Endoscopic treatment of pancreatic diseases via Duodenal Minor Papilla: 135 cases treated by Sphincterotomy, Endoscopic Pancreatic Duct Balloon Dilation (EPDBD), and Pancreatic Stenting (EPS)

Treatments via the minor papilla is effective where the deep cannulation via the major papilla is impossible in such cases as [1] the Wirsung’s duct is inflammatory narrowed, bent or obstructed by impacted stones [2] pancreatic duct divisum (complete or incomplete) [3], maljunction of pancreatico-biliary union with stones [4], pancreatic stones in the Santorini’s duct. In [1,2] cases, the pancreatic juice flow via the major papilla decreases, while that of the minor papilla increases. Then the size of minor papilla and its orifice shows corresponding enlargement. This substitutional mechanism is an advantage when undertaking our new method. Since the pancreatic juice flow is maintained via the minor papilla in these cases, accurate and careful endoscopic skills are necessary to prevent pancreatitis due to the occlusion of the Santorini’s duct after this procedure. We have experienced 135 cases treated via minor papilla in these 27 years, so we would like to report about its safety and efficacy

Gender difference in NASH susceptibility: Roles of hepatocyte <i>Ikkβ</i> and <i>Sult1e1</i>

<div><p>Myeloid cell and hepatocyte IKKβ may mediate the genesis of obesity and insulin resistance in mice fed high fat diet. However, their gender-specific roles in the pathogenesis of non-alcoholic steatohepatitis (NASH) are not known. Here we demonstrate myeloid IKKβ deficiency prevents Western diet-induced obesity and visceral adiposity in females but not in males, and attenuates hyperglycemia, global IR, and NASH in both genders. In contrast, all metabolic sequela including NASH are aggravated by hepatocyte IKKβ deficiency (<i>IkbkbΔhep</i>) in male but not female mice. Gene profiling identifies sulfotransferase family 1E (<i>Sult1e1)</i>, which encodes a sulfotransferase E1 responsible for inactivation of estrogen, as a gene upregulated in NASH in both genders and most conspicuously in male <i>IkbkbΔhep</i> mice having worst NASH and lowest plasma estradiol levels. LXRα is enriched to LXRE on <i>Sult1e1</i> promoter in male WT and <i>IkbkbΔhep</i> mice with NASH, and a <i>Sult1e1</i> promoter activity is increased by LXRα and its ligand and augmented by expression of a S32A mutant of IκBα. These results demonstrate striking gender differences in regulation by IKKβ of high cholesterol saturated fat diet-induced metabolic changes including NASH and suggest hepatocyte IKKβ is protective in male due at least in part to its ability to repress LXR-induced <i>Sult1e1</i>. Our findings also raise a caution for systemic IKK inhibition for the treatment of NASH as it may exacerbate the disease in male patients.</p></div