Ablative therapy continues to develop. The most recent option is radiofrequency ablation which in one study had a very high reported efficacy, with 97% of patients who had find more their non-dysplastic BE ablated being free of metaplasia 30 months post-therapy.86 Unfortunately, in the US, ablative therapy is already being widely used in

patients with non-dysplastic BE by “competitive” clinicians before adequate definition of the risk/benefit balance.15 This reality should not distract researchers from the strong possibility that if ablative therapy permanently removes the need for ongoing endoscopic surveillance, it would be cost effective87 (Fig. 2). All should be revealed in the next 10 years! As discussed above, the diagnosis of low-grade dysplasia when confirmed by a www.selleckchem.com/hydroxysteroid-dehydrogenase-hsd.html pathologist expert in BE (which eliminates up to 85% of low grade dysplasia diagnoses), indicates substantial EA risk. This risk level, which has been defined very recently,49,50,65 argues strongly for use of ablative or even mucosal resective therapies.47,87 Radiofrequency ablation has achieved promising results in patients with low-grade dysplasia.88 The choice of therapy for primary management of high-grade dysplasia seems such a politically charged topic that even very recent general reviews are disappointingly

circumspect in their discussion of this.2–4 Major guidelines for BE management were published in 2005 (two), 2006 and 2008, and all list esophagectomy as an appropriate primary therapy for high-grade dysplasia.2,3 These guidelines would have taken at least one year to formulate and publish, so they rely on the literature available between 3 and 6 years ago. So much has been learnt since then about high-grade dysplasia and its management by endoscopic therapy that the recommendations of these guidelines for management of high-grade

dysplasia are seriously outdated. Presence of high-grade dysplasia does not indicate that EA (even selleck chemicals llc intramucosal) will develop in the immediate future (see above). If the worst case estimate of EA risk, that of Overholt is used69,70 (Fig. 4), the yearly risk of EA development in one patient is just over 10%. There is time to digest the following information. Several expert centers have shown that endoscopic therapy is highly effective at removing and preventing recurrence of high-grade dysplasia for up to more than 5 years, with minimal risk and morbidity.89–94 Some of the data for high-grade dysplasia are a little difficult to tease out separately from outcomes of endoscopic therapy of intramucosal EA, but the excellent outcomes for EA attest to what endoscopic therapy can also achieve in high-grade dysplasia95 (Fig. 5).

The three HP+ patient who were resistant to fluoroquilolones were HetEM (*2/*1).

Eradication with 14 days regime (PPI+clarithromycin+amoxycilin) was near 96%. Conclusion: More epidemiological data in Greek population are needed to establish the real prevalence of the CYP2C19 polymorphisms which, combined with the antibiotic resistant molecular test could be useful for difficult to treat patients. Key Word(s): 1. CYP2C19; 2. Helicobacter Selleck NVP-AUY922 pylori; 3. Resistance; 4. Eradication; Presenting Author: LIAOSHENG YIN Additional Authors: CHENJIAN YONG, HUJIAN FANG Corresponding Author: CHENJIAN YONG Affiliations: The People’s Hospital of JianXi Province; The People’s Hospital of JianXI Province; The People’s Hospital of Jianxi Province

Objective: To Study the gastric mucosal proteins expression in chronic gastictis rat with damp-heat FK506 cell line syndrome of spleen-stomach and investigate the pathogenesis related to the chronic gastictis. To observe the differential expression of gastric mucosal protein in chronic gastictis rat model with damp-heat syndrome of spleen-stomach after treatment with sanren decoction and investigate the mechanism of sanren decoction in chronic gastictis Methods: The rats models were reproduced by quantified method. Proteomic two-dimensional gel electrophoresis technique was used to separate total gastric mucosal protein. The two-dimensional gel electrophoresis maps were analysised to decect protein spots expressed differently by

PDquest 8.0 software, the protein spots expressed differently was identified by MALDI-TOF/TOF-MS. Results: the protein spots were 1025 ± 39, 994 ± 51, 1087 ± 33, deteced from two-dimensional gel electrophoresis profiles of normal control group, model group and sanren decoction group respectively. The protein spots of differential expression were 74 between model group and normal control group,30 spots up-regulated in model group while 44 spots down-regulated; The protein spots of differential expression were 75 between sanren decoction group and model group,49 spots up-regulated in sanren decoction group while 26 spots down- regulated. this website Five protein spots of differential expression were identified successfully. The identificated results are: heat shock protein 72, heat shock protein 60, protein disulfide-isomerase, malate dehydrogenase, unnamed protein Conclusion: The pathogenesis of chronic gastictis with damp-heat syndrome of spleen-stomach may be related to energy metabolism disorders and stress, the mechanism of sanren decoction in the chronic gastritis with damp-heat syndrome of spleen-stomach may adjust the differential expression of gastric mucosal protein. Key Word(s): 1. chronic gastritis; 2. Damp-heat syndrome; 3. proteome; 4. Sanren decoction; Presenting Author: YINGLIAN XIAO Additional Authors: FRÉDÉRIC NICODÈME, ZHIYUE LIN, SABINE ROMAN, PETER J.

The three HP+ patient who were resistant to fluoroquilolones were HetEM (*2/*1).

Eradication with 14 days regime (PPI+clarithromycin+amoxycilin) was near 96%. Conclusion: More epidemiological data in Greek population are needed to establish the real prevalence of the CYP2C19 polymorphisms which, combined with the antibiotic resistant molecular test could be useful for difficult to treat patients. Key Word(s): 1. CYP2C19; 2. Helicobacter Selleck ABT263 pylori; 3. Resistance; 4. Eradication; Presenting Author: LIAOSHENG YIN Additional Authors: CHENJIAN YONG, HUJIAN FANG Corresponding Author: CHENJIAN YONG Affiliations: The People’s Hospital of JianXi Province; The People’s Hospital of JianXI Province; The People’s Hospital of Jianxi Province

Objective: To Study the gastric mucosal proteins expression in chronic gastictis rat with damp-heat R428 syndrome of spleen-stomach and investigate the pathogenesis related to the chronic gastictis. To observe the differential expression of gastric mucosal protein in chronic gastictis rat model with damp-heat syndrome of spleen-stomach after treatment with sanren decoction and investigate the mechanism of sanren decoction in chronic gastictis Methods: The rats models were reproduced by quantified method. Proteomic two-dimensional gel electrophoresis technique was used to separate total gastric mucosal protein. The two-dimensional gel electrophoresis maps were analysised to decect protein spots expressed differently by

PDquest 8.0 software, the protein spots expressed differently was identified by MALDI-TOF/TOF-MS. Results: the protein spots were 1025 ± 39, 994 ± 51, 1087 ± 33, deteced from two-dimensional gel electrophoresis profiles of normal control group, model group and sanren decoction group respectively. The protein spots of differential expression were 74 between model group and normal control group,30 spots up-regulated in model group while 44 spots down-regulated; The protein spots of differential expression were 75 between sanren decoction group and model group,49 spots up-regulated in sanren decoction group while 26 spots down- regulated. selleck screening library Five protein spots of differential expression were identified successfully. The identificated results are: heat shock protein 72, heat shock protein 60, protein disulfide-isomerase, malate dehydrogenase, unnamed protein Conclusion: The pathogenesis of chronic gastictis with damp-heat syndrome of spleen-stomach may be related to energy metabolism disorders and stress, the mechanism of sanren decoction in the chronic gastritis with damp-heat syndrome of spleen-stomach may adjust the differential expression of gastric mucosal protein. Key Word(s): 1. chronic gastritis; 2. Damp-heat syndrome; 3. proteome; 4. Sanren decoction; Presenting Author: YINGLIAN XIAO Additional Authors: FRÉDÉRIC NICODÈME, ZHIYUE LIN, SABINE ROMAN, PETER J.

Portal hemodynamics were assessed by HVPG measurement, whereas vWF-Ag levels were measured by enzyme-linked immunosorbent assay. During follow-up, complications of liver cirrhosis, death or transplantation were recorded. Two hundred LY2606368 cell line and eighty-six patients (205 male and 81 female; mean age, 56 years) with liver cirrhosis were included. vWF-Ag correlated with HVPG (r = 0.69; P < 0.0001) and predicted CSPH independently of Child Pugh score. Higher vWF-Ag levels were associated with varices (odds ratio [OR] = 3.27; P < 0.001), ascites (OR = 3.93; P < 0.001) and mortality (hazard ratio: 4.41; P < 0.001).

Using a vWF-Ag cut-off value of ≥241%, the AUC for detection of CSPH in compensated patients was 0.85, with a positive predictive value and negative predictive value of 87% and 80%, respectively. Compensated DAPT cell line patients had 25% mortality after 53 months if the vWF-Ag was <315% compared to 15 months in patients

with vWF-Ag >315% (P < 0.001). Decompensated patients had a mortality of 25% after 37 and 7 months if their vWF-Ag was <315% and >315%, respectively (P = 0.002). In compensated patients with a vWF-Ag >315% median time to decompensation or death was 32 months compared with 59 months in patients with vWF-Ag <315%. vWF-Ag equals Model for End-Stage Liver Disease (MELD) in mortality prediction (area under the curve [AUC] = 0.71 for vWF-Ag versus AUC = 0.65 for MELD; P = 0.2). Conclusion: vWF-Ag is a new, simple and noninvasive predictor of CSPH. A vWF-Ag cut–off value at 315% can clearly stratify patients with compensated and decompensated liver cirrhosis in two groups with completely different survival. vWF-Ag

may become a valuable marker for the prediction check details of mortality in patients with liver cirrhosis in clinical practice. (HEPATOLOGY 2012) Portal hypertension (PH) accounts for the major complications of liver cirrhosis, such as ascites, variceal hemorrhage and decompensation. Early diagnosis of PH is essential for the management of patients with cirrhosis. In previous studies, it has been shown that early diagnosis, leading to adequate treatment, can significantly reduce the mortality rate of PH-related complications.1, 2 Recent guidelines recommend the diagnosis of PH by the measurement of hepatic venous pressure gradient (HVPG).3 Clinically significant portal hypertension (CSPH; HVPG ≥10 mmHg) is associated with a higher risk of liver-related mortality, development of varices, and other PH-related complications. An HVPG ≥12 mmHg is associated with a higher risk of bleeding from varices.1 Measurement of HVPG is an invasive procedure and is only available in specialized centers. Noninvasive markers could be a clear advantage for the management of patients with cirrhosis, but none of the markers investigated, so far, have shown satisfactory specificity and sensitivity to enter clinical routine.

The results of pathogenicity test, morphology studies and sequence analyses based on ITS and β-tubulin loci indicated that the disease was caused by Colletotrichum truncatum. The pathogen produced elliptic, yellow spots with chlorotic halos on the surface of the fruit, and the lesion become depressed gradually. Grey to black acervuli appeared on the lesion surface in concentric circles later. This is the first report of dragon fruit anthracnose caused by this pathogen in China. “
“Botrytis disease of tea

was reported for the first time from Rize, Turkey. The causal agent was identified as Botrytis cinerea based on morphological and cultural characteristics. Also, the species-specific PCR assays confirmed the identification of all B. cinerea isolates. The pathogen caused blight of shoots, buds, flowers and young leaves, shoot canker Olaparib clinical trial and leaf spots. The disease was observed in Rize central district and Derepazarı, Çamlıhemşin, Çayeli, Pazar, Hemşin, İkizdere, Ardeşen and AZD1152 HQPA İyidere districts. “
“In

July 2010, symptoms suggestive of phytoplasma infection were observed on Rose Balsam (Impatiens balsamina) around Yangling, China. Nested polymerase chain reaction with universal 16S rDNA phytoplasma primers P1/P6 and R16F2n/R16R2 yielded amplicons of expected size (1.2 kb) from all symptomatic, but not asymptomatic, leaf samples. Sequencing results and NCBI BLASTn analysis of the 1246 bp products (R16F2n/R16R2) showed that the phytoplasma belonged to group 16SrI. Restriction fragment length polymorphism and phylogenetic analysis showed the

phytoplasma had a close relationship to subgroup 16SrI-D. This is the first report of a phytoplasma infecting Rose Balsam. “
“Leaf curl disease symptoms were observed in tomato crop grown in a tomato field at Matera district of Bahraich, India, in March 2013 with an 85% disease incidence. The infected plants exhibited leaf curl symptoms accompanied with puckering, vein swelling and stunting of the whole plant. PCR carried out with begomovirus coat protein gene and DNA beta-specific primer sets resulted in positive amplification of ~775 bp and 1.35 kbp, respectively, with all symptom-bearing plant samples. BLASTn and phylogenetic analyses of CP gene sequences showed highest and close relationship selleck chemicals llc with Croton yellow vein mosaic virus (CYVMV) isolates, while the phylogenetic study of betasatellite sequence showed distinct relationships with other begomovirus associated betasatellites reported from India and abroad. This is a first report of a CYVMV associated with tomato leaf curl disease in India. “
“Virus-like chlorotic symptoms were observed on tomato plants, cv. Velocity, grown in a greenhouse, region of Plovdiv. Samples collected from the leaves with interveinal yellowing and with initial interveinal chlorosis were tested for virus presence.

In addition, bile acids were determined by gas chromatography in hepatovenous effluate pooled between minute 55 and 115. Quantification of bile acid levels by capillary gas chromatography was performed as described earlier.25, 26 For details, see Supporting

Information Data. Biliary bile acids were further characterized by LC-MS/MS in order to discriminate between conjugated and nonconjugated check details bile acids as described earlier.27 Biliary bile acid concentrations lower than 0.01 mmol/L were set as zero. Biliary secretion of the Mrp2 substrate, GS-DNP, was determined spectrofluorometrically as described earlier.13, 14 For details, see Supporting Information Data. For quantification of hepatocellular damage, activity of lactate dehydrogenase (LDH) in the hepatovenous AG-014699 in vitro effluate was determined by an enzymatic assay as described.28 Active caspase-3 and cleaved cytokeratin 18 were determined by immunofluoresecence on cryosections of rat liver tissue as described previously.25,

29 Caspase-3–positive hepatocytes with concomitant cytokeratin intermediate filament breakdown were counted in 40 different high-power fields per sample for quantification of apoptotic cell death. Human HepG2 hepatoblastoma cells were stably transfected with a pcDNA3.1/Na+-taurocholate cotransporting polypeptide (Ntcp) construct (Ntcp-HepG2 cells).30 After cultivation, the cells were incubated in minimal essential medium (Eagle) with bile acids or DMSO (0.025%, vol/vol; control) for 4 hours. After fixation, Ntcp-HepG2 cells were incubated with an anti-cleaved caspase-3 antibody for quantification of apoptosis. Subsequently, cells learn more were incubated with a secondary anti-rabbit immunoglobulin G antibody. Nuclear DNA fragmentation was disclosed with Hoechst 33342. The studies were conducted on a Zeiss Axiovert 135TV microscope. Living and dead cells were counted by two examiners independently, and results were expressed as percentage of total cells. For details, see Supporting Information Data. Ntcp-transfected HepG2 cells were cultured and exposed to bile acids. Quantification of

apoptosis was performed by immunoblotting31 and fluorescence techniques. For details, see Supporting Information Data. Results were expressed as mean ± standard deviation (SD). Differences between the various groups were assessed for statistical significance by analysis of variance (ANOVA) with Tukey’s post-hoc test. Statistical significance was assumed when P values were <0.05. Bile flow in rat livers was 1.1 ± 0.1 μL/minute/g liver (n = 65) after 45 minutes of perfusion with KRB, reflecting an adequate secretory function of IPRL. Addition of CDNB (30 μmol/L), the precursor of the Mrp2 model substrate GS-DNP, between minute 65 and 75 led to a transient increase of bile flow due to its choleretic property as observed previously.

Advanced patient age is not a contraindication for surgical treatment. Key Word(s): 1. advanced gastric cancer; 2. metastatic; 3. palliation; 4. surgery Presenting Author: XUEYUAN CAO Additional Authors: DONG HUI CAO, JING JIANG, TETSUYA TSUKAMOTO, MASAHIRO OSHIMA Corresponding Author: XUEYUAN CAO Affiliations: First Hospital of Jilin University, First Hospital of Jilin University, School of Medicine,

Fujita Health University, Kanazawa University Objective: 18β-Glycyrrhetinic acid (GRA), extracted from Liquorice root (Glycyrrhiza glabra), is known for its anti-tumor properties. And the anti-tumor properties might correlates with miRNA expression level, while the mechanism and target genes are not clear. K19-C2mE transgenic

(Tg) mice model could spontaneously develop the hyperplastic tumors in stomach. The purpose of this study was to systematically identify miRNAs correlated with hyperplastic tumor progression using K19-C2mE GSK126 concentration Tg mice model. Methods: K19-C2mE transgenic animal model of gastric tumor was established by Oshima M. Six-week-old K19-C2mE Tg mice were randomly divided into two groups: Control group (n = 40) and GRA-treated group ((n = 40, drinking water containing 0.05% GRA). After 52 weeks, total RNA enriched in miRNA samples were extracted from the tumors of Control group and GRA-treated group Caspase inhibitor clinical trial (mirVana™ miRNA Isolation Kit, ambion), reverse-trancribed (TaqMan® MicroRNA Reverse Transcription Kit) and assayed using Affymetrix GeneChip miRNA 3.0 Array. The incidence of gastric tumors was also detected. Results: The tumor incidence was decreased from 77.8% (28/36) to 33.4% (13/39) (P = 0.002) after GRA selleck inhibitor administration. MicroRNA array analysis found 30 miRNAs expression levels changed significantly (P 2.0), and 19 microRNAs were up-regulated and 11 miRNAs were down-regulated by GRA treatment. Two miRNAs correlated with tumor growth, MiRNA-128 and miRNA-30 were significantly down-regulated. And the abnormal

expression of miRNA-128 and miRNA-30 was correlated with Wnt/β-Catenin/BCL9 signaling pathway. Conclusion: 18β-Glycyrrhetinic acid could inhibit hyperplastic tumor growth and progression in K19-C2mE transgenic mice, and the inhibition effects might correlate with miRNA modulation. This work was supported by Norman Bethune Program of Jilin University [2013025], National Natural Science Foundation of China (81072369 and 81273065). Key Word(s): 1. miRNA-128; 2. miRNA-30; 3. 18ß-glycyrrhetinic acid; 4. gastric tumors; 5. transgenic mice Presenting Author: DONG HUI CAO Additional Authors: XUEYUAN CAO, JING JIANG, TETSUYA TSUKAMOTO, MASAHIRO OSHIMA Corresponding Author: XUEYUAN CAO Affiliations: First Hospital of Jilin University, First Hospital of Jilin University, School of Medicine, Fujita Health University, Kanazawa University Objective: Canolol (4-vinyl-2, 6-dimethoxyphenol), a natural antioxidant product, was shown anti-inflammatory and anti-tumor effects.

18–22 Finally, the p.G191R variant in the serine protease 2 (PRSS2) gene encoding anionic trypsinogen was shown to afford protection against chronic pancreatitis.23 Taken together, the genetic studies indicate that chronic pancreatitis is a multigenic disease, and the balance between risk and protective genetic factors determines susceptibility. The genetics LDE225 ic50 of PRSS1, PRSS2, SPINK1, and CFTR mutations in chronic pancreatitis has been the subject of excellent reviews.2,3,14,15,24,25 Functional studies with mutant cationic trypsinogens demonstrated that

the most frequently and consistently found phenotypic change was an increased propensity for trypsin-mediated trypsinogen activation, also referred to as autoactivation.26–30 On the basis of these findings, we proposed that most PRSS1 variants are gain-of-function mutations that cause chronic pancreatitis by promoting premature C646 nmr trypsinogen activation in the pancreas. We and others showed that genetic variants in the SPINK1 gene are loss-of-function

mutations that diminish the expression of the inhibitor, either at the mRNA or at the protein level, thereby impairing its protective function.31–35 Finally, in contrast to the pathogenic PRSS1 and SPINK1 mutations, we found that the p.G191R variant in PRSS2 results in rapid autodegradation of anionic trypsinogen, and thereby affords protection against chronic pancreatitis.23 Conceptually, the properties of p.G191R are noteworthy because they highlight the protective

role of trypsinogen degradation against chronic pancreatitis. Taken together, the genetic and biochemical evidence defines a pathological pathway in which the imbalance between intrapancreatic trypsinogen activation, trypsinogen degradation, and trypsin inhibition increases the risk for the development of chronic pancreatitis (Fig. 1). In 2007, an international team of scientists reported that loss-of-function variants in the chymotrypsin C (CTRC) gene are risk factors for chronic pancreatitis, and this finding was replicated by an independent study published shortly thereafter.36,37 Screening of CTRC in patients affected by chronic pancreatitis was stimulated by selleck inhibitor biochemical studies from our laboratory, which demonstrated that CTRC plays an important role in regulating trypsinogen activation and degradation. The initial genetic experiments took place at the University of Leipzig in Germany, where Niels Teich and Jonas Rosendahl used direct DNA sequencing to investigate 100 patients with idiopathic and hereditary chronic pancreatitis and found variants in four patients. The senior author of this review visited Leipzig in 2006 and still recalls the palpable excitement these initial observations elicited.

Histopathologic examination revealed epitheloid granulomatous with caseating necrosis and presence of Langerhan’s giant cells. Therefore, postoperative diagnosis Cell Cycle inhibitor was revealed tuberculosis of cholecystitis. The patient tolerated the procedure well and was discharge 1 week following surgery without any problems. The patient was started on anti tubercular treatment. Conclusion: Herein, we present a case of tuberculous cholecystitis with cholecysto-colonic fistula.

Key Word(s): 1. tuberculosis cholecystitis; 2. cholecysto-colonic fistula Presenting Author: JIN KYEONG CHO Additional Authors: Na Corresponding Author: JIN KYEONG CHO Affiliations: Seoul Medical Center Objective: Introduction After successful common bile duct (CBD) stone removal by endoscopic retrograde cholangiopancreatography (ERCP), high prolonged jaundice is very confused for the next decision (ERCP for remnant stone or other rare causes). With assurance of removal see more of CBD stone and no remnant stone, Liver biopsy may be useful for jaundice of parenchymal origin but invasive. In such cases, steroid challenge test is useful both diagnosis and treatment. Case description

A 62-year-old male presented with colicky right upper quadrant pain. Laboratory tests showed total bilirubin of 7.6 mg/dL, aspartate aminotransferase (AST) 60 IU/L, alanine aminotransferase (ALT) 15 IU/L, alkaline phosphatase (ALP) 60 IU/L and gamma-glutamyltranspeptidase

(γ-GT) 71 IU/L. At abdomen CT, There was single 1.3 cm sized distal CBD stone and diffuse dilatation of upstream bile duct and cystic duct. The patient underwent endoscopic retrograde biliary drainage (ERBD) by plastic stent because of long procedure time for cannulation. But 5 days after the ERBD, his total bilirubin increased to 18.7 mg/dL. A second ERCP was carried out, which revealed patent biliary stent and CBD stone was removed successfully. After 2 days of second ERCP, total bilirubin level increased to 19.5 mg/dL. At second abdomen CT, there was no remnant stone. It was presumed that intrahepatic cholestasis was occurred by intrahepatic bile duct inflammation from contrast agent or pethidine. selleck kinase inhibitor P rednisolone was started (30 mg/day) for three days, which caused a significant improvement of jaundice and bilirubin level. But 7 days later, his bilirubin raised up to 20.3 mg/dL. It was certain that prednisolone improved his cholestasis. Prednisolone started again and after use of 30 mg/day of prednisolone for 7 days, total bilirubin fell to 10 mg/dL, and his jaundice was progressively declined. Steroid was used and tapered off during a month. He had normal bilirubin level and normal liver function tests. Key Word(s): 1. ERCP; 2.

HEPATOLOGY 2010 A diagnosis of hepatotoxicity must be considered when liver injury is identified in a person taking a prescription drug, herbal, or over-the-counter product, even Abiraterone clinical trial if there is already preexisting liver disease.1-5 Because there is currently no specific marker of drug-induced liver injury (DILI), the diagnosis rests on excluding other conditions that can mimic such injury. The diagnosis is especially difficult when affected persons are taking multiple products, any one of which might be responsible, and because of possible synergism between drugs.1, 6-8 In the traditional diagnostic approach to suspected DILI, which involves

clinical, biochemical, and histological evaluation, www.selleckchem.com/products/Imatinib-Mesylate.html attempts are made to establish the latency between the start of the drug and the onset of injury, its clinical signature, the exclusion of alternate etiologies, evidence of improvement of the liver injury upon drug withdrawal (dechallenge), and the effect of deliberate or inadvertent rechallenge. When performed by an experienced clinician, the assessment is considered by expert opinion. However, even for experts, the diagnosis of DILI can be problematic because of the inherently subjective nature of this approach. Efforts have therefore turned toward developing more objective diagnostic strategies through the creation of specific instruments such as the Roussel-Uclaf Causality Assessment

Method (RUCAM), the Maria and Victorino method, and the Naranjo scale, the last designed to assess all forms of adverse drug reactions.9-13 In a head-to-head comparison of these instruments, RUCAM has been found to perform best for diagnosing hepatotoxicity, but it is cumbersome and therefore is rarely used in clinical

practice. The Drug-Induced Liver Injury Network (DILIN) is a multicenter study whose primary aims are to identify and collect information on bona fide cases of drug-induced liver disease and to obtain serum, DNA, and liver tissue to allow for mechanistic investigation. When the study was being planned, the decision was made to assess causality with both expert opinion and RUCAM. A highly structured expert opinion method was developed that was specifically designed to include standardized terminology and specific methodology, and it is hereafter called find more structured expert opinion. It was hypothesized that this approach may have certain advantages in comparison with RUCAM. This report describes how the expert opinion approach was developed and refined and compares its effectiveness to that of RUCAM.14 ALT, alanine aminotransferase; AP, alkaline phosphatase; AST, aspartate aminotransferase; CRF, case report form; DCC, data coordinating center; DILI, drug-induced liver injury; DILIN, Drug-Induced Liver Injury Network; INR, international normalized ratio; MAD, maximum absolute difference; RUCAM, Roussel-Uclaf Causality Assessment Method; ULN, upper limit of normal.