identify the risk factors for PDAC development during the follow-up period of BD-IPMN. Subjects and Methods: We investigated 230 patients undergoing follow-up of BD-IPMN; the median follow-up period was 56.9 months, and the range was 3-276 months. Among these patients, 10 developed pancreatic cancer (PDAC, 7; intraductal papillary mucinous carcinoma [IPMC], 3). The 230 patients were divided into 2 groups: PDAC group, which included 7 patients; and non-PDAC group, which included 223 patients. The PDAC and non-PDAC groups were compared with respect to the following factors: sex; age; follow-up period; number of BD-IPMNs; size of BD-IPMNs; diameter of the main pancreatic duct (MPD); size of mural nodules; family history of pancreatic cancer (within the second degree of relationship); family history of digestive organ cancer, except pancreatic cancer (within the second degree of relationship); diabetes mellitus; adiposis (body mass index [BMI] ≥ 30 kg/m2); chronic pancreatitis; and history of smoking. A chi-square test and a t test were used for univariate analysis, and logistic regression was used for multivariate analysis. Results:Univariate analysis showed that adiposis (p = 0.016), chronic pancreatitis (p = 0.038), and a family history of pancreatic cancer (p = 0.006) were the factors significantly associated with PDAC development. Multivariate analysis of these 3 factors showed that adiposis (p = 0.000, odds ratio = 60.93, 95% confidence interval [CI] = 6.18-599.92), chronic pancreatitis (p = 0.023, odds ratio = 13.0, 95% CI = 1.42-119.35), and a family history of pancreatic cancer (p = 0.003, odds ratio = 21.1, 95% CI = 2.87-156.49) were independently associated with PDAC development. Conclusions: Our results showed that adiposis (BMI ≥ 30 kg/ m2), chronic pancreatitis, and a family history of pancreatic cancer (within the second degree of relationship) were risk factors for PDAC development during the follow-up period of BD-IPMN patients.

Backgrounds: Recently, two distinct histological patterns of autoimmune pancreatitis (AIP), type 1 AIP and type 2 AIP, have been recognized. Type 2 AIP has been reported mainly in western countries and is known to be rare in Asia. The aim of this study was to compare the prevalence, clinical profiles, radiological findings and response to steroids of type 1 and type 2 AIP in Korea. Methods: From 120 patients diagnosed with AIP between January 2003 and March 2010, 52 patients with histologically confirmed type 1 (n=37) or type 2 (n=15) AIP were included. We reviewed the prospectively collected data on these patients. Results: The type 2 AIP patients' median age (34 years) was significantly lower than that of the type 1 AIP patients (61 years) (p 1,800 mg/dL, 54.1% in type 1 AIP vs. 0% in type 2, p 135 mg/dL, 70.3% in type 1 AIP vs. 0% in type 2 AIP, p