6 These effects have been observed despite concomitant increases in liver TAG levels. According to these metabolic considerations, promoting FAO seems to conflict with the antidiabetic outcomes reported in db/db mice expressing CPT1AM in the liver. An analysis of the molecular mechanism or mechanisms underlying the antidiabetic effects resulting from the greater activity of liver FAO perhaps may open new approaches to modulating GNG in type 2 diabetes. One scientific inaccuracy in this work is the erroneous report by the authors that β-hydroxybutyryl coenzyme A in the liver is an intermediate of ketone body metabolism (see Table 1 and p 825 of their

article). D-β-Hydroxybutyrate is a ketone body enantiomer oxidized through find more the formation of acetoacetate and not through its esterification to coenzyme A, whereas the enantiomer L-β-hydroxybutyl coenzyme A is an intermediate of FAO.7, 8 Arduino Arduini M.D.*, Mario Bonomini M.D.†, * R&D Department, CoreQuest Sagl, Bioggio,

Switzerland, † Institute of Nephrology, Department of Medicine, G. d’Annunzio University, Chieti, Italy. “
“Nodular gastritis (NG) is defined as antral gastritis with endoscopic findings usually characterized by a miliary pattern resembling “goose flesh.” There is a possible association between NG and gastric cancer. The aim of our study is to Lapatinib investigate whether there are some differences between young and elderly people in incidence and characteristics of NG and estimate potential risk factors for gastric cancer in adults with NG. Patients underwent upper gastrointestinal medchemexpress endoscopy for abdominal symptoms or cancer screening. Incidence rates and relationship between an elderly group (40 years or older) and young group (< 40 years) were assessed by endoscopic grade of NG, atrophic grade, concomitant diseases, and serum pepsinogen (PG). NG was found in 62 cases (0.94%) out of 6623 patients who underwent endoscopy, with a mean

age of 47.3 ± 13.3 years. Female patients were present at a significantly higher rate in the elderly group (P < 0.001). The grade of neutrophil infiltration in the greater curvature of the upper gastric body was recognized at a significantly higher rate in the elderly group (P < 0.05). PG II was present at a higher rate and PG I/II at a lower rate in the elderly group (P < 0.05). The odds ratio for the risk of gastric cancer in patients with NG was 2.1 (95% confidence interval 0.3–15.3) in the elderly group. NG in the elderly was also suggested to be a risk factor for gastric cancer as well as in the young. "
“Background and Aim:  Reflux esophagitis needs maintenance therapy. Data on comparison between trademark and generic medications are not available. Complaints and use of acid-suppressive therapy 10 years after diagnosis were determined.

HVPG-Free and HVPG-IVC had similar ROC curves (AUC: 0.66 and 0.67). HVPG-Free or HVPG-IVC discriminate 2 populations of pts with significantly Selleck HDAC inhibitor different OLT-free survival. The best cutoff value significantly change within either strategy (16 mmHg for HVPG-Free and 18 for HVPG-IVC) in the whole cohort and also when only considering the “discordant” pts. Importantly,

when HVPG-IVC was measured but HVPG-free cutoff was applied, the prognostic value was lost (no significant differences in OLT-free survival in pts with a HVPG-IVC > or below 16mmHg). Conclusions: HVPG-Free or HVPG-IVC, together with MELD, are independent predictors of death/OLT in pts with cirrhosis regardless of FVHP/IVC discrepancy ≥2mmHg. However, the cut-off value for HVPG-IVC is 2mmHg higher than for HVPG- Free and therefore they can not be interchangeable. This is special relevant in patients with large differences among FHVP and IVC. Disclosures: Jaime Bosch – Consulting: Falk, Gilead Science, Norgine, ONO-USA, Intercept pharma, Exalenz, Almirall, Conatus; Grant/Research Support: Gore Juan Carlos

Garcia-Pagan – Grant/Research Support: GORE The following people have nothing to disclose: Gilberto Silva-Junior, Anna Baiges, Fanny Turon, Karina G. Ramirez Ibarra, Tamoxifen mouse Vera Costa Santos, Annalisa Berzigotti, Virginia Hernandez-Gea Background: We have reported the usefulness of measuring the sheer wave velocity (Vs) using Virtual Touch Quantification (VTQ) in diagnosing fibrosis. This VTQ measurements can also be performed in the spleen. Fibrosis developed in liver cirrhosis can lead to portal hypertension, splenomegaly, and collateral circulation. We studied the diagnostic performance of spleen Vs in esophageal and gastric varices. Patients and Methods: 143 patients

who were diagnosed with esophageal and gastric varices using an upper gastrointestinal endoscopy (GIF) (84 male, age 64.8±12.5; 19 HBsAg(+), 86 HCVAb(+), 38 HBsAg(-)/HCVAb(-)) were included. Diagnosis were made according to the General rules for study of portal hypertension in Japan. The diagnostic ability of 上海皓元 liver and spleen Vs, biochemical exam, and Spleen Index (SI) were compared using receiver operating characteristic analysis (ROC). Results: The form of esophageal varies were F0/F1/F2/F3, 58/60/25/0, respectively. Liver Vs were 1.46/2.27/2.47m/s and spleen Vs were 2.58/3.06/3.71m/s, respectively. Liver and spleen Vs were significantly higher with the development of varices (p<0.001). The red color sign (RC) were RC(-)/(+), 122/21, respectively, and liver Vs and spleen Vs according to RC were 1.90/2.36m/s, 2.88/3.59m/s, respectively. The result showed significantly higher Vs in the group that required treatment (p<0.001). The area under ROC (AUROC) for distinguishing F0-1 from F2 for spleen Vs was 0.904, and it showed the highest diagnostic ability. The cut off value was 3.

The nls mutation in zebrafish is a loss-of-function allele of the raldh2 gene that was generated by the ENU approach. Originally, nls was isolated in an in situ hybridization screen and was detected by its effects on neural AP patterning.8 The nls embryos lack pectoral fin buds and fins. A similar phenotype has been reported for a natural

loss-of-function raldh2 mutation in zebrafish called no-fin.10 In addition to their lack of FDA approved drug high throughput screening fins, nls embryos do not express the hepatocyte and pancreatic cell markers that are detectable in WT zebrafish embryos.22 Stafford and Prince22 also showed that exogenous RA treatment of WT zebrafish embryos resulted in the anterior expansion of the pancreatic anlage. Thus, RA signaling is a determinant of the regionalization of both neuroectoderm and endoderm, and defects in raldh2 function prevent the development of the endodermal region in which liver and pancreatic cells would normally appear. In contrast, our medaka hio mutation does not have severe effects on neuroectoderm

and endoderm regionalization, and the liver in hio embryos, although find more reduced in size and delayed in appearance, eventually forms in the normal location. Thus, hio is a unique mutation affecting liver organogenesis, and continued study of this mutation should yield new insights into the involvement of RA signaling in liver specification. It remains to be elucidated how medaka hio mutants escape the defect in endodermal regionalization associated with zebrafish MCE公司 nls mutations. The

availability of two closely related fish model systems, medaka and zebrafish, for studies in genetics, experimental embryology, and molecular biology is unique among vertebrates and advantageous for two reasons. First, the evolutionary distance between these two species is particularly well suited for comparative functional genomics. Second, and more importantly, the parallel existence of medaka and zebrafish transforms the perceived weakness of studying genetics in fish, namely, the many analogous groups of genes formed because of genomic duplications, into an advantage: the study of a gene in one species may shed light on a gene function that is hidden in the other species.28 For example, RALDH2′s function in AP patterning is not apparent in medaka hio mutants, and RALDH2′s function in liver specification is not apparent in zebrafish nls mutants. Our results clearly demonstrate that a comparison of two related species can be a powerful means of dissecting genetic and molecular mechanisms underlying vertebrate development. The authors thank numerous members of the Nishina and Katada laboratories for excellent fish care, technical assistance, and helpful discussions. Additional Supporting Information may be found in the online version of this article. “
“Aim:  There is an ongoing need for predictors of long-term outcomes for patients with primary biliary cirrhosis (PBC).

In Kang et al.’s model, NrasG12V alone was not able to drive hepatic tumorigenesis in wildtype mice. Surprisingly, NrasG12V did drive massive tumor development in CD4−/− hosts, implicating a role for the adaptive immune system (Th cells) in surveillance of cells undergoing oncogenic stress. Furthermore, the authors found Nras G12V peptide epitope-specific Th cells indicating specificity for the driving oncogene. The authors also presented evidence that monocytes/macrophages function as effectors in Dabrafenib chemical structure clearing initiated cells but

antibody-mediated depletion of neutrophils and NK cells showed only marginal or no effect. It has been noted that immunosuppressed individuals display a higher cancer rate (reviewed22) and in the case

of hepatitis C, senescent hepatocytes build-up in infected livers of immunosuppressed patients.19 This is consistent with immune-mediated surveillance of senescence providing a major barrier to tumorigenesis by eliminating the reservoir of premalignant senescent cells that are primed for escape to transformation. However, additional studies, including single-cell analyses, are needed to formally exclude the possible preexistence of senescence-resistant or otherwise transformed cells. The Myc oncogene has been Kinase Inhibitor Library chemical structure implicated in hepatocellular senescence (tumor regression), malignant progression, and tumor-dependent immunoregulation. Overexpression of wildtype Myc is a feature in most HCC patients. Induction of Myc-driven genes also marks the transition from dysplastic nodules to “early” HCC,23 indicating medchemexpress that Myc may initiate or be an “effector” of transformation in HCC. Myc is the only oncogene24 in its wildtype form that can induce high penetrance tumors with short latencies in most transgenic

models. The Myc transgenic tumor model displays decreased latencies in response to hepatotoxins and hydrodynamic damage, implying that Myc may collaborate with inflammation-driven signaling pathways.25 Interestingly, Myc is an addictive oncogene in models of lymphoma and HCC where tumor regression occurs when Myc is shut down. In lymphoma, Myc evokes apoptosis that attracts and signals macrophages to secrete TGF-β inducing senescence. Just as CD4 T cells are required for successful surveillance of NrasG12V-induced senescent cells, sustained tumor regression following Myc inactivation also depends on CD4 T cells for induction of senescence, collapse of angiogenesis, and long-term suppression of minimal residual disease.26 Myc-driven transgenic HCC models also display the ability to modulate the adaptive immune response.

Pharmacogenetics may one day prove to be the best application of personalized medicine: Once a “library” is constructed, it may allow the prediction of drug toxicities as with ribavirin (RBV)-induced anemia.24 By using DNA samples collected from >1,000 recruits a trial comparing pegylated interferon alpha (Peg-IFNα)-2ba to Peg-IFNα-2b, the influence of genetic control of response to treatment was evaluated: see more Specific variations

in the IL28B gene correlated excellently with sustained virologic response (SVR).25 Do I think such “personalized medicine” is the way of the future? Frankly, not soon anyway; even IL28B genotyping as currently performed seems insufficiently reliable to decide whether to fund or not fund VX-770 in vivo antiviral therapy to an individual with CHC. Experiences in both the liver clinic and emergency room settings have made me realize that, particularly in the management of liver failure, whatever the cause, we have failed to translate what we know—at least to primary care physicians, such as the following: 1. Patients with acute alcoholic hepatitis (AH) with a Maddrey Discriminant Function test result of >32 or, as more recently reported a Glasgow AH score of

9 or more, fail to receive treatment with corticosteroids with or without reevaluation after the first week of therapy.26, 27 Thus, it would appear that education in the management of liver failure is “poorly” delivered. Why is this? Could it be that most trials in this field are investigator initiated and thus their findings fail to be delivered verbally to the front-line physician? Could Web-based education be an effective alternative? We

are now at the start of a very exciting era of antiviral therapy that involves directly targeting the viral lifecycle or the host machinery of viral replication. The first two agents recently licensed are telaprevir and boceprevir, which both enhance SVR rates in treatment-naïve patients and some previously treated with Peg-IFNα plus ribavirin.36-40 Shorter duration of therapy, along with enhanced efficacy MCE公司 for CHC, is uppermost on every infected patient’s agenda. There are advantages and disadvantages to both of these drugs. The trial design of the registration trials were very different, so only time will tell which will become (albeit for a very short while) the optimal therapy; both are toxic and require new management skills both of treating physicians and their nursing assistants. Toxicity issues will doubtless become more apparent as access to these two agents becomes available worldwide. Currently, RBV appears to be indispensable in patients prescribed either new drug. But, both Peg-IFN and RBV-free strategies are what patients want. Early reports of two direct-acting antivirals (DAAs) given simultaneously to patients with CHC (genotype 1) and one DAA with RBV to those with G2/G3 infection suggest that an interferon (IFN)-free drug regimen may be shortly on the horizon.

7%, 1-year survival 29.2%, no severe toxicity) [40]. The effect of sunitinib as second-line treatment in patients with GC has been assessed in a German phase II trial [41]. The overall response rate was 3.9% with a PFS of 1.28 months, an OS of 5.81 months, and a 1-year survival rate of 23.7%. These results do not support the application of sunitinib in this setting. Efforts are made to use the rapidly developing biostatistical approaches of gene-coexpression network profiling for the

identification of novel target genes or promising candidate compounds for the treatment of advanced GC [42]. Several studies have suggested that chronic infection with H. pylori may moderately increase the risk for colorectal cancer [43-45]. The background for this hypothesis is that infection with H. pylori leads to an increase of plasma gastrin levels. Hypergastrinemia stimulates mucosal cell proliferation. Chronic H. pylori PLX3397 molecular weight Silmitasertib manufacturer infection results in gastric atrophy, cell

mutation, and transformation of gastric mucosal cells into gastrin-producing cells, which also express gastrin receptors serving to stimulate cell proliferation and tumor growth [46-48]. Two meta-analysis reported that there is a modest increase in the risk of colorectal cancer owing to H. pylori infection [49, 50]. However, the studies had several weaknesses as thus included a small sample size of studies with high heterogeneity and made note or confounding controls. Recently, a large population-based case control study was conducted in Germany to investigate the association between H. pylori and colorectal cancer [51]. Serum anti-H. pylori antibodies and anti-CagA antibodies were measured in 1712 patients with colorectal cancer and 1669 controls. There was a high 上海皓元 H. pylori seroprevalence in the study population (mean age 69 years) with more than 40% in both arms. Overall, H. pylori infection

was more prevalent in colorectal cancer cases (46.1%) than in controls (40.1%). The authors performed a stratified analysis which showed risk elevation to be essentially confined to left-sided colorectal cancer, with an odds ratio (OR) of 1.22 (95% CI: 1.02–1.45). The results of this large population-based study suggest that H. pylori infection may be associated with an increased risk for the selected group after the neoplasia of the left colorectum. Colorectal cancer development is based on the adenoma-carcinoma sequence. Thus, a study investigated correlation between H. pylori infection or chronic atrophic gastritis (CAG) and risk of colorectal adenoma [52]. In this study, H. pylori infection was a risk factor for adenoma as a whole. The analysis of distal adenoma cases showed that adenoma risk was significantly increased in the presence of H. pylori infection when chronic atrophic gastritis was present. In a large cross-sectional study from Korea, 2195 eligible subjects undergoing screening colonoscopy have been evaluated for the prevalence of H.

Peginterferon alfa-2b is registered in some Asia-Pacific selleck compound countries, including mainland China. Tenofovir has been registered in Australia as

well as Europe and North America and registration in Asia-Pacific regions is ongoing. Clevudine is registered only in Korea and the Philippines, but not in other countries due to the risk of myopathy. In the American and European recommendations, entecavir and tenofovir are the preferred oral antiviral agents due to their potent antiviral effect and very low risk of drug resistance.46,47 However, in the Asia-Pacific consensus statement, no clear recommendation has been made on the choice of antiviral agents.45 The major reason is the vast difference in the economic situation and medical reimbursement arrangements between different Asia-Pacific countries. In fact, the estimated annual cost of antiviral drugs, if accepted across the affected population, might exceed the gross national income per capita in countries such as India, Indonesia, the Philippines and Papua New Guinea.5 In economic deprived countries, lamivudine may be the only reimbursable antiviral agent due to its low cost.71 In Taiwan, Indonesia and Korea, antiviral drugs are only reimbursed for a limited duration of time.71 In Hong Kong, although entecavir can

be reimbursed indefinitely, the indication for reimbursement is very restricted and most patients need to pay for their

antiviral treatment.72 Daporinad mw 上海皓元 Detailed cost-effective analysis is therefore warranted to guide usage policies for HBV antiviral drugs in the Asia-Pacific region. One possibility is the roadmap-approach, in which an inexpensive antiviral drug is started as the first-line treatment and the drug regime is modified according to the on-treatment HBV DNA response.73,74 However, the emergence of lamivudine- or Adefovir-resistant mutant forms of HBV, which rapidly develop entecavir (but not tenofovir) resistance would be a concern with this approach. Most pivotal clinical trials on antiviral drugs are based on their efficacy at 1–2 years.47 However, relapse of hepatitis is common (> 70% cases) after premature drug cessation. Some authorities recommend long-term extended treatment by antiviral drugs. In the Asia-Pacific consensus, it was recommended to stop the antiviral drug when HBeAg seroconversion has developed for more than 6 months among HBeAg-positive patients.45 However, HBeAg seroconversion induced by antiviral drugs is not as sustained as that induced by interferon therapy.75 In two small case series’ in Hong Kong and Taiwan, 27% to 45% of HBeAg-positive patients had HBV DNA relapse after cessation of lamivudine despite maintenance lamivudine post-HBeAg seroconversion according to the regional recommendation.

— Reversible changes in brain magnetic resonance imaging (MRI) weighted in diffusion-weighted images (DWI) and apparent water diffusion coefficient (ADC) maps have been reported in acute stroke, epilepsy, eclampsia, and hypoglycemia, but they are contradictory regarding to migraine aura. Objective.— A 41-year-old

woman with known basilar migraine for 5 years consulted about a persistent visual aura (visual snow phenomenon) plus bilateral paresthesias in the extremities for GS-1101 cost 4 days. The headache was treated with success with 10 mg of wafer rizatriptan and 600 mg of ibuprophen. Methods.— The neurologic and ophthalmologic examination were normal. An urgent brain MRI detected no lesions in T1, T2, fluid-attenuated inversion recovery, and DWI, but an abnormal signal appeared in the left occipital lobe in ADC and (r)ADC maps. The brain MRI angiography, carotid ultrasound study, transesophageal echocardiography, 24-hour cardiac Holter monitoring, and thrombophilia study were normal. Results.— A new brain MRI 8 days after did not show any previous lesion in the same sequences. Conclusions.— We present a patient with migraine and transitory abnormal signals in the ADC map of an occipital region during persistent visual aura. The clinical-radiological relationship is congruent. Some similar cases have showed these MRI signals during the aura, suggesting cytotoxic edema, without ischemic lesions

in the MRI controls. Theses ADC images probably appear in complex auras. “
“(Headache 2011;51:300-305) Remission of hemicrania Palbociclib order continua (HC) and transformation from HC to chronic paroxysmal hemicrania (CPH) are unusual. We report a patient with left-sided HC who, after a period of remission, presented as CPH. The continuous HC headache disappeared completely after initiating treatment with cyclooxygenase (COX)-2 inhibitor, but reappeared on the same side after 14 months remission with paroxysmal, frequent, intense and short-lasting headache attacks accompanied by ipsilateral cranial autonomic symptoms. This happened shortly after

MCE the treatment was discontinued because of withdrawal of the COX-2 inhibitor from the market. The response to indomethacin was prompt, and the patient became completely free from her paroxysmal headache with a dose of 50 mg 2 times daily. This case questions a possible modification effect on the course of HC by use of COX-2 inhibitor, as well as further supporting that some aspects of the pathophysiology of HC may resemble those of CPH, and may argue for common biological mechanisms in HC and CPH. “
“(Headache 2011;51:1212-1227) Background.— Medication-overuse headache (MOH) refers to headache attributed to excessive use of acute medications. The role of personality needs studies to explain the shifting from drug use to drug abuse. The main aim of this study is to study personality, according to Minnesota Multiphasic Personality Inventory, comparing MOH, episodic headache, substance addicts (SA) vs healthy controls.

3) shows significant

effect of daclizumab (RR 0.82; CI 0.71-0.95; P = 0.007; 12 trials/cohorts) but not basiliximab (RR 0.87; CI 0.73-1.03; P = 0.11; seven trials), but this Dabrafenib mw does not seem to be a systematic effect because meta-regression does not indicate a significant effect of type of IL-2Ra (P for test of moderators = 0.67; Table 3) and inspection of the funnel plot (Supporting Fig. 4) shows that both types of studies are distributed similarly. Meta-regression also showed that concomitant use of MMF (in both arms) seems to amplify the effect of IL-2Ra (ratio of RR 0.83; CI 0.69-1.01; P = 0.06). Analysis of the type of CNI did not show significant effects, but trials in comparison 2 also had a lower RR compared to trials in comparison 1 (Table 3). This effect may be explained by the fact that MMF was used in all trials in comparison 2. After adjusting for MMF, the effect in comparison 2 alone is no longer

seen. We did not RO4929097 nmr observe significant heterogeneity in any of the analyses and observed only marginal changes of residual heterogeneity in meta-regression (Table 3). However, we observed considerable heterogeneity of overall rejection rates (i.e., the sums in the experimental and control groups of each trial) ranging from over 55%36 to less than 10%38 (see Supporting Table 2). Similar differences have also been observed in other meta-analyses concerning organ transplantation.42 We sought sources of heterogeneity using GLMM and found that the overall rejection rate was significantly higher in studies that required protocol biopsies (OR 3.10;

CI 1.93-4.99; P < 0.001; 19 trials/cohorts). These studies reported not only treated rejections but also histological signs of rejection without clinical correlates. Subgroup analysis of trials with and without protocol biopsies (five trials/cohorts with 435 patients and 14 trials with 2,526 patients, respectively) showed a significant effect on acute rejection only in studies without protocol biopsies (RR 0.81; CI 0.71-0.92) but not in studies that performed protocol biopsies (RR 0.92; CI 0.76-1.11). Meta-regression does not provide any evidence for a significant MCE公司 effect of protocol biopsies on acute rejection (P value for test of moderators 0.26) and the inspection of the funnel plot (Supporting Fig. 5) shows that the distribution of both groups of studies is comparable. Furthermore, the analysis of overall rejection rate showed that the use of MMF decreased the incidence of acute rejection in both study arms (OR 0.49; CI 0.31-0.77; P = 0.002; 19 trials/cohorts). After adjustment for use of MMF and type of biopsy the effect of IL-2Ra was still highly significant (OR 0.76; CI 0.64-0.90; P = 0.002; 19 trials/cohorts). Funnel plot analysis for acute rejection showed significant asymmetry (P = 0.01). Using the trim-and-fill method we augmented the data (Supporting Fig. 6) and these supposedly missing studies all had a risk ratio above 1.

Infants with perinatal subtype of BA have higher tissue levels of PROM1 expression than those with embryonic subtype. Conclusion: Expansion of collagen-producing PROM1pos cells within regions of

periportal fibrosis is associated with activated FGF and TGFβ pathways in both experimental and human BA. PROM1pos cells may therefore play an important role in the biliary selleck chemicals fibrosis of BA. (Hepatology 2014;60:941–953) “
“This chapter contains sections titled: Epidemiology Histopathology Etiology and pathophysiology Clinical features and diagnosis One or two diseases? Treatment of microscopic colitis References “
“The reported prevalence of cancer associated with a primary choledochal cyst ranges from 2.5%[1]to 26%.[2] Total cyst excision is the standard procedure to prevent malignant changes. An essential part of this surgery is the termination of the Trichostatin A in vivo reflux of pancreatic juice into the bile duct through the anomalous pancreaticobiliary duct union, so as to avoid activation of pancreatic enzymes involved in the pathogenesis of bile duct carcinoma. Theoretically, biliary malignancy should not develop after excision of the choledochal cyst because the presumed cause was abrogated by separation-operation. However, although the incidence of biliary malignancy after excision of choledochal cyst was 0.6% in Korean multicenter

study[3] and 0.7% in a Japanese nationwide study,[4] far lower than that associated with unresected choledochal cysts, it is still higher (about 200 times) than the incidence of biliary cancer in the general population in Japan. The main issues about the biliary malignancy after cyst excision are the perspective it might give on risk factors for oncogenesis, the relevance of cyst excision as a standard treatment and risk factors. In this issue of the Journal of Gastroenterology and Hepatology, Ohashi et al.[5] provided cumulative incidence data on subsequent biliary malignancy increase

more than 15 years after choledochal cyst excision, describe unfavorable outcomes, and provide a comprehensive review of biliary malignancy after cyst excision. However, several questions mentioned remained unanswered. The authors searched only the English literature. Because choledochal cyst is a relatively rare disease in the West and 上海皓元医药股份有限公司 more than half of the reported cases have occurred in Japan, we searched both English and Japanese language literature. Between 1970 and 2011, 58 cases were identified, and among them, data of site of malignancy can be available in 54 cases[3, 6-47] (Table 1). According to Todani’s classification, 24 of 41 patients (59%) were classified into type IVa, and 17 (42%) were into type I. The most common site of involvement in 54 cases was the hepatic duct, at or near the choledocho-enteric anastomosis (43%) followed by the intrahepatic duct (41%) and distal choledochus (17%).