7%) of the colonies that formed originated from CD49fhi cells (Fig. 2D). These data, together with the LDA results, definitively demonstrate that CD49f enriches for candidate gallbladder stem cells. We observed the formation of two distinct types of colonies in EpCAM+CD49f+ gallbladder cultures at p0. The http://www.selleckchem.com/products/BI6727-Volasertib.html first type consisted of large colonies with an undifferentiated phenotype comprising small cells with a large nuclear-cytoplasmic ratio (Fig 3A,B, red arrowheads). We termed these the “flat colonies.” The second type was smaller, more organized colonies called “glandular colonies” with an organotypic phenotype consisting of cells organized around a lumen (Fig. 3A,B, white

arrowheads). Flat colonies were more numerous than glandular ones. TEM on the flat colonies revealed a single layer of cuboidal epithelial cells (Fig. 3C). These cells have defined apical-basolateral polarity, apical microvilli, and appear to secrete basement membrane at their basolateral surface. They also have interdigitating lateral membranes and junctional apparatus typical of gallbladder

epithelial cells. Conversely, the glandular colonies consist of columnar epithelial cells organized around a central lumen (Fig. 3C) and exhibit junctional apparatus. Unlike PDGFR inhibitor flat colonies, numerous secretory granules are seen in their apical cytoplasm, and secretory products are present in their lumen (Fig. 3C). The flat and glandular colonies are distinct by morphology and ultrastructure. Importantly, only the flat colonies are observed at late passages (Fig. 3A), indicating that the glandular colonies are not capable of long-term Amisulpride self-renewal (>p3). To test this hypothesis, we passaged single colonies from p0 cultures. None of the glandular colonies could be successfully repassaged (Fig. 3D). This suggests that serial passage of the gallbladder cells past the first expansion enriches for EpCAM+CD49f+ cells that form

flat colonies. Because we found no additional markers to further purify gallbladder stem cells, we hypothesized that the cells past the first expansion are candidate stem cells. To determine their stemness, we tested whether the expanded EpCAM+CD49f+ gallbladder cells could satisfy the stem cell criteria of clonogenic self-renewal and lineage commitment. We developed a novel invitro differentiation assay by utilizing the basement membrane extracellular matrix, Matrigel. Matrigel has been shown to promote or maintain the differentiation or three-dimensional (3D) morphogenesis of numerous cell lines and primary cells, including hepatocytes and IHBD cells.23-25 In our assay, expanded EpCAM+CD49f+ gallbladder cells (>p1) were mixed with serum-free media and layered above with Matrigel (Fig. 4A). Within 1 week, we noticed the formation of two distinct morphogenetic structures—ductular structures that adhered to the plastic (Fig. 4B) and cysts that were suspended in the Matrigel (Fig. 4C).

7%) of the colonies that formed originated from CD49fhi cells (Fig. 2D). These data, together with the LDA results, definitively demonstrate that CD49f enriches for candidate gallbladder stem cells. We observed the formation of two distinct types of colonies in EpCAM+CD49f+ gallbladder cultures at p0. The ABT-263 mw first type consisted of large colonies with an undifferentiated phenotype comprising small cells with a large nuclear-cytoplasmic ratio (Fig 3A,B, red arrowheads). We termed these the “flat colonies.” The second type was smaller, more organized colonies called “glandular colonies” with an organotypic phenotype consisting of cells organized around a lumen (Fig. 3A,B, white

arrowheads). Flat colonies were more numerous than glandular ones. TEM on the flat colonies revealed a single layer of cuboidal epithelial cells (Fig. 3C). These cells have defined apical-basolateral polarity, apical microvilli, and appear to secrete basement membrane at their basolateral surface. They also have interdigitating lateral membranes and junctional apparatus typical of gallbladder

epithelial cells. Conversely, the glandular colonies consist of columnar epithelial cells organized around a central lumen (Fig. 3C) and exhibit junctional apparatus. Unlike selleck chemical flat colonies, numerous secretory granules are seen in their apical cytoplasm, and secretory products are present in their lumen (Fig. 3C). The flat and glandular colonies are distinct by morphology and ultrastructure. Importantly, only the flat colonies are observed at late passages (Fig. 3A), indicating that the glandular colonies are not capable of long-term Edoxaban self-renewal (>p3). To test this hypothesis, we passaged single colonies from p0 cultures. None of the glandular colonies could be successfully repassaged (Fig. 3D). This suggests that serial passage of the gallbladder cells past the first expansion enriches for EpCAM+CD49f+ cells that form

flat colonies. Because we found no additional markers to further purify gallbladder stem cells, we hypothesized that the cells past the first expansion are candidate stem cells. To determine their stemness, we tested whether the expanded EpCAM+CD49f+ gallbladder cells could satisfy the stem cell criteria of clonogenic self-renewal and lineage commitment. We developed a novel invitro differentiation assay by utilizing the basement membrane extracellular matrix, Matrigel. Matrigel has been shown to promote or maintain the differentiation or three-dimensional (3D) morphogenesis of numerous cell lines and primary cells, including hepatocytes and IHBD cells.23-25 In our assay, expanded EpCAM+CD49f+ gallbladder cells (>p1) were mixed with serum-free media and layered above with Matrigel (Fig. 4A). Within 1 week, we noticed the formation of two distinct morphogenetic structures—ductular structures that adhered to the plastic (Fig. 4B) and cysts that were suspended in the Matrigel (Fig. 4C).

Downstream from hypoxia-induced caspase-1 activation, cleavage and release of proinflammatory cytokines interleukin (IL)-1β and -18 occurred. We further demonstrate that overexpression of HMGB1 or treatment with recombinant HMGB1 enhanced the invasiveness of HCC cells, whereas stable knockdown of HMGB1 remarkably reduced HCC invasion. Moreover, in a murine model of HCC pulmonary metastasis, stable PF-02341066 clinical trial knockdown of HMGB1 suppressed HCC invasion and metastasis. Conclusion: These results suggest

that in hypoxic HCC cells, HMGB1 activates TLR4- and RAGE-signaling pathways to induce caspase-1 activation with the subsequent production of multiple inflammatory mediators, which, in turn, promote cancer invasion and metastasis. (HEPATOLOGY 2012;55:1866–1875) A worldwide increase in mortality associated with hepatocellular carcinoma (HCC) has recently been reported.1 Clinical treatment of HCC remains challenging because of a lack of effective chemotherapy and clearly defined endpoints for clinical protocols.2, 3 The advanced nature of disease at presentation, often in the background of steatosis4 and chronic hepatitis C,5 is a major change in the etiology from that observed in

the past.6 The main cause of death in HCC patients, irrespective of etiology, is cancer metastasis within or outside the liver. The underlying mechanisms responsible for invasiveness and metastatic spread of HCC are still not fully understood. Farnesyltransferase Hypoxia is found in a wide range of human malignancies, including liver, breast, prostate, and pancreatic cancers as well BGB324 as brain tumors and melanoma.7 The extent of hypoxia is associated with tumor progression and poor clinical outcomes. Hypoxia has a dual role: Insufficient oxygen limits tumor cell division while, at the same time, selecting for

more malignant cells and induces cell adaptations that allow for more invasive behavior.8 Cancer cells may promote tumor metastasis through the release of paracrine or endocrine signals that enhance invasiveness and promote the tumor premetastatic niche.9-11 Tumor-derived mediators not only inhibit apoptosis of tumor cells, but also promote cell invasiveness and metastasis. High-mobility group box 1 (HMGB1) is an evolutionarily conserved, chromatin-binding protein that has been implicated in several disease states, including sepsis, arthritis, ischemia-reperfusion injury, and cancer.12, 13 Cancer cells that have undergone necrotic cell death can release HMGB1 into the local microenvironment. HMGB1 is also actively secreted by inflammatory cells, acting as an endogenous danger signal and binding with high affinity to several receptors, including the receptor for advanced glycation endproducts (RAGE) as well as Toll-like receptors (TLRs)-2, -4, and -9.12 Extracellular HMGB1 can lead to chronic inflammatory-reparative responses that, in the setting of cancer, may lead to tumor cell survival, expansion, and metastases.

Downstream from hypoxia-induced caspase-1 activation, cleavage and release of proinflammatory cytokines interleukin (IL)-1β and -18 occurred. We further demonstrate that overexpression of HMGB1 or treatment with recombinant HMGB1 enhanced the invasiveness of HCC cells, whereas stable knockdown of HMGB1 remarkably reduced HCC invasion. Moreover, in a murine model of HCC pulmonary metastasis, stable R788 cell line knockdown of HMGB1 suppressed HCC invasion and metastasis. Conclusion: These results suggest

that in hypoxic HCC cells, HMGB1 activates TLR4- and RAGE-signaling pathways to induce caspase-1 activation with the subsequent production of multiple inflammatory mediators, which, in turn, promote cancer invasion and metastasis. (HEPATOLOGY 2012;55:1866–1875) A worldwide increase in mortality associated with hepatocellular carcinoma (HCC) has recently been reported.1 Clinical treatment of HCC remains challenging because of a lack of effective chemotherapy and clearly defined endpoints for clinical protocols.2, 3 The advanced nature of disease at presentation, often in the background of steatosis4 and chronic hepatitis C,5 is a major change in the etiology from that observed in

the past.6 The main cause of death in HCC patients, irrespective of etiology, is cancer metastasis within or outside the liver. The underlying mechanisms responsible for invasiveness and metastatic spread of HCC are still not fully understood. Afatinib mw Hypoxia is found in a wide range of human malignancies, including liver, breast, prostate, and pancreatic cancers as well RG7204 chemical structure as brain tumors and melanoma.7 The extent of hypoxia is associated with tumor progression and poor clinical outcomes. Hypoxia has a dual role: Insufficient oxygen limits tumor cell division while, at the same time, selecting for

more malignant cells and induces cell adaptations that allow for more invasive behavior.8 Cancer cells may promote tumor metastasis through the release of paracrine or endocrine signals that enhance invasiveness and promote the tumor premetastatic niche.9-11 Tumor-derived mediators not only inhibit apoptosis of tumor cells, but also promote cell invasiveness and metastasis. High-mobility group box 1 (HMGB1) is an evolutionarily conserved, chromatin-binding protein that has been implicated in several disease states, including sepsis, arthritis, ischemia-reperfusion injury, and cancer.12, 13 Cancer cells that have undergone necrotic cell death can release HMGB1 into the local microenvironment. HMGB1 is also actively secreted by inflammatory cells, acting as an endogenous danger signal and binding with high affinity to several receptors, including the receptor for advanced glycation endproducts (RAGE) as well as Toll-like receptors (TLRs)-2, -4, and -9.12 Extracellular HMGB1 can lead to chronic inflammatory-reparative responses that, in the setting of cancer, may lead to tumor cell survival, expansion, and metastases.

CYP7A1 represents the key enzyme catalyzing BA biosynthesis. In one human study, investigating patients with obstructive cholestasis, hepatic CYP7A1 mRNA tended to be increased, similar to the results in our fatty liver patients.32 High serum cholestenone levels confirm the increased CYP7A1 mRNA expression in our study at the functional level. SHP also represses hepatocyte BA uptake by transcriptional repression of NTCP.33 In experimental obstructive cholestasis in rodents, NTCP is down-regulated by activation of FXR and subsequently induction of the repressor SHP. This mechanism prevents excessive BA transport from portal blood and uptake GDC-0980 into the hepatocytes.10

Similar mechanisms are in action for human NTCP where SHP has been shown to suppress the glucocorticoid receptor-mediated transactivation of the human NTCP promoter.34 In human fatty livers, we observed an increase in NTCP expression, which in contrast to Cyp7A1 decreased with progression to NASH. The observed attenuation of baseline SHP activity under steatotic conditions was confirmed in our in vitro experiments. FFA treatment led selleck chemicals llc to a significant up-regulation

of NTCP and Cyp7A1. Similar to our findings in NASH regarding NTCP expression, BA (CDCA) treatment attenuated these effects, most likely by way of FXR-SHP activation. This is consistent with recent data from ob/ob mice where SHP-induction and down-regulation of NTCP is absent despite retention of BAs.35 In a recent study, Wanninger et al.36 observed an up-regulation of hepatic CYP7A1 mRNA expression, in line with elevated serum triglyceride levels in adiponectin knockout

mice. We also observed lower adiponectin levels with advanced stages Ketotifen of NAFLD and our in vitro data also confirm a negative regulation of Cyp7A1 by adiponectin. As Aranha et al.6 have shown, BAs within the liver are elevated in patients with steatohepatitis. In agreement with our data, this would suggest an increased BA uptake and production. Elevated intrahepatic BA amounts would lead to activation of FXR and subsequently enhanced BSEP expression, which we also observed.29 On the other hand, impaired adaptation of BSEP expression may lead to increased BA accumulation in hepatocytes and enhanced cell death. Interestingly, steatotic hepatocytes were shown to be more susceptible to BA-induced apoptosis.37 Even low elevations of BAs normally not considered harmful could enhance hepatocyte apoptosis in patients with NAFLD. However, in our in vitro studies we did not observe alterations in viability upon FFA and CDCA cotreatment. An altered intestinal FGF19 production and/or altered hepatic responsiveness to FGF19 may accordingly contribute to the dysregulation of BA homeostasis observed in our patients with NAFLD, as has previously been shown that a rather moderate increase in BA flux may superimpose an influence of FGF15.

A precontrast computed tomography scan showed a diffusely hyperdense liver and a large amount of ascites (Panel A). Transjugular liver biopsy demonstrated cirrhosis with polymorphonuclear infiltrate, Mallory bodies (arrows), and ballooning degeneration (arrowheads) (Panel B). Electron microscopy showed lysosomal myeloid bodies with dense deposits

(asterisks) within hepatocytes (Panel C). On the basis of clinical history and histologic findings, amiodarone-induced liver cirrhosis was diagnosed, and the drug was replaced with another antiarrhythmic agent (propafenone). He was discharged with improved general condition with marked reduction of ascites. Although asymptomatic elevations of aminotransferases have been reported in up to 25% of the patients

treated with long-term amiodarone therapy, symptomatic liver dysfunction has been reported to occur in fewer than 1% of these patients.1, 2 However, amiodarone-induced Selleck PLX3397 hepatitis can progress to cirrhosis, resulting in decompensated hepatic failure, although this rarely happens.1, 2 Amiodarone is one of the cationic amphiphilic drugs (CADs) that can cause phospholipidosis in liver.3 In this case, the findings demonstrating intralysosomal myelin figures and electron-dense material on electron microscopy are compatible with the findings of CAD-induced phospholipidosis.4 However, the functional consequences of phospholipidosis on cellular or tissue function have not been well explained. Rather, liver damage is considered to be caused by amiodarone-induced find more inhibition of mitochondrial β-oxidation.5 “
“We read with great interest the article by Lange and coworkers.1 It is known that mitochondrial toxicity related to the nucleoside analogues can result in macrovesical hepatic steatosis and lactic acidosis. In vivo, these results were shown as side effects of long-term lamivudine use in patients with human immunodeficiency virus (HIV).2 It was noted that the amount of mitochondrial DNA

defects is a predictive marker for the clinical expression of mitochondrial toxicity.2 In case of the severity of the underlying liver dysfunction due to cirrhosis, or acute exacerbation of chronic liver disease, the function of mitochondria in hepatocytes declines immediately. In light of these data, severe mitochondrial 4-Aminobutyrate aminotransferase dysfunction leading to lactic acidosis can be aggravated by nucleoside analogues in patients with an underlying disease, as discussed above. Moreover, hepatic steatosis may be an additional risk factor for these patients with hyperlactatemia who are using entecavir. Obesity was reported as a possible risk factor for mitochondrial toxicity in patients with HIV who are undergoing highly active antiretroviral therapy.3 So, in spite of the small numbers of patients with lactic acidosis under entecavir, we worry about the effect of body mass index on treatment toxicity. Akif Altınbas MD*, Fuat Ekiz MD*, Osman Yuksel MD, Assoc. Prof.

Angiotenzyn – II (AT-II), produced by angiotenzin converting enzyme (ACE), has important role in liver fibrogenesis. Dual antiviral therapy with PEG-IFN and ribavirin beside antiviral effect, leads to the reduction of liver parenchyma fibrosis. Aim: To determine ACE value in serum of

patients with chronic hepatitis C before and after dual antiviral therapy, as well as reduction of liver fibrosis in liver tissue before and after the antiviral www.selleckchem.com/products/crenolanib-cp-868596.html treatment Methods: We analysed 50 patients treated at Gastroenterohepatology Department, in the period of four years. Patient were treated with pegylated interferon alfa 2a or 2b and ribavirin with treatment duration depending on genotype. Value of ACE in serum, was determined by Olympus AU 400 device, with application of kit “Infinity TN ACE Liquid Stable Reagent.” HCV RNA levels in sera

were measured by real time PCR. HCV RNA test was performed with Napabucasin concentration modular analysis AMPLICOR and COBAS AMPLICOR HCV MONITOR test v2.0, which has proved infection and was used for monitoring of the patients respond to the therapy. Liver histology was evaluated in accordance to the level of necroinflammation activity and stadium of fibrosis. Results: Antiviral therapy in chronic hepatitis C statistically decreases serum activities of ACE (p = 0,02) with indirect affects on the fibrogenesis of the liver parenchyma. Among the patients who accepted repeated biopsy after the treatment (35% of total number), 60% had a regression in fibrosis stage. Conclusion: Our results suggested that serum activity of the ACE is valuable indirect parameter of the liver damage, and can be used as a marker of non invasive assessment of intensity of liver damage. Antifibrotic effect of antiviral therapy was also proven by quantification of changes

in liver tissue. Key Word(s): 1. angiotenzin converting enzyme; 2. antiviral therapy; 3. chronic hepatitis C Presenting Author: ILHAMD Additional Authors: ADLIN Chloroambucil HERY, MASRUL LUBIS, LUKMAN HAKIM ZAIN Corresponding Author: ILHAMD Affiliations: University of Sumatera Utara, University of Sumatera Utara, University of Sumatera Utara Objective: Over the past 40 years, endoscopy has been used with increasing frequency in the investigation of upper gastrointestinal symptoms. Upper gastrointestinal endoscopy is currently the main diagnostic modality in the work-up of dyspeptic patients. Despite most dyspeptic patient either have no identifiable cause of dyspepsia (non-ulcer dyspepsia, NUD), performing endoscopy in patients with dyspepsia is to detect underlying ulcer disease, gastric cancer or pancreatic disease. The aim of this study was to establish the etiology of dyspeptic symptoms on upper endoscopic investigation.

MAIN OUTCOME MEASURE: Mortality from all causes, cardiovascular disease, cancer, and liver disease (up to 18 years of follow-up). RESULTS: The prevalence of non-alcoholic fatty liver disease with and without increased levels of liver

enzymes in the population was 3.1% and 16.4%, respectively. Compared with participants without steatosis, selleck products those with non-alcoholic fatty liver disease but normal liver enzyme levels had multivariate adjusted hazard ratios for deaths from all causes of 0.92 (95% confidence interval 0.78 to 1.09), from cardiovascular disease of 0.86 (0.67 to 1.12), from cancer of 0.92 (0.67 to 1.27), and from liver disease of 0.64 (0.12 to 3.59). Compared with participants without steatosis, those with non-alcoholic fatty liver disease and increased liver enzyme levels had adjusted hazard ratios for deaths from all causes of 0.80 (0.52 to 1.22), from cardiovascular disease of 0.59 (0.29 to 1.20), from cancer of 0.53 (0.26 to 1.10), and from liver disease of 1.17 (0.15 to 8.93). CONCLUSIONS: Non-alcoholic fatty liver disease was not associated with an increased risk of death from all causes, cardiovascular Trametinib nmr disease, cancer, or liver disease. Charlton MR, Burns JM, Pedersen RA, Watt KD, Heimbach JK, Dierkhising RA. Frequency and outcomes of liver transplantation for nonalcoholic steatohepatitis in the United

States. Gastroenterology 2011;141:1249-1253. (Reprinted with permission.) BACKGROUND & AIMS: The relative frequency of nonalcoholic steatohepatitis (NASH) as an indication for liver transplantation and comparative outcomes following transplantation are poorly Methane monooxygenase understood. METHODS: We analyzed the Scientific Registry of Transplant Recipients for primary adult liver transplant recipients from 2001 to 2009. RESULTS: From 2001 to 2009, 35,781 patients underwent a primary liver transplant, including 1959 for who NASH was the primary or secondary indication. The percentage of patients undergoing a liver transplant for NASH increased from 1.2% in 2001 to 9.7% in 2009.

NASH is now the third most common indication for liver transplantation in the United States. No other indication for liver transplantation increased in frequency during the study period. Compared with other indications for liver transplantation, recipients with NASH are older (58.5±8.0 vs 53.0±8.9 years; P<.001), have a larger body mass index (>30 kg/m2) (63% vs 32%; P<.001), are more likely to be female (47% vs 29%; P<.001), and have a lower frequency of hepatocellular carcinoma (12% vs 19%; P<.001). Survival at 1 and 3 years after liver transplantation for NASH was 84% and 78%, respectively, compared with 87% and 78% for other indications (P=.67). Patient and graft survival for liver recipients with NASH were similar to values for other indications after adjusting for level of creatinine, sex, age, and body mass index.

The success of the procedure and the complete removal of lithiasis in this first study were: in group A 97.1% and 70% , in group B 100% and 86.4%, respectively, without significant differences. Seven or ten Fr plastic stent was placed in group A 30.4% and group B 18.2%, without selleck compound significant differences. Comparing only the giants stones was noted that the successful stones extraction in the first ERCP was in group A 58.6% and group B 89.3% (p = 0.019). The use of mechanical lithotripsy in group A was 44.8% and in

group B 21.4%, without significant difference. With respect to complications in group A was 5.8% (1 perforation, 2 cholangitis and 1 binding of basket) and in group B was 6.8% (2 mild pancreatitis, 1 cholangitis). There was no death in both groups following the ERCP. Conclusion: The combination of sphincterotomy and large volumes balloon dilation in the treatment of difficult stones is equally effective and safe as in sphincterotomy alone. The combination therapy was

more effective in the management of giant stone. Key Word(s): 1. choledocholithiasis; Presenting Author: HUIJER HWANG Additional Authors: RAUL MATANO, MARTIN GUIDI, JULIO DE MARIA, ESTEBAN PROMENZIO, FERNANDO ALK inhibitor RAGONE, JUAN VISCARDI Corresponding Author: HUIJER HWANG Affiliations: El Cruce Hospital Objective: Hiliar tumors (HT) are neoplasms with a poor prognosis and most patients die within a year of diagnosis. While surgery is the standard for curative treatment, in most cases the

PAK5 goal is palliative treatment. Endoscopic biliary drainage (EBD) and percutaneous biliary drainage (PBD) are two minimally effective invasive techniques. It is not known with certainty what is the approach of choice. Several studies have shown that EBD can be difficult in Bismuth III and IV tumors because of the high risk of post-procedure cholangitis. Aim: To report the effectiveness and complications of EBD and PBD in the palliative management of HT. Methods: Descriptive observational retrospective analysis of the management of HT in a Trainning Center of ERCP, from October 2008 to March 2012. We analyzed the following variables in the groups treated with EBD and PBD: rate of effective drain, reintervention rate, survival, complications and death associated with the procedure. Results: We included in EBD group: 40 patients and 52 procedures and in PBD group: 22 patients and 28 interventions. The final success in the first group was 85% and the second 90.9% (p = 0.788). Five patients (4 HT Bismuth IV) required combined approach. The global rate of success was 95.16%. Twelve patients of EBD group were Bismuth IV, whose effectiveness was 58.3%. Meanwhile, 11 patients of PBD group were Bismuth IV, whose effectiveness was 81.8% (p = 0.442). Overall survival in EBD group was 7.9 months, while in PBD group was 4.8 months. With respect to complications in the EBD group was 11.

The success of the procedure and the complete removal of lithiasis in this first study were: in group A 97.1% and 70% , in group B 100% and 86.4%, respectively, without significant differences. Seven or ten Fr plastic stent was placed in group A 30.4% and group B 18.2%, without ABT-888 in vivo significant differences. Comparing only the giants stones was noted that the successful stones extraction in the first ERCP was in group A 58.6% and group B 89.3% (p = 0.019). The use of mechanical lithotripsy in group A was 44.8% and in

group B 21.4%, without significant difference. With respect to complications in group A was 5.8% (1 perforation, 2 cholangitis and 1 binding of basket) and in group B was 6.8% (2 mild pancreatitis, 1 cholangitis). There was no death in both groups following the ERCP. Conclusion: The combination of sphincterotomy and large volumes balloon dilation in the treatment of difficult stones is equally effective and safe as in sphincterotomy alone. The combination therapy was

more effective in the management of giant stone. Key Word(s): 1. choledocholithiasis; Presenting Author: HUIJER HWANG Additional Authors: RAUL MATANO, MARTIN GUIDI, JULIO DE MARIA, ESTEBAN PROMENZIO, FERNANDO Bortezomib RAGONE, JUAN VISCARDI Corresponding Author: HUIJER HWANG Affiliations: El Cruce Hospital Objective: Hiliar tumors (HT) are neoplasms with a poor prognosis and most patients die within a year of diagnosis. While surgery is the standard for curative treatment, in most cases the

Phosphoprotein phosphatase goal is palliative treatment. Endoscopic biliary drainage (EBD) and percutaneous biliary drainage (PBD) are two minimally effective invasive techniques. It is not known with certainty what is the approach of choice. Several studies have shown that EBD can be difficult in Bismuth III and IV tumors because of the high risk of post-procedure cholangitis. Aim: To report the effectiveness and complications of EBD and PBD in the palliative management of HT. Methods: Descriptive observational retrospective analysis of the management of HT in a Trainning Center of ERCP, from October 2008 to March 2012. We analyzed the following variables in the groups treated with EBD and PBD: rate of effective drain, reintervention rate, survival, complications and death associated with the procedure. Results: We included in EBD group: 40 patients and 52 procedures and in PBD group: 22 patients and 28 interventions. The final success in the first group was 85% and the second 90.9% (p = 0.788). Five patients (4 HT Bismuth IV) required combined approach. The global rate of success was 95.16%. Twelve patients of EBD group were Bismuth IV, whose effectiveness was 58.3%. Meanwhile, 11 patients of PBD group were Bismuth IV, whose effectiveness was 81.8% (p = 0.442). Overall survival in EBD group was 7.9 months, while in PBD group was 4.8 months. With respect to complications in the EBD group was 11.