Common bile duct dilation after bariatric surgery.

BACKGROUND: Biliary dilation suggests obstruction and prompts further work up. Our experience with endoscopic ultrasound and endoscopic retrograde cholangiopancreatography in the symptomatic post-bariatric surgery population revealed many patients with radiographically dilated bile ducts, but endoscopically normal studies. It is unclear if this finding is phenomenological or an effect of surgery. Additionally, it is unknown whether the type of bariatric surgery alters biliary pathophysiology. Thus, we studied whether a change occurs in biliary diameter following Roux-en-Y gastric bypass (RYGB) and sleeve gastrectomy (SG). METHODS: A single-center retrospective study assessing biliary diameter before and after RYGB or SG based on radiographic imaging. All adult patients undergoing RYGB or SG from January 2010 to December 2013 who had imaging studies before and > 3 months after surgery were included. Those with known obstructive etiologies and those without post-operative imaging were excluded. Common bile duct (CBD) diameter was re-read by a radiologist at the same location in the CBD for pre- and post-operative imaging. Baseline clinical factors and cholecystectomy status were collected. RESULTS: 269 patients met inclusion criteria (193 RYGB;76 SG). Between the groups, there were no significant differences in pre-operative characteristics. Average time from surgery to repeat imaging was 24.1 months. After adjusting for pre-operative factors, subjects who underwent an RYGB had an increase in CBD diameter of 1.4 mm (95% CI 0.096, 0.18), which was greater than the change following SG 0.5 mm(95% CI - 0.007, 0.11). The magnitude of this change did not depend on prior cholecystectomy in the RYGB cohort. Within the SG group, for patients without a prior cholecystectomy, there was a significant increase in post-operative CBD diameter of 0.8 mm(95% CI 0.02, 0.14). CONCLUSION: Bariatric surgery results in CBD dilation, with changes more pronounced after RYGB. Biliary dilation occurs irrespective of cholecystectomy status. Further work is necessary to determine the cause and clinical implications of this phenomenon.

Engaging Ly-6A/Sca-1 triggers lipid raft-dependent and -independent responses in CD4+ T-cell lines.

INTRODUCTION: The lymphocyte antigen 6 (Ly-6) supergene family encodes proteins of 12-14 kda in molecular mass that are either secreted or anchored to the plasma membrane through a glycosyl-phosphatidylinisotol (GPI) lipid anchor at the carboxy-terminus. The lipidated GPI-anchor allows localization of Ly-6 proteins to the 10-100 nm cholesterol-rich nano-domains on the membrane, also known as lipid rafts. Ly-6A/Sca-1, a member of Ly-6 gene family is known to transduce signals despite the absence of transmembrane and cytoplasmic domains. It is hypothesized that the localization of Ly-6A/Sca-1 with in lipid rafts allows this protein to transduce signals to the cell interior. METHODS AND RESULTS: In this study, we found that cross-linking mouse Ly-6A/Sca-1 protein with a monoclonal antibody results in functionally distinct responses that occur simultaneously. Ly-6A/Sca-1 triggered a cell stimulatory response as gauged by cytokine production with a concurrent inhibitory response as indicated by growth inhibition and apoptosis. While production of interleukin 2 (IL-2) cytokine by CD4+ T cell line in response to cross-linking Ly-6A/Sca-1 was dependent on the integrity of lipid rafts, the observed cell death occurred independently of it. Growth inhibited CD4+ T cells showed up-regulated expression of the inhibitory cell cycle protein p27kip but not of p53. In addition, Ly-6A/Sca-1 induced translocation of cytochrome C to the cytoplasm along with activated caspase 3 and caspase 9, thereby suggesting an intrinsic apoptotic cell death mechanism. CONCLUSIONS: We conclude that opposing responses with differential dependence on the integrity of lipid rafts are triggered by engaging Ly-6A/Sca-1 protein on the membrane of transformed CD4+ T cells.