Conclusions:  Complications

Conclusions:  Complications selleck chemical are rare during EUS-guided drainage of PFC and can be managed successfully in most patients. “
“Hypoxia has been shown to have a role in the pathogenesis of several forms of liver disease. The hypoxia inducible factors (HIFs) are a family of evolutionarily conserved transcriptional

regulators that affect a homeostatic response to low oxygen tension and have been identified as key mediators of angiogenesis, inflammation, and metabolism. In this review we summarize the evidence for a role of HIFs across a range of hepatic pathophysiology. We describe regulation of the HIFs and review investigations that demonstrate a role for HIFs in Dasatinib clinical trial the development of liver fibrosis, activation of innate immune pathways, hepatocellular carcinoma, as well as other liver diseases in both human disease as well as murine models. (HEPATOLOGY 2012;) The liver has a unique anatomical and functional niche in the body that profoundly affects its physiology and pathophysiology, including its oxygen homeostasis. Afferent blood flow to the liver derives from both highly oxygenated blood in the hepatic artery

as well as oxygen-depleted blood in the hepatic portal vein. Furthermore, the directional flow of mixed oxygenated and deoxygenated blood toward the central vein of the hepatic lobule creates a physiological oxygen gradient.1 This gradient has been reported to result in oxygen tensions from about 60-65 mmHg in periportal blood, falling to about 30-35 mmHg in perivenous portions

of the liver parenchyma; by comparison, physiological arterial oxygen concentration in most other body tissues is about 74-104 mmHg, and venous oxygen concentration is 34-46 mmHg.1 Hypoxia has profound consequences for tissues of an aerobic organism. In recent decades, our knowledge of the homeostatic response to hypoxia has increased to molecular genetic mechanisms. The hypoxia inducible factors (HIFs) are a family of heterodimeric Dichloromethane dehalogenase transcription factors that act as master regulators of a homeostatic transcriptional response to hypoxia in virtually all cells and tissues. Active HIF consists of an alpha subunit and a beta subunit. Three alpha subunits, termed HIF1α, HIF2α, and HIF3α, have been described in humans, mice, and rats; all bind to a common β subunit named, alternatively, HIF1β, or the aryl-hydrocarbon-nuclear receptor translocator [ARNT].2 Active HIF is termed by its (1)alpha subunit; hence, HIF1 is the active transcription factor consisting of HIF1α and ARNT, HIF2 is the dimer of HIF2α and ARNT, etc. HIF1 and HIF2 are the major hypoxia-inducible factors in humans, mice, and rats. Far less is known about the function of HIF3.2 Posttranslational degradation by the proteasome is a major pathway of HIF regulation.

Papillary dilation using large-bored (12–20 mm) balloon dilation

Papillary dilation using large-bored (12–20 mm) balloon dilation catheter was performed through the percutaneous transhepatic route. We analyzed the efficacy of the stone retrieval and post-procedure complications after the procedure. Results: The success rate for the complete duct clearance was 100%. There was no patient who needs use of basket to remove the stone buy Staurosporine after PPLBD. Electrohydraulic lithotripsy was required in 2 (18.2%) patients. The median time to complete stone removal after PPLBD was 17.8 minutes. There was no any complications

occurred after PPLBD. Asymptomatic hyperamylasemia did not occur in all patients. Conclusion: The current data suggested that PPLBD is safe and effective for removal of large CBD stones. Keywords: Balloon Dilation, Choledocholithiasis N MAQBOUL,1 S GUPTA1,2 1Princess Alexandra Hospital, Brisbane, Australia, 2The Wesley Hospital, Brisbane, Australia Introduction: EUS plays an important role in the characterisation of gastro-intestinal and pancreatic lesions. EUS/FNA allows real-time sampling with minimal risk of complications. The Echotip Procore 25-gauge (Cook Medical) is a novel needle designed to obtain tissue for both cytology and histology, potentially increasing diagnostic yield with fewer needle passes. Methods: A retrospective review of all EUS performed between June 2012 and May 2013 at two tertiary referral academic

centres in Brisbane, Australia. All PF-02341066 purchase EUS were carried out by a single endoscopist. EUS/FNA procedures utilising the Echotip Procore 25-gauge needle were included for analysis. A positive result was defined GBA3 as adequate cellular yield and cytology concordant with the predicted diagnosis at the time of EUS. Assessment of tissue for histology was not routinely performed. Results: A total of 82 EUS/FNA were performed using the Echotip Procore 25-gauge needle in 49 males and 33 females. Indication for EUS/FNA was further characterisation of a pancreatic mass (67.1% of cases), gastric/duodenal lesions (13.4%), mediastinal masses/lymphadenopathy/lung

lesions (13.4%), liver lesions (4.9%) and evaluation of a rectal lesion (1.2%). On-site cytopathology service was utilised when available. Positive results were obtained in 72 of the 82 cases (87.8%); one was a second procedure in a patient with an initial negative result. Negative, or non-diagnostic, results were seen in 10 of the 82 cases (12.2%). The mean number of passes in the positive group was 3.40, compared with 3.60 in the negative group. There were no immediate complications with this technique. Conclusion: Our initial experience utilising the Echotip Procore 25-gauge needle resulted in high diagnostic yield with very few passes, and low complication rates. Given the higher cost associated with this needle in Australia, a randomised trial comparing yield against the standard 25-gauge needle would be needed to determine cost-effectiveness.

1A) and spotted necrosis (Supporting Fig 1) in wild-type (WT) C5

1A) and spotted necrosis (Supporting Fig. 1) in wild-type (WT) C57BL/6 mice by 16 hours postinjection. However, to our surprise, α-Galcer induced 5- to 6-fold higher serum ALT and AST levels and a larger area of necrosis in IL-4−/−IFN-γ−/− dKO mice than those in WT mice at 16 hours after α-Galcer injection (Fig. 1; Supporting Fig. 1). In addition, administration of α-Galcer induced an accumulation of inflammatory foci in the livers of BMS-907351 datasheet WT mice, with the peak effect occurring

at 72 hours postinjection (Supporting Fig. 1), and the number of inflammatory foci was also much higher in dKO mice than that in WT mice (Supporting Fig. 1). To determine the role of early production of IL-4 in α-Galcer-induced liver injury, we examined the effects in IL-4−/− and IL-4R−/− Z VAD FMK mice. As illustrated in Fig. 2A,B, α-Galcer-induced elevation of serum ALT and AST was lower in IL-4−/− and

IL-4R−/− mice than in WT controls. Liver histology analyses further revealed that IL-4−/− and IL-4R−/− mice had reduced liver necrosis and fewer inflammatory foci than WT control mice after α-Galcer administration (Figs. 2C-D). The number of myeloperoxidase (MPO)-positive neutrophils was also lower in IL-4−/− and IL-4R−/− mice than in WT mice 72 hours after α-Galcer administration (Fig. 2C,D). The above findings indicated that the number of inflammatory foci (iNKT expansion) in the liver was lower in IL-4−/− or IL-4R−/− mice than in WT mice 72 hours post-α-Galcer injection, which may have been due to IL-4-mediated promotion of iNKT proliferation, Mannose-binding protein-associated serine protease as demonstrated previously.[17] Fluorescence-activated cell sorting (FACS) analyses of liver MNCs revealed that WT and IL-4−/− mice had a similar number of iNKT cells at the early timepoints post-α-Galcer injection (data not shown), which does not explain the reduced liver injury in IL-4−/− mice. To further explore the mechanisms underlying α-Galcer-induced liver injury, we examined NK cells and neutrophils in the liver. In this case, FACS analyses revealed that the number of NK cells was not increased post-α-Galcer injection and that depletion of NK cells using an anti-ASGM1

antibody did not affect α-Galcer-induced liver injury in mice (data not shown), suggesting that NK cells are not involved in this process. In contrast, there was a striking increase in the percentage and total number of neutrophils in the liver after α-Galcer injection. As illustrated in Fig. 3A,B, the percentage of neutrophils was elevated 4-fold, whereas the total number of neutrophils was elevated 30-fold at 3 hours post-α-Galcer administration. Moreover, depletion of neutrophils markedly reduced serum ALT and AST levels (Fig. 3C), suggesting that the accumulation of neutrophils contributes to α-Galcer-induced hepatocellular damage. Figure 3D shows that the percentage and total number of hepatic neutrophils were lower in IL-4−/− mice than in WT mice at 3 hours post-α-Galcer administration. Furthermore, Fig.

(HEPATOLOGY 2011;) Hepatitis C virus (HCV) infects over 3% of the

(HEPATOLOGY 2011;) Hepatitis C virus (HCV) infects over 3% of the population, causing severe liver disease. Current therapy comprising pegylated interferon (IFN) and ribavirin (Rib) is inadequate, which, combined with high cost and poor patient compliance, has driven the demand for new virus-specific drugs.1 Future standard of care will replace IFN/Rib with combinations of specific inhibitors, such as seen for human immunodeficiency virus (HIV) therapy. However, extensive HCV variability raises concerns 3-deazaneplanocin A nmr over the ability of relatively few compounds to suppress resistance. Thus, great effort focuses on expanding the repertoire of HCV drug targets, expedited by the availability

of the Japanese fulminant hepatitis clone 1 (JFH-1) infectious isolate.2 HCV is the prototype member of the Hepacivirus genus within the Flaviviridae.3

It is enveloped and possesses a positive-sense single-stranded RNA genome of ∼9.6 kb. An internal ribosome entry site in the 5′ untranslated region drives translation selleck chemical of a polyprotein that is cleaved into 10 mature products. The core and envelope glycoproteins with the RNA genome comprise the virion, whereas nonstructural (NS) proteins modulate host metabolism and replication of the viral RNA. JFH-1 has permitted the study of particle production, and it has become clear that, in addition to canonical virion components, other viral proteins are required.4-13 HCV p7 forms a cation channel in vitro,14-16 and both deletions and point mutations markedly reduce the production of infectious virions in culture.4, 5 It is comprised of two trans-membrane domains separated by a cytosolic loop and forms both hexameric and heptameric complexes.14, 17, 18 We have recently shown that p7 acts as a proton channel within infected cells, which is directly required for the production PD184352 (CI-1040) of infectious virions.19 p7 is required for HCV to replicate in chimpanzees20 and small molecules block both channel function in vitro and virion production in culture, rendering it an attractive antiviral target.21, 22 Skepticism concerning

p7 inhibitors heralds from trials where p7 inhibitor monotherapy, or combinations with IFN/Rib failed to significantly improve responses.23 However, evidence from meta-analyses24, 25 and patient virus loads at early time points26, 27 supports a specific antiviral effect, and selection of specific nonsynonymous mutations occurs within patient isolate p7 sequences.28, 29 Because HCV displays genotype (GT)-dependent p7 inhibitor sensitivity,21 changes in amino acid sequence could interfere with the binding of drug molecules, making it likely that the emergence of resistant quasispecies accounts for trial outcomes. Here, we identify p7 resistance mutations specific to adamantane and IS drugs, indicative of a genuine antiviral effect that supports their inclusion in future combination therapies.

Third, risk of NAFL is undoubtedly associated with obesity and me

Third, risk of NAFL is undoubtedly associated with obesity and metabolic syndrome and has been traditionally associated with more affluent living standards. In the current study too, even

nonobese subjects with NAFL had worse metabolic parameters and higher income than their age-matched and sex-matched counterparts who did not have NAFL. Nevertheless, coexistence of intrauterine and neonatal malnutrition and c-Met inhibitor the development of obesity, type 2 diabetes, and related comorbidities have been confirmed in a number of studies in humans and animal models.2 Moreover, it has been shown that, in humans, the intrahepatic lipid content increase following starvation also may be due to reduced apolipoprotein B-100 production and hepatic lipid export, and/or impaired mitochondrial function;

this could have implications for exacerbations of steatohepatitis that is sometimes seen with rapid weight loss, anorexia nervosa, and parenteral nutrition.3 Therefore, in contrast to the popular view, malnutrition rather than obesity at different stages of life may well be an explanation for pathogenesis of NAFL in this predominantly poor population. Sujoy Maitra M.D., MRCP Dr.*, * Consultant Hepatologist, Columbia Small molecule library Asia Hospital Calcutta, India. “
“Background and Aim:  The aim of this study was to evaluate endoscopic band ligation plus argon plasma coagulation versus scleroligation. Methods:  Patients were randomized to: Group I, 50 patients subjected to endoscopic injection sclerotherapy; Group II, 50 patients subjected to variceal band ligation; Group III, 50 patients subjected to combined endoscopic sclerotherapy and band ligation; and Group IV, 50 patients

subjected to endoscopic band ligation plus argon plasma coagulation. Results:  A comparison of the number of therapeutic sessions showed that group III underwent significantly fewer sessions. As regards post-treatment complications, Group I showed a high incidence Ureohydrolase of transient pyrexia, transient dysphagia and/or retrosternal pain and ulceration, while in group II a higher incidence of rebleeding was demonstrated, as well as a higher incidence of esophageal varix recurrence after eradication during the follow-up period. A higher mortality incidence was detected in groups I and II. The follow-up incidence did not significantly differ between the different study groups. Conclusion:  Scleroligation allows very rapid eradication of varices, has a low recurrence rate, avoids the disadvantage of high recurrence of band ligation alone, and does not require special skills over sclerotherapy or band ligation. Also, band ligation plus argon plasma coagulation allows for very rapid eradication of varices, and a low recurrence rate, with no obvious recorded complications, but it has the disadvantage of being the most expensive technique and requires special equipment that is only available in a few endoscopic centers.

41%) were H pylori positive The prevalence reached a peak at th

41%) were H. pylori positive. The prevalence reached a peak at the age of 30–39 years (90.82%). There was significant difference between sexes and women had a higher infection rate than men. The prevalence of

H. pylori infection was also associated with eating kipper food and fried food. No association between H. pylori prevalence and smoking or drinking was found. Compared to healthy individuals, people with dyspeptic diseases (peptic ulcer, gastroenteritis) click here presented a high prevalence of H. pylori infection. Using multivariate logistic regression analysis, age, history of peptic ulcer and gastroenteritis were the independent predictors for H. pylori infection. Conclusion: Yangzhong country, a persistent high risk area of gastric carcinoma, had a high prevalence of H. pylori infection and was related to several risk factors. The underlying mechanisms are needed to be further investigated. Key Word(s): 1. Helicobacter pylori; 2. risk factor; 3. Jiangsu province; 4. gastric cancer; Presenting Author: YIN ZHU Additional Authors: HONGSHENG WANG, YAN SUN, MING YAN, JUNGSOO JOO, JIAFANG SUN, WEIPING CHEN, CHENFENG QI, NONGHUA LV, HERBERTCARPENTER Paclitaxel manufacturer MORSE, III, WILLIAMG COLEMAN, JR Corresponding Author: HERBERTCARPENTER MORSE, III,, WILLIAMG COLEMAN, JR Affiliations: National Institutes of Health, NIDDK; the First Aiilated Hospital of NanChang Univerisity, the Department of

Gastroenterology; National Institutes of Health, NIAID; the First Affiliated Hosptial of Nanchang University,

the Department of Gastroenterology Objective: Interferon Regulatory Factor 8 (IRF8) is a transcription factor Avelestat (AZD9668) of the interferon regulatory factor (IRF) family and has many functions involved in the regulation of development, growth and host defense in hematopoietic lineage cells including innate and adaptive immune responses. However, expression and function of IRF8 in non-hematopoietic cells remain poorly understood. Methods: We used microarray analysis to monitor host responses to Helicobacter pylori (H. pylori) infection. The expression of IRF8 was detected by quantitative PCR and western blot in the gastric epithelial cell line (GSM06) and macrophage cell line (RAW264.7) infected by H. pylori. We generated an IRF8-EGFP fusion protein reporter mice (IRF8-EGFP mice) to monitor IRF8 expression during H. pylori infection using immunofluorescence and qPCR. Results: The results of microarray analysis showed that the IRF8 gene was up-regulated (fold changes > 2, p < 0.0001). Both IRF8 mRNA expression and IRF8 protein level increased in GSM06 and RAW264.7 after infected by H. pylori. The protein of IRF8 expressed in gastric epithelial cells from IRF8-EGFP mouse stomach, mostly localized in the nucleus. The fluorescence of IRF8 increased on gastric epithelial cells with the extension of H. pylori infection. IRF8 mRNA expression of stomach tissues increased significantly in IRF8-EGFP mice infected by H. pylori, compared with wild type control mice (p < 0.05).

Thus, there is a significant unmet need in terms of effective ava

Thus, there is a significant unmet need in terms of effective available treatments and this unmet need may be overcome by adopting alternate therapeutic strategies such as (1) employing different agents to improve insulin resistance (e.g., GLP-1 agonists) and oxidative stress (betaine, SAMe); (2) exploring agents affecting different targets such as apoptosis (e.g., GS 9450) and FXR (e.g., obeticholic acid), or stellate cell activation (losartan); or (3) investigating a combination buy PD-0332991 of agents affecting different targets/pathways. In this issue of HEPATOLOGY, Harrison’s

group6 report the results of their randomized controlled trial that investigated two different combination therapies to treat NASH. Angiotensin II receptors have been identified on hepatic stellate cells (HSC) and their activation leads Alisertib cell line to HSC proliferation. Angiotensin II receptor knockout

mice when challenged with carbon-tetrachloride had significantly reduced hepatic fibrosis when compared to wildtype mice, suggesting angiotensin receptor II is a novel target to improve hepatic fibrosis.7 Losartan, an angiotensin II receptor blocker (ARB), has been shown in mice models to have beneficial effects on liver fibrosis,8, 9 and in a small study consisting of seven patients with NASH, Yokohama et al.10 suggested that losartan may improve necroinflammation and fibrosis. Torres et al.6 randomized 137 subjects with biopsy-proven NASH to a 48-week course of rosiglitazone

4 mg twice daily alone, or in combination with either metformin 500 mg twice daily or losartan 50 mg daily. The primary endpoint was change in hepatic histology as evidenced by at least one point improvement in steatosis, inflammation, and fibrosis. Steatosis, inflammation, and oxyclozanide fibrosis improved between baseline and the end of treatment within each treatment arm, but the changes in liver histology were statistically not different between the three treatment groups.6 Randomized controlled trials of NASH with histological endpoints are expensive and difficult to conduct, and thus Harrison’s group must be applauded for undertaking this study and for their other important contributions to the field. However, we suggest caution in interpreting the results of this study because of some of its limitations. This study was prematurely stopped due to severe restrictions imposed by the Food and Drug Administration on rosiglitazone use in the United States, leading to an underpowered sample size. The presence of fibrosis was not a prerequisite at baseline and yet its improvement was required to achieve the primary outcome.

10, 11 An elevation of serum endothelin-1 has been noted in NASH,

10, 11 An elevation of serum endothelin-1 has been noted in NASH, and has been positively related to the severity of liver fibrosis.12 An enhanced peripheral vasoconstrictive response to endothelin-1

has been widely reported in NASH patients and rats.12, 13 However, studies investigating Nutlin-3 research buy an enhanced intrahepatic vasoconstrictive response to endothelin-1 in NASH cirrhotic livers are still limited. Endocannabinoids are lipid mediators that increase in liver of diet-induced obesity models. Besides hyperleptinemia, an activated hepatic endocannabinoid system is significantly involved in the pathogenesis of NASH and cirrhosis.14, 15 Nonetheless, the relationship between hyperleptinemia, activated endocannabinoids system, aggravated hepatic steatosis, and fibrogenesis and increased IHR in NASH cirrhotic rats remains unclear. Collectively, our study aims to explore the possible contribution of hyperleptinemia to the pathogenesis of the endothelin-1 and endocannabinoids-mediated mechanisms that cause increased IHR and portal hypertension in NASH cirrhotic rats. HF/MCD, high fat/methionine-choline-deficient; PCI-32765 nmr HSC, hepatic stellate cells; IHR, intrahepatic resistance; NASH, nonalcoholic steatohepatitis; OBRb: leptin receptor. Detailed Materials

and Methods are provided in the Supporting Information. The Zucker rats, which bear a mutation (fa) in the leptin receptor (OBRb) gene, fed HF/MCD diets were used.4-6, 13 The HF/MCD diet used consisted of 37% calories

(Cal) from fat (corn oil), 24.5% Cal from protein (lactalbumin hydrolysate), and 38.5% Cal from carbohydrate (dextrose) together with vitamins and minerals (Dyets, Bethlehem, PA) deficient in methionine and choline as recommended. The normal diet was a paired feeding protocol that controlled calorie intake using a methionine choline-sufficient diet. Alanine-glyoxylate transaminase In the first series of studies (n = 8 in each group), two groups of 3-week-old Zucker rats and two groups of age-matched lean rats were fed either the HF/MCD or normal diet for 16 weeks. This resulted in four groups: HF/MCD-Zucker rats, normal-Zucker rats, HF/MCD-lean rats, and normal-lean rats. Among the above four groups, NASH cirrhotic livers and hyperleptinemia were only observed in the HF/MCD-Zucker rats. Thus, normal-Zucker rats, HF/MCD-lean rats, and normal-lean rats that were without NASH cirrhotic livers and hyperleptinemia served as the controls for this study. In a second series of studies, the exogenous administration of mouse endotoxin free recombinant leptin (100 μg/kg/day, intraperitoneal) was given to HF/MCD+leptin-lean and normal+leptin-lean rats (n = 6) in order to directly explore the leptin-related hepatic effects in rats that have intact OBRb. In our preliminary experiments, different durations (5, 7, 10, and 13 weeks) of leptin were administrated.

14 In order to validate the relevance of the mAb

D32 10 i

14 In order to validate the relevance of the mAb

D32.10 in vivo, we used the D32.10 epitope as a probe to look for the presence of anti-E1E2A,B D32.10 epitope-binding antibodies in the serum of HCV-infected patients. The prevalence of anti-E1E2 antibodies in serum was high in patients who either resolved the infection spontaneously, or who achieved a sustained viral response (SVR) after antiviral therapy. Thus, the E1E2A,B D32.10 epitope-binding antibody response appears as associated with control of HCV infection in vivo and may be predictive of the response to HCV treatment. aa, amino acid; C, cured patients; CR, complete responders; ELISA, enzyme-linked immunosorbent assay; HDL, high-density lipoprotein; HCV, hepatitis C virus; HCVcc, infectious cell culture HCV particle; HCVpp, HCV pseudotyped particle; HCVsp, serum-derived HCV particle; HVR1, hypervariable region 1; IgG, immunoglobulin Roxadustat in vivo G; mAb, monoclonal antibody; NHS, normal human serum; NPV, negative predictive value; NR, nonresponder; NT, never-treated chronic carriers; OD, optical density; PBS, phosphate-buffered saline; PBSTG, PBS–Tween–goat serum;

PEG-IFN, Protein Tyrosine Kinase inhibitor pegylated interferon; PPV, positive predictive value; SD, standard deviation; SVR, sustained viral response; Trt, treatment; ULN, upper limit of the normal range. Human serum samples positive for HCV antibody were obtained from 194 individuals, tested by third-generation enzyme-linked immunosorbent assay (ELISA; Ortho Diagnostics), and classified according to four groups. Group 1: Fifty-two samples negative for HCV RNA were from 22 patients who had spontaneously resolved symptomatic or asymptomatic acute HCV infection in the past (≥ 10 years), and from pentoxifylline 30 patients whose date of acute infection was unknown. Only 50% (26 of 52) of samples were analyzed

for genotyping, and 25 of 26 were of genotype 1 (Table 1). Group 2: Fifty serum samples were from never-treated (NT) HCV chronic carriers. Fifty-eight percent (28 of 48) were of genotype 1 (Table 1). Their median HCV viral load was 5.8 log10 IU/mL (range: 3.4-7.8 log10 IU/mL) for 44 of 47 cases (Table 1). A total of 54% (26 of 48) showed elevated aminotransferases (median = 1.4 × upper limit of the normal range [ULN], range = 1.06-4.90 × ULN) whereas 46% (22 of 48) had normal levels (median = 0.75 × ULN, range = 0.3-1 × ULN). A total of 77% (27 of 35) exhibited no or low Metavir activity score (A0-A1) and 63% (27 of 43) had a Metavir fibrosis score of F0-F1 (Table 1). Group 3: Forty serum samples were from chronically infected patients who did not respond to multiple successive antiviral therapies with standard or pegylated interferon (PEG-IFN) in association with ribavirin in the majority of cases (77%, 30 of 39; Table 1). HCV RNA levels showed a median of 5.7 log10 IU/mL (range: 4.7-6.9 log10 IU/mL) for 27 of 35 cases (Table 1).

Although arterial embolisation of pulmonary and hepatic AVMs have

Although arterial embolisation of pulmonary and hepatic AVMs have been successfully described before, the widespread distribution of AVMs and rapid systemic deterioration in our patient precluded any chance of successful haemostasis. Although rare, women with HHT should be screened for AVMs and monitored closely during pregnancy. Contributed by “
“President:

Dr. Udom Kachintorn Vice-President: Dr. Pisaln Mairiang Dr. Teerha Piratvisuth Secretary General: Dr. Tawesak Tanwandee Vice-Secretary General: Dr. Chinnavat Sutthivana Dr. Phunchai Charatcharoenwitthaya Treasurer: Dr. Chomsri Kositchaiwat Vice-Treasurer: Dr. Sombat Treeprasertsuk Chairman, Social Affairs: Dr. Somchai Leelakusolvong Vice Chairman, Social Affairs: Dr. Taya Kitiyakara Chairman, Scientific Program: Dr. Varocha Mahachai Vice Chairman, PLX3397 concentration Scientific

Program: Dr. Pisit Tangkijvanich Chairman, Abstract Submissions: Dr. Polrat Wilairat Chairman, Dabrafenib chemical structure Publications: Dr. Piyawat Komolmit Chairman, Press/Media: Dr. Anuchit Chutaputti Chairman, AV Committee: Dr. Nopporn Anukulkarnkusol Chairman, Fund Raising: Dr. Satawat Thongsawat Chairman, Postgraduate Course: Dr. Abhasnee Sobhonslidsuk Chairman, Young Investigators Awards: Dr. Wattana Sukeepaisarnjaroen Chairman, Surgery: Dr. Soottiporn Chittmittrapap Chairman, Endoscopy: Dr. Rungsun Rerknimitr Advisory Board Members: Dr. Bancha Ovartlarnporn Dr. Chutima Pramoolsinsap Dr. Darin Lohsirirwat Dr. Kamthorn Phaosawasdi Dr. Kannikar Pornputkul Dr. Ong-Ard Praisontarangkul Glutamate dehydrogenase Dr. Pinit Kullavanijaya Dr. Sasiprapa Boonyapisit Dr. Sathaporn Manatsathit Dr. Sawadh Hitanant Dr. Sinn Anuras Dr. Surapon Chuenrattanakul Dr. Termchai Chainuvati Dr. Thawee Ratanachu-Ek Dr. Thongdee Chaipanich Dr. Uthai Khowean “
“A 67-year-old woman was admitted to our hospital with weakness, fatigue, fever, and persistent vomiting for 2 days. Physical examination showed reduced general condition and adiposity, but no abdominal tenderness. Laboratory tests revealed elevated levels of serum gamma glutamyltransferase (50 U/L [normal

< 28 U/L]) and C-reactive protein (16 mg/dL [normal < 1 mg/dL]). Serum levels of total bilirubin and direct bilirubin were normal. Blood cultures were negative. Ultrasound examination of the abdomen showed multiple hyperechoic and hypoechoic liver lesions accentuated in the right liver lobe. The further diagnostic workup included a magnetic resonance cholangiopancreatography (MRCP) which showed multiple hyperintense liver lesions. There was no visible communication between the cystic lesions and the normal biliary system (Fig. AB). In some parts of the liver, the lesions were surrounded by fibrosis. Due to persisting uncertainty of the pathology, the patient underwent ultrasound-guided fine-needle biopsy, which showed chronic portal and periportal inflammation.