We describe the prevalence of diabetes and the parameters indicat

We describe the prevalence of diabetes and the parameters indicative of an adequate diabetes care according the recommended international standards. RESULTS: 147 (47%) out of the 312 patients were patients with diagnosis of diabetes.There were no differences between the

DM (n=147) and non-DM group (n=165) with respect to arterial hypertension (62% vs 53%) and chronic renal failure (14%vs18%) prevalences. Dyslip-idemia (44%DM-group vs 21% selleck products no-DM group,p=<0.01) and cardiovascular disease (20% vs 9%,p=0.03) occurred more frequently in the DM-group. 69% of diabetic patients were obese/ overweight and 85% had abdominal obesity. With regards to diabetic care based on accepted international standards, it included drug therapy (insulin in 54%, oral antidiabetic

drugs in 39.5%), exercise (moderate in 33%), diabetic diet (62)%, and diabetic management education (40%). However, hemoglobin A1c levels were adequately controlled in only 27% of patients. A free diet was followed by 36% of the patients, and a sedentary life and/ or light Daporinad in vitro physical exercise was practised by 65%. Moreover, screening for complications of diabetes had never been performed in 50% of patients in terms of ret-inopathy, nephropathy and cardiovascular disease., and less than 10% had been screened for neuropathy and diabetic foot. CONCLUSIONS: 1.Prevalence of diabetes and common diabetes-associated conditions in LTR are high;2.Control of DM in LTR is poor,with low control of risk factors associated withD-M,a poor screening of DM complications and poor glycemic control;3.Treatment is focused on the use of antidiabetic drugs disregarding other treatments,such as exercise and diet;4.The role of the LT team is important to improve control of DM but ultimately a multidisciplinary approach is required. Disclosures:

José Ignacio Herrero – Speaking and Teaching: Roche, Astellas, Novartis; Stock Shareholder: Roche, Novartis, Abbott, GlaxoSmitthKline Martin Prieto – Advisory Committees or Review Panels: Bristol, Gilead The following people have PAK5 nothing to disclose: Beatriz Rodríguez-Medina, Diego Alvarez de Sotomayor, Carla Satorres, Trinidad Serrano, Manuel De la Mata, Carmen Vinaixa, Victoria Aguilera, Angel Rubin, Marina Berenguer BACKGROUND: Over the past decade, cardiovascular disease has emerged as a major cause of long-term complications after liver transplantation (LT). However, little is known about early major adverse cardiac events (MACE) following transplant. AIM: To determine the cumulative risk and predictive factors for early (30-day and 1-year) MACE after LT. METHODS: We identified all adult recipients of a first LT at our institution from 2/2002-12/2012.

7 Although β-catenin itself does not bind DNA, it can interact

7 Although β-catenin itself does not bind DNA, it can interact

with other transcription factors (especially the more studied T-cell factor/lymphoid enhancer factor [TCF/LEF] family of transcription factors) to induce www.selleckchem.com/products/chir-99021-ct99021-hcl.html target gene expression. Feng et al. have recently linked the β-catenin and AR pathways in a feed-forward loop through CCRK in HCC. 6 In an effort to identify AR-dependent mechanisms and thus address the male predominance of HCC, Feng and colleagues took advantage of chromatin immunoprecipitation (ChIP)-chip analysis and identified CCRK as a direct target of AR in two androgen-expressing HCC cell lines—Huh7 and PLC5. In fact, 212 target genes that were common between the two cell lines were identified; 21 of these 212 genes were cell cycle regulators, and CCRK was identified as having the highest binding affinity to AR. Through multiple means it was shown that AR strongly

bound and transactivated Tyrosine Kinase Inhibitor Library price the CCRK promoter. AR knockdown diminished the CCRK promoter activity, and, conversely, the AR agonist R1881 induced AR binding and transactivation of the CCRK reporter; additional validation was provided through site-directed mutagenesis. The same authors also transfected the AR gene in two cell lines with low endogenous AR (SK-Hep1 and LO2) and identified a significant increase in CCRK expression, which was also substantiated by immunofluorescence (IF). The authors then proceeded to determine the functional relevance of CCRK expression control by the AR. Whereas AR stimulation led to cell cycle progression, CCRK down-regulation under such circumstances abrogated tumor cell proliferation. Conversely, ectopic expression of CCRK was able to significantly reverse proliferation and cell cycle arrest following AR inhibition. A similar relationship was also evident

in focus assays and anchorage-independent soft agar assays and further corroborated a direct relationship between http://www.selleck.co.jp/products/Metformin-hydrochloride(Glucophage).html AR and CCRK in promoting cellular proliferation and transformation. To further test the biological relevance of these findings in vivo, the authors demonstrated that injection of PLC5 hepatoma cells expressing shRNA to CCRK led to significantly diminished tumor formation compared to the controls in tumor xenograft studies. Conversely, stably transfected LO2 cells expressing CCRK displayed incredible tumor growth, with 20-fold mean tumor volumes compared with empty vector controls. These results undoubtedly demonstrate the oncogenic properties of CCRK.


Thirty-four strains had single nucleotide mutat


Thirty-four strains had single nucleotide mutations in dupA that lead to premature stop codon creating smaller products than the predicted 1839 bp product and, for this reason, were considered as dupA-negative. Intact dupA was more frequently observed in strains isolated from duodenal ulcer patients (65.5%) than in patients with gastritis only (46.2%) or with gastric carcinoma (50%). In logistic analysis, the presence of the intact dupA independently associated with duodenal ulcer (OR = 5.06; 95% CI = 1.22–20.96, p = .02). Conclusion:  We propose the primer walking methodology as a simple technique to sequence the gene. When we considered as dupA-positive only those strains that carry dupA gene without premature stop codons, the gene was associated with duodenal buy Sorafenib ulcer ERK inhibitor and, therefore, can be used as a marker for this disease in our population. “
“Chronic infection with Helicobacter pylori (H. pylori) is causally linked with gastric carcinogenesis. Virulent H. pylori strains deliver bacterial CagA into gastric epithelial cells. Induction of high motility and an elongated phenotype is considered to be CagA-dependent process. Casein kinase 2 plays a critical role in carcinogenesis through signaling pathways related to the epithelial mesenchymal transition. This study was

aimed to investigate the effect of H. pylori infection on the casein kinase 2-mediated migration and invasion in gastric epithelial cells. AGS or MKN28 cells as human gastric epithelial cells and H. pylori strains Hp60190 (ATCC 49503, CagA+) and Hp8822 (CagA−) were used. Cells were infected with H. pylori at multiplicity of infection of 100 : 1 for various times. We measured in vitro kinase assay to examine casein kinase 2 activity and performed immunofluorescent

staining to observe E-cadherin complex. We also examined β-catenin transactivation through promoter assay and MMP7 expression by real-time PCR and ELISA. H. pylori upregulates casein kinase 2 activity and inhibition of casein kinase 2 in H. pylori-infected cells profoundly suppressed cell invasiveness and motility. We confirmed that casein kinase 2 mediates membranous α-catenin depletion through dissociation of the α-/β-catenin complex in H. pylori-infected cells. We also found that H. pylori Florfenicol induces β-catenin nuclear translocation and increases MMP7 expressions mediated through casein kinase 2. We show for the first time that CagA+ H. pylori upregulates cellular invasiveness and motility through casein kinase 2. The demonstration of a mechanistic interplay between H. pylori and casein kinase 2 provides important insights into the role of CagA+ H. pylori in the gastric cancer invasion and metastasis. “
“Background:  Novel helicobacter infections and associated disease are being recognized with increasing frequency in animals and people. Yet, the pervasiveness of infection in distantly related animal taxa, genetic diversity of helicobacters, and their transmissability are not known.

Additional Supporting Information may be found in the online vers

Additional Supporting Information may be found in the online version of this article. DAPT price
“Mass screening with abdominal ultrasonography (AUS) has been suggested as a tool to control adult hepatocellular carcinoma (HCC) in individuals, but its efficacy in reducing HCC mortality has never been demonstrated. This study aimed to assess the effectiveness

of reducing HCC mortality by mass AUS screening for HCC based on a program designed and implemented in the Changhua Community-based Integrated Screening (CHCIS) program with an efficient invitation scheme guided by the risk score. We invited 11,114 (27.0%) of 41,219 eligible Taiwanese subjects between 45 and 69 years of age who resided in an HCC high-incidence area to attend a risk score-guided mass AUS screening between HDAC inhibition 2008 and 2010. The efficacy of reducing HCC mortality

was estimated. Of the 8,962 AUS screening attendees (with an 80.6% attendance rate), a total of 16 confirmed HCC cases were identified through community-based ultrasonography screening. Among the 16 screen-detected HCC cases, only two died from HCC, indicating a favorable survival. The cumulative mortality due to HCC (per 100,000) was considerably lower in the invited AUS group (17.26) compared with the uninvited AUS group (42.87) and the historical control group (47.51), yielding age- and gender-adjusted relative mortality rates of 0.69 (95% confidence interval [CI]: 0.56-0.84) and 0.63 (95% CI: 0.52-0.77), respectively. Conclusion: The residents invited to community-based AUS screening for HCC, compared with those who were not invited, showed a reduction in HCC mortality by ∼31% among subjects aged 45-69 years who had not been included in the nationwide vaccination program against hepatitis B virus PAK6 infection. (Hepatology 2014;59:1840–1849) “
“Background:  Autofluorescence (AF) videoendoscopy has an advantage over ordinary videoendoscopy in the diagnosis

of gastric neoplasias, and the aim of the present study was to evaluate the effectiveness of using the SAFE-3000 videoendoscopy system to diagnose superficial gastric neoplasias. Methods:  Ordinary videoendoscopy, AF videoendoscopy, and chromoendoscopy (CE) were used to diagnose the tumor existence and extent in 14 patients with gastric adenoma, 40 patients with intestinal-type early gastric cancer (EGC) (10 protruded, and 30 depressed), and nine patients with diffuse-type EGC. The diagnostic accuracies of the three kinds of images were evaluated by comparison with the results of histopathological assessment of resected specimens. Results:  For gastric adenomas the diagnostic accuracy between the AF images and white light (WL) images did not differ significantly, and for protruded intestinal-type EGCs and diffuse-type EGCs the diagnostic accuracy did not differ significantly between any of the types of images.

Expression levels of established LXRα target genes,


Expression levels of established LXRα target genes,

however, were unaffected in sequestrant-treated lean and db/db mice, suggestive of unchanged LXRα signaling. Yet, investigation in sequestrant-treated Lxrα−/− mice revealed that lipogenic gene expression was not increased in these mice compared with untreated wild-type littermates. Our results from colesevelam-treated Fxr−/− and Lxrα−/− mice confirm earlier findings that FXR and LXRα are both involved in regulation of bile salt–mediated changes in lipogenic pathways.17 The exact molecular mechanisms through which these nuclear receptors signal regulate the lipogenic response to bile salt sequestration exceed the scope of this report. At a physiological level, bile salt–mediated signaling pathways are dependent on the concentration of bile salts see more in the liver acinus. We speculate Doxorubicin ic50 that the concept of metabolic zonation43 might

add to the understanding of the observed hepatic effects upon bile salt sequestration. Hepatocytes localized around the portal vein display different metabolic activities than those lining the central vein; for example, bile salt and fat synthesis are pericentrally localized processes, whereas cholesterol synthesis is performed mainly by portal hepatocytes.43 As we show in the current report, the amount of bile salt molecules reabsorbed in the ilea of colesevelam-treated mice was decreased by ≈30% with a subsequent reduction in plasma bile salt levels and, hence, reduced bile salt signaling in periportal hepatocytes. Newly synthesized bile salts, which accommodate a much larger fraction of the bile salt pool of colesevelam-treated mice compared with controls, are primarily secreted by pericentrally localized cells and possibly exert differential signaling functions.

Selective periportal fat accumulation and differentially affected expression levels of hepatic FXR target genes support this hypothesis. Additionally, it was shown that Cyp7a1, which is exclusively expressed in pericentral hepatocytes,44 translocates to a larger area of the liver lobulus with more involvement of periportally localized cells in sequestrant-treated rats.45 Our working model is summarized in Supporting Fig. 5. It should be stressed that this hypothesis requires dedicated investigation. In conclusion, we show that colesevelam about treatment increases lipogenesis and chain elongation in mice that, at least at the level of gene expression, is dependent on FXR and LXRα. A shift from reabsorption to de novo synthesis as the source of biliary bile salts affects the sinusoidal gradient of bile salts.46 This shift modifies the regulation of genes and proteins involved in bile salt synthesis and bile salt–mediated regulation of metabolism and possibly underlies the phenotypical response to colesevelam treatment in mice. We are indebted to Rick Havinga for excellent contributions to the mouse studies performed.

Conclusions: Gastric varices are a noteworthy issue in patients w

Conclusions: Gastric varices are a noteworthy issue in patients with portal hypertension, primarily due to the associated risk of bleeding, which occurred in 20% of our patients. Although not significantly linked to a fatal outcome, patients with IGV-1 or large varices and those without portal hypertensive gastropathy or NSBB appear to have an increased risk of bleeding. In these circumstances, primary

prophylaxis should be considered, and the use of NSBB seems to be a suitable option. Disclosures: The following people have nothing to disclose: Tiago Curdia Goncalves, Joana Magalhaes, Carla M. Marinho, Jose Cotter Purpose: Liberal use of blood products to correct coagulopathy prior

to invasive procedures in patients with cirrhosis is a common practice, but evidence increasingly supports learn more a restrictive transfusion strategy for blood products in a variety of clinical scenarios, prompting this systematic review. Methods: Using a pre-established search engine, two reviewers independently evaluated and retrieved papers in EMBASE, PUBMED RG-7388 and reference lists, with no date or language restriction until December 2013. Only reports with cirrhotic patients undergoing elective minor procedures including data on bleeding complications were included. Papers on major surgeries were excluded. Results 3,972 abstracts were reviewed, of which 12 met the inclusion criteria. Four studies (4 case series) evaluated upper endoscopy (EGD), colonoscopy, and Orotic acid transesophageal echocardiography (TEE). Data from these studies are shown in the TABLE. Four studies (3 case series and 1 randomized controlled trial (RCT)) evaluated liver biopsy and found overall low rates of bleeding often without correction of coagulopathy, though the study of mini-laparascopic biopsy found bleeding

requiring hemostasis in 60% of cirrhotics. Three studies (2 RCTs and one case series) examined dental procedures and found bleeding in <6% of patients in the two RCTs (both in groups receiving and not receiving blood products) and in 23% in the case series. Finally, a RCT using eltrombopag vs placebo in cir-rhotics with platelets <50K followed by a supplemental platelet transfusion if needed prior to invasive procedures found bleeding complications in 17% of the eltrombopag group vs 23% of the placebo group (95% CI -15 to 3). Conclusion: Most of the evidence for correction of coagulopathy in cirrhotic patients comes from case series. Overall the data suggest that bleeding complications are infrequent. Given the potential complications of the over-transfusion of blood products, further RCTs or high-quality observational studies are needed to determine the best transfusion strategy in cirrhotic patients undergoing invasive procedures. TABLE.

“Journal of Zoology is pleased to introduce the first Thom

“Journal of Zoology is pleased to introduce the first Thomas Henry Huxley Review, which aims to celebrate Huxley’s outstanding contributions to zoological research and, in particular, his research on comparative anatomy, physiology and evolutionary biology. Indeed, between 1861 and 1880, Huxley published many of these papers in the Proceedings and Transactions of the Zoological Society London, which merged in 1965 to form the Journal of Zoology. As well as conducting his own research, Huxley was dedicated to improving the understanding and acceptance of the theory of evolution by the scientific community and the wider public. Renowned for his

exploration of the philosophical issues in science, Huxley both advanced the status of scientific research and founded a generation of researchers whose discoveries remain relevant and inspiring Navitoclax datasheet today. In accordance with Huxley’s many achievements in the field of zoology, the Thomas Henry Huxley Review will examine our current understanding of a selected zoological theme, and suggest

and inspire research that will improve our knowledge in the future. The journal annually invites a distinguished researcher who has made a major contribution to zoological science to write the review. The first paper in this series, ‘How stupid not to have thought of that: RG-7388 clinical trial post-copulatory sexual selection’, is written by Tim Birkhead and provides a historical and contemporary account of an area of biology Darwin largely ignored, post-copulatory sexual selection. Professor of Behaviour and Evolution at the University of Glycogen branching enzyme Sheffield, Tim is dedicated to expanding the minds of undergraduates through his lectures on animal behaviour and the history and philosophy of science. Tim currently serves on the management committee of the Darwin Correspondence Project and has been President of the International Society for Behavioural Ecology. In addition to his passion for research, Tim is committed to advancing the public understanding of science, particularly

through his articles. He has written for New Scientist, BBC Wildlife, Natural History magazine and The Independent and has a regular column in the Times Higher Education. Tim’s outstanding career was further acknowledged when he was elected to a Fellowship of the Royal Society. Given Tim’s extensive research on promiscuity and sperm competition in birds and his flair for writing, he provides an eloquent account of our current understanding of post-copulatory sexual selection as well as an overview of how we have eventually arrived at this current explanation for some of the more unusual phenomena in the biological world. We hope you enjoy reading the first Thomas Henry Huxley Review.

The data were log or square root-transformed to meet the assumpti

The data were log or square root-transformed to meet the assumptions of homogeneity and normality. All response variables were affected by at least two of the factors tested. The rate of algal growth, Pnmax, dark-adapted Fv/Fm, and Rdark tended to be at their lowest values in August, and were mostly governed by the interaction of Time (August vs. November) and Scenario. Growth was enhanced by the PI treatment in November, and slightly reduced

in August in response to the A1FI treatment (three-way factorial ANOVAs, F(3,32) = 6, P < 0.002; post hoc: November-PI > Other, August-A1FI < November-PD, Fig. 1). CX-4945 The average values for temperature and pCO2 were 26.2° ± 0.9°C (mean ± SD) and 990 ± 175, respectively, under LY2109761 August-A1FI treatments, and 24.4° ± 0.9°C and 345 ± 47, respectively, under November-PI treatments (Table 1). Weekly growth rates, calculated as an average between August and November experiments, decreased with increasing temperature and acidification

offsets, and was lowest under A1FI treatment (+4.0°C, +681 μatm) and highest under the PI treatment (−1°C, −100 μatm). The mean dark-adapted Fv/Fm showed a significant temporal effect and an interaction between Time × Scenario (Fig. 2; Table 2). This interaction (three-way factorial ANOVA, F(3,32) = 4, P = 0.02) led to significantly elevated dark-adapted Fv/Fm in November PI grown algae compared to either August-PI or August-A1FI grown algae (Fig. 2). Pnmax (μmol · h−1 · gfw−1) was governed by Scenario (Fig. 2, three-way factorial ANOVA, F(3,32) = 5.3, P = 0.004; Table 2). Pnmax was greatest under A1FI, having significantly higher values than those obtained under PD and PI scenarios. The response of algal Rdark (μmol · h−1 · gfw−1) was dominated by a three-way

Isotretinoin interaction (Fig. 2, three-way factorial ANOVA, F(3,32) = 4.2, P = 0.01; Table 2). As a main effect, algae grown under the November-A1FI scenario had significantly higher dark respiration rates than algae grown under November-PI and November-PD scenarios (two-way factorial ANOVA, F(3,16) = 5.2, P = 0.01; Table 2). However, a weak interaction between Nutrients and Scenario led to increased respiration under A1FI ambient nutrients compared with the nutrient enriched PI and ambient nutrient PD thalli (two-way factorial ANOVA, F(3,16) = 3.5, P = 0.04; Table 2). In August, an interaction between Scenario and Nutrients led to opposing effects. This interaction had a tendency to lead to reduced Rdark under ambient nutrients combined with PD or PI scenarios, but nutrient enrichment increased Rdark under these same scenarios. Under B1 and A1FI scenarios, nutrient enrichment led to lower respiration rates, while Rdark was increased under ambient nutrients. Pigments showed complex responses to the different treatments (Fig. 3; Table 3). Pigment responses were governed by interactions amongst the factors.

As shown in Fig 4A, we observed robust up-regulation of the BH3-

As shown in Fig. 4A, we observed robust up-regulation of the BH3-only protein, Bnip3, by GANT61 in all three HCC cell lines; the expression of other Bcl-2 family proteins (including Bim, Noxa, Puma, Bcl2, and Bclxl) were not significantly affected, although the level of Mcl-1 was NSC 683864 mouse slightly reduced in two of the three HCC cell lines. GANT61 induced a 4.39-fold, 2.84-fold, and 1.97-fold increase in Bnip3 mRNA level in Huh7, Hep3B, and HepG2 cells, respectively, as determined by qRT-PCR (Fig. 4B). The effect of GANT61 on Bnip3 expression was dose-dependent (at 24- and 48-hour timepoints) (Fig. 4C). The role of Bnip3 in GANT61-induced autophagy was supported by the observations that siRNA knockdown

of Bnip3 prevented GANT61-induced LC3II accumulation (Fig. 4D, left panel) and that overexpression of Bnip3 enhanced GANT61-induced LC3II accumulation (Fig. 4D, right panel) and reversed SAG-induced LC3II reduction (Fig. 4E). We sought to further investigate the mechanism by which Hh signaling regulates Bnip3. As the Bnip3 promoter does not contain the Gli consensus DNA-binding sequences, it is likely that Hh signaling might regulate Bnip3 through an indirect mechanism. Given that Bnip3 is a downstream target of the MEK/ERK signaling pathway[11, 12]

and that Hh and MEK/ERK signaling pathways are known to interconnect in other cells,[13-15] we performed experiments http://www.selleckchem.com/products/ulixertinib-bvd-523-vrt752271.html to determine whether inhibition of Hh by GANT61 might induce Bnip3 expression by way of activation of MEK/ERK. As shown in Fig. 4F, GANT61 treatment increased the phosphorylation of MEK and ERK1/2

(but did not below affect the levels of total MEK and ERK1/2). We observed that inhibition of MEK by U0126 prevented GANT61-induced phosphorylation of ERK1/2, expression of Bnip3, and accumulation of LC3II (Fig. 4G). These findings suggest that GANT61-induced Bnip3 expression is mediated at least in part through activation of the MEK/ERK pathway. Although Bnip expression is known to be regulated by nuclear factor kappa B (NF-κB),[16] p53,[17] and DNA methyltransferase-1 (DNMT-1),[18] these molecules were not altered by GANT61 treatment in our system (Supporting Fig. S3). Beclin-1, the mammalian ortholog of yeast Atg6, is a well-known key regulator of autophagy; it is a critical component of the class III phosphatidylinositol-3-kinase complex (PI3KC3) required for autophagy. The overall structure of Beclin-1/Atg6 and its essential role in autophagosome formation is evolutionarily conserved throughout all eukaryotic phyla. Whereas Beclin-1 expression promotes autophagy, Beclin-1 reduction decreases autophagic activity.[19] Sequence alignment and structural modeling indicate that Beclin-1 contains a putative BH3-like domain (amino acids 112-123), which is known as a novel BH-3 domain only protein.[20] The BH-3 domain of Beclin-1 interacts with Bcl-2, which leads to inhibition of autophagy.

At the end of treatment, we found a significant expansion of the

At the end of treatment, we found a significant expansion of the total serum bile acid pool and marked UDCA and LCA enrichment in the UDCA-treated patients versus the placebo group when pretreatment levels were compared. Additionally, we found that the increases in serum bile acid levels seemed to correlate with worse outcomes because the subset of patients that reached the clinical endpoints of disease progression during UDCA therapy tended to have higher bile acid levels. The proposed UDCA mechanisms of action in hepatobiliary disorders include expansion of

the hydrophilic bile acid pool and hypercholeresis.16 Early studies in gallstone patients showed that UDCA administration this website could modify the composition of circulating bile acids and lead to UDCA predominance.17, 18 Multiple subsequent studies, most of them in patients with primary biliary cirrhosis, Selleck GSK1120212 have verified this modification and have generally revealed an overall expansion

of the total bile acid pool.8, 9, 13, 14, 19-22 Rost et al.13 in a study of biliary bile acid composition in patients with PSC specifically indicated that UDCA enrichment was augmented (43.1% ± 0.3% to 58.6% ± 2.3% of total bile acids) parallel to an escalating dose of UDCA (10-13 to 22-25 mg/kg/day) and reached a plateau at the highest dose. This enrichment did not further increase beyond that dose.13 In our study, the mean changes in UDCA and total bile acid levels post-treatment were significantly higher in the UDCA group compared to the placebo group (P < 0.0001). The mean posttreatment UDCA percentage in the bile acid pool was 74%, far higher than that ever reported in any other study, and

this implies that enrichment is increased proportionally to the dose. Nonetheless, this high enrichment did not correspond to a better outcome. Therefore, further investigation of biliary enrichment has to be performed, especially with respect to clinical outcome. Changes in the levels of other bile acids under UDCA treatment have been generally considered to follow an inverse relationship between the increase in UDCA levels also and the decrease in CA, CDCA, DCA, and LCA levels. Results, however, are not homogeneous, and the changes are not significant in the majority of cases.13, 21, 22 In PSC patients, one study has suggested that LCA levels are not increased, even after high-dose UDCA treatment.13 Nonetheless, the antibiotics administrated in that study during the endoscopic retrograde cholangiography procedure used to obtain samples for bile acid analysis might have interfered with the results. Nonsignificant changes between the two treatment groups for CDCA, CA, and DCA levels were observed in our study after treatment. Levels of CDCA, CA, and DCA were slightly decreased in the placebo group, whereas in the UDCA group, CA showed a tendency to decrease, and DCA and CDCA were slightly increased.