Using air cholangiography to reduce postendoscopic retrograde cholangiopancreatography cholangitis in patients with malignant hilar obstruction.

Background: Cholangitis after endoscopic retrograde cholangiopancreatography (ERCP) is a major problem for patients with hilar biliary obstruction. To date, it remains unclear whether air-contrast cholangiography (ACC) can reduce cholangitis in these patients. For this reason, our study assesses the efficacy of reducing cholangitis through ACC. Methods: This paper presents a retrospective study conducted at a tertiary university hospital. We enrolled patients who were diagnosed with hilar structures and underwent ERCP between January 2012 and December 2018. From 2015 onwards, ACC was performed following the successful selective cannulation into the dilated intrahepatic bile duct of these patients. The primary aim was to assess patients with cholangitis in both an ACC group and iodine contrast cholangiography (ICC) group. Results: This study included 80 patients, 35 of whom received ACC and 45 who received ICC. There were no differences between the 2 groups in terms of the number of patients who underwent endoscopic papillotomy, endoscopic nasobiliary drainage, endoscopic biliary stent placement, or other technical procedures or complications. A total of 19 patients (23.8%) presented with fever (cholangitis) after the ERCP procedure (4 ACC, 15 ICC; 11.4% vs. 33.3%, respectively; P=0.03). One patient in the ICC group who obtained a plastic stent for palliative drainage died 2 weeks post-ERCP. Among the other 18 cholangitis patients, 8 (1 ACC, 7 ICC) were treated with additional ERCP or percutaneous transhepatic biliary drainage (PTBD), while the remaining 10 only received antibiotics. One patient in the ICC group who obtained a plastic stent for palliative drainage died 2 weeks post-ERCP. Conclusions: We found that ACC significantly reduced the incidence of cholangitis in patients with hilar obstruction.

Sulforaphane alter the microbiota and mitigate colitis severity on mice ulcerative colitis induced by DSS.

Sulforaphane (SFN) is a kind of natural isothiocyanate, which exists in cruciferous plants. Only few studies were about the anti-inflammatory effects of sulforaphane in ulcerative colitis. In this study, our purpose is to explore the effects of sulforaphane on the intestinal microbial community of UC mice. The severity of mice colitis were measured by colon length, survial rate, body weight and disease activity index (DAI) score. Histological and morphological evaluation of colon tissues were performed by HE. 16S rRNA gene amplicon pyrosequencing was used to analyza the changes of mouse flora. The variety of flora expression were explored using quantitative PCR. Sulforaphane treated mice had larger body weight and longer colon length than DSS-induced mice. The colon tissues of DSS group showed congestion and edema. Meanwhile, treatment with sulforaphane effectively reducted the damage scores and MPO activity. Sulforaphane reversed DSS-induced gut dysbiosis. Sulforaphane would shift the balance to Butyricicoccus on inflammation. The possible anti-inflammatory mechanism of sulforaphane is to coordinate with the probiotics such as Butyricicoccus. In summary, these findings proved that sulforaphane might be a useful content and serve as a potential therapy in the treatment of UC.

HOXB13 expression is correlated with hepatic inflammatory activity of patients with hepatic fibrosis.

Liver fibrosis is a common pathological process of chronic hepatic injury, preceded by the chronic inflammation. The homeobox B13 (HOXB13) gene, a member of HOX family, plays diverse biological roles in embryonic development, carcinogenesis, and many inflammatory diseases. However, the expression of HOXB13 in chronic liver diseases including hepatic fibrosis remains to be defined. In present study, 55 patients with hepatic fibrosis, 15 patients of hepatocellular carcinoma, and 17 healthy controls were enrolled in this study. Pathological specimens were collected through liver biopsy or surgical resection. The degree of hepatic inflammation (G0-G4) and fibrosis (S0-S4) of hepatic fibrosis was scored based on the modified histology activity index. Intrahepatic HOXB13 expression was analyzed using immunohistochemistry analysis. Compared with healthy subjects, both patients with hepatic fibrosis and patients with hepatocellular carcinoma exhibited significant accumulations of HOXB13+ cells in the liver (p < 0.05). Additionally, the number of HOXB13+ cell was significantly elevated along with the increment of hepatic inflammatory activities, but not fibrosis stages, among these liver fibrosis samples (p < 0.01). Furthermore, the quantity of HOXB13+ cells were also positively correlated with hepatic enzymes, alanine transaminase (r = 0.299, p = 0.041) and aspartate aminotransferase (r = 0.317, p = 0.013) in our cohort of hepatic fibrosis. In conclusion, our study identified a strong hepatic expression of HOXB13 among patients with hepatic fibrosis, which strongly associated with the degree of hepatic inflammatory activity for patients with hepatic fibrosis, suggesting an important role of HOXB13 during the pathogenesis of liver fibrogenesis.