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Background: Endoscopic fully‐covered self‐expandable metal stents (FCSEMSs) are used to treat benign biliary strictures (BBSs); however, treatment for perihilar BBSs is technically challenging. The aim of this study was to evaluate the usefulness of an unflared FCSEMS designed for intraductal placement in patients with refractory perihilar BBS. Methods: Twenty‐two consecutive patients with perihilar BBS unresolved by endoscopic plastic stent placement at 13 tertiary medical centers were prospectively enrolled. The FCSEMS was placed above the papilla and removed after 4 months. The primary outcome was stricture resolution at 4 months, and the secondary outcomes were technical success, stent removal, adverse events, and recurrence. Results: The technical success rate of intraductal FCSEMS placement was 100%, and plastic stent placement at contralateral or side branch was performed in 86% of patients. The rate of successful stent removal at 4 months was 100%, and stricture resolution was observed in 91% of patients. Stent migration or stent‐induced de novo stricture did not occur in any patient. The stricture recurrence rate was 16%, and the median (interquartile range) follow‐up duration was 2.8 (1.6‐3.3) years. Conclusions: Intraductal placement of unflared FCSEMS is effective treatment for refractory perihilar BBS. [ABSTRACT FROM AUTHOR]

Background and Aim: Bleeding is an inevitable and often severe complication after endoscopic sphincterotomy (EST). We aimed to investigate the factors associated with post‐EST bleeding in patients treated with anticoagulants. Methods: The data of patients who underwent EST at 15 hospitals between July 2015 and June 2017 were extracted. We investigated the incidence of post‐EST bleeding and risk factors for bleeding in patients treated with anticoagulants. Results: One hundred forty‐nine patients undergoing EST who met the inclusion criteria were included in this study. The total‐EST bleeding (bleeding occurring during or after EST) rate did not differ between the heparin replacement (8.0%, 6/75) and continuation (16.6%, 2/12; P = 0.37) groups of warfarin users. The total‐EST‐bleeding rate in the heparin replacement group (12.9%, 4/31) was significantly higher than that in the continuation group (0%, 0/31; P = 0.016) in direct oral anticoagulant (DOAC) users. The rate of total‐EST bleeding with continuation of DOAC (0%, 0/31) was significantly lower with continuation of warfarin (16.6%, 2/12; P = 0.021). During‐EST bleeding (bleeding occurring during EST) (P = 0.0083) and precut (P = 0.033) were significant risk factors for post‐EST bleeding in all 149 patients. Heparin replacement was only a significant risk factor for total‐EST bleeding (P = 0.033) in DOAC users. Conclusion: Heparin replacement was a significant risk factor for post‐EST bleeding in DOAC users; however, there was no significant difference between the bleeding rate of heparin replacement and that of continuation groups in patients taking warfarin. During EST and precut were significant risk factors for post‐EST bleeding in all patients treated with anticoagulants. [ABSTRACT FROM AUTHOR]

In the present study, we have analyzed the amount of precore wild-type hepatitis B virus (HBV) (wild-type) and precore mutant HBV (nt 1896: G→A) (precore mutant) of HBV carriers; 31 asymptomatic healthy carriers (ASC) and 28 patients with chronic hepatitis (CH). Wild-type and precore mutant were quantified using sensitive and specific quantification methods: competitive wild-type-sequence-specific assay and competitive mutation-site-specific assay with different sets of specific primers and internal controls. Median serum levels of wild-type and precore mutant were 9.60 and 8.60 log copies/ml (median percentages of precore mutant in total HBV-DNA: 11.7%) in HBeAg(+) ASC, 8.48 and 8.00 (33.3%) in HBeAg(+) CH, and 6.30 and 6.85 (84.7%) in anti-HBe(+) CH, respectively, showing higher levels of the relative amount of precore mutant to wild-type along with HBeAg/anti-HBe status. Only precore mutant, but not wild-type was detected in anti-HBe(+) ASC. Although median percentages of precore mutant at the anti-HBe(+) ASC and CH stages were much higher than those at the HBeAg(+) ASC and CH stages, a substantial amount of precore mutant was found even at the HBeAg(+) stages. Existence of a substantial amount of precore mutant even in HBeAg(+) ASC suggests that the occurrence of precore mutant is not always closely associated with seroconversion from HBeAg to anti-HBe. [Copyright &y& Elsevier]