Among those CM patients with CGRP levels below 72 pg/mL, 28% had

Among those CM patients with CGRP levels below 72 pg/mL, 28% had low VIP levels and just 33.3% responded as compared with 77.4% responders in the remaining 72% who had high VIP levels. Therefore, the probability of being a responder in CM

patients with CGRP levels below the threshold was significantly higher in those patients with high VIP levels vs those with low VIP levels (OR: 6.857; 95% CI: 1.583-29.707; P = .012). Among CM patients with CGRP levels above the threshold, there was only one nonresponder who also had high VIP levels. As already reported by our group using in part subjects included here, this study first confirms that interictal CGRP and VIP levels measured in peripheral blood are increased in a large series of CM learn more patients this website vs healthy subjects with no headache history. In fact, both CGRP and VIP levels in CM were twice those of controls, which should be interpreted as distant signs of activation of the sensory and parasympathetic arms of the TVS, respectively. The levels of these two neuropeptides, and especially of CGRP due to its lower variability, measured in peripheral blood and outside migraine attacks have been proposed as the first biomarkers helpful for a more objective diagnosis of CM in the context of a patient with daily or almost daily headaches and a history of migraine, which could

be of value for a better selection of treatment for CM patients.[9, 10] The impact of CM in terms of quality of life and economic burden is very relevant.13-15 Treatment of CM is not easy.[14] Even selleckchem though in clinical practice we use oral preventatives with efficacy in EM, objective evidence of efficacy in CM is available only for topiramate16-18 and, to a lesser degree, for valproic acid.[19] It was not until

this decade that the efficacy of pericranial injections of 155-195 U of onabotA was shown in two large controlled phase III trials.[11] This efficacy has also been reported in several open studies20-23 and in this series in which three quarters of our patients showed an objective and subjective response to onabotA injections. The exact mechanism of action of pericranial injections of onabotA leading to migraine prevention is still unclear, and reliable potential predictors of response have not yet been identified. In the pooled analysis of the 2 phase III trials with onabotA in CM, there was no positive correlation between 85 possible clinical predictors and response to onabotA.[11] The main finding of the present work is that interictal CGRP, and to a lesser degree, VIP levels are potentially of great help on predicting response to onabotA. In fact, both CGRP and VIP levels were significantly higher in CM patients responding to onabotA as compared with nonresponders.

Therefore, we conducted a prospective cohort study in a clinical

Therefore, we conducted a prospective cohort study in a clinical setting to assess bleeding risk attributable to gastric biopsy in patients taking antiplatelet agents and the validity of performing endoscopic biopsy with small cup biopsy forceps. Methods: The study was performed during

the 1-year for 5374 scheduled esophagogastroduodenoscopy performed. 1128 patients, PD 332991 including 65 patients taking antiplatelet agents underwent gastric biopsy with small cup biopsy forceps, and 2025 biopsy specimens were obtained from each part of the stomach. Clinical bleeding was investigated during and after endoscopy. Two pathologists assessed the presence of muscularis mucosae in biopsy specimens in addition to the suitability of specimens for histological diagnosis. Results: Ratio of appropriate

specimens obtained with small cup biopsy forceps was 99.3% (2010/2025) and muscularis mucosae was detected BTK inhibitor price in 27.8% (538/1394) of specimens. After endoscopy, 1 patient of 1049 patients who took no antithrombotic agents experienced major bleeding (0.095%); however, 65 patients receiving antiplatelet treatment experienced no bleeding. Conclusion: Endoscopic forceps with a small cup is useful and the absolute risk attributable to gastric biopsy in patients taking antiplatelet agents seems to be low. Key Word(s): 1. endoscopic biopsy; 2. antiplatelet agent; 3. bleeding; 4. biopsy forceps; 5. antithrombotic agent Presenting Author: KUNIO IWATSUKA Additional Authors: TAKUJI GOTODA, SHIN KONO, SHO SUZUKI, NAOKO YAGI, CHIKA KUSANO, MASAKATSU FUKUZAWA, TAKASHI KAWAI, FUMINORI MORIYASU Corresponding Author: KUNIO IWATSUKA Affiliations:

Tokyo Medical University, Tokyo Medical University, Tokyo Medical University, Tokyo Medical University, Tokyo Medical University, Tokyo Medical University, Tokyo Medical University Hospital, Tokyo Medical University Objective: Despite improvements in pharmacological click here and endoscopic hemostasis, gastrointestinal bleeding (GIB) remains fatal clinical event in the elderly patients. With increasing numbers of the elderly population, endoscopists might face such kind of serious cases. The aims of this study are to research treatment outcomes and clinical features of GIB in elderly patients. Methods: Medical records of 185 patients (mean age 68.2 years, range 10–99 years, male/female 123/62) with GIB who underwent esophagogastroduodenoscopy or colonoscopy from April 2012 to March 2014 were reviewed. Clinical outcomes and clinicopathological features including pre-existing co-morbidities, prescribed drugs (antiplatelet agent, anticoagulant, NSAIDs, corticosteroid) were compared between younger <70 years old) and elderly groups (≤70 years old). Results: Following features were specifically found in elderly patients (N = 100) compared to non-elderly patients (N = 85): presence of co-morbid diseases (90.0% vs. 62.4%: p < 0.001), low hemoglobin level (9.0 vs. 10.6 g/dl: p < 0.

Further investigation into the societal cost of cognitive dysfunc

Further investigation into the societal cost of cognitive dysfunction in cirrhosis is Bortezomib important to encourage routine diagnosis and therapy of MHE beyond the research setting. “
“See article in J. Gastroenterol. Hepatol. 2010; 25: 1416–1419. Drainage is needed for symptomatic or infected intraabdominal/pelvic fluid collections. The options are surgical, imaging-guided and endoscopic drainage. The surgical approach allows greater access, facilitates more thorough drainage and debridement,

and may address the predisposing condition at the same setting, but at the expense of being more invasive and associated with greater morbidity.1 An imaging-guided approach using computer tomography and ultrasound Everolimus price by the interventional radiologist is less invasive than surgical drainage. However, access for drainage may be limited by interposed organs, blood vessels, nerves and bony structures. There is also the possibility of inadvertent puncture of undetected interposed organs and vessels. Furthermore there is a need to insert an external indwelling drainage catheter for a prolonged period of time which can be uncomfortable for patients; the catheter may also be prone to slippage. Endoscopic transenteric drainage is less invasive than surgery, and may be able to access collections not possible with the imaging-guided approach. In addition, it does away with the need for an indwelling external drainage catheter because an internal

transenteric stent can be inserted, thus improving patient comfort. In the past, before the introduction of endoscopic ultrasound (EUS), endoscopic transenteric drainage was performed by puncturing the endoscopically visible intraluminal bulge caused by the fluid collection, after which guidewire and transenteric

stent insertion were performed under fluoroscopic guidance. Increasingly endoscopic drainage is being performed under real time EUS guidance.1 The difference between EUS and non-EUS guided endoscopic drainage is that during EUS-guided drainage, EUS is used to visualize the fluid collection and guide the initial puncture and guidewire insertion. All subsequent steps such as balloon dilatation of the puncture tract and stent insertion are similar between both approaches, and usually performed with fluoroscopic click here monitoring. EUS has made it possible for endoscopic drainage to be performed even in the absence of endoscopic bulging, because the collection can now be visualized directly, thus extending the spectrum of cases that are treatable endoscopically.2,3 With the use of colour Doppler ultrasound during EUS-guided drainage, EUS may potentially decrease the risk of puncturing interposed blood vessels.4 Most published data for EUS-guided drainage are in the context of pancreatic fluid collections, although drainage of liver and subphrenic abscesses has been reported.1,5 There are limited data concerning EUS-guided drainage of pelvic abscesses.

Further investigation into the societal cost of cognitive dysfunc

Further investigation into the societal cost of cognitive dysfunction in cirrhosis is PLX3397 important to encourage routine diagnosis and therapy of MHE beyond the research setting. “
“See article in J. Gastroenterol. Hepatol. 2010; 25: 1416–1419. Drainage is needed for symptomatic or infected intraabdominal/pelvic fluid collections. The options are surgical, imaging-guided and endoscopic drainage. The surgical approach allows greater access, facilitates more thorough drainage and debridement,

and may address the predisposing condition at the same setting, but at the expense of being more invasive and associated with greater morbidity.1 An imaging-guided approach using computer tomography and ultrasound VX-809 mw by the interventional radiologist is less invasive than surgical drainage. However, access for drainage may be limited by interposed organs, blood vessels, nerves and bony structures. There is also the possibility of inadvertent puncture of undetected interposed organs and vessels. Furthermore there is a need to insert an external indwelling drainage catheter for a prolonged period of time which can be uncomfortable for patients; the catheter may also be prone to slippage. Endoscopic transenteric drainage is less invasive than surgery, and may be able to access collections not possible with the imaging-guided approach. In addition, it does away with the need for an indwelling external drainage catheter because an internal

transenteric stent can be inserted, thus improving patient comfort. In the past, before the introduction of endoscopic ultrasound (EUS), endoscopic transenteric drainage was performed by puncturing the endoscopically visible intraluminal bulge caused by the fluid collection, after which guidewire and transenteric

stent insertion were performed under fluoroscopic guidance. Increasingly endoscopic drainage is being performed under real time EUS guidance.1 The difference between EUS and non-EUS guided endoscopic drainage is that during EUS-guided drainage, EUS is used to visualize the fluid collection and guide the initial puncture and guidewire insertion. All subsequent steps such as balloon dilatation of the puncture tract and stent insertion are similar between both approaches, and usually performed with fluoroscopic find more monitoring. EUS has made it possible for endoscopic drainage to be performed even in the absence of endoscopic bulging, because the collection can now be visualized directly, thus extending the spectrum of cases that are treatable endoscopically.2,3 With the use of colour Doppler ultrasound during EUS-guided drainage, EUS may potentially decrease the risk of puncturing interposed blood vessels.4 Most published data for EUS-guided drainage are in the context of pancreatic fluid collections, although drainage of liver and subphrenic abscesses has been reported.1,5 There are limited data concerning EUS-guided drainage of pelvic abscesses.

(HEPATOLOGY 2011;) The detection of hepatitis B surface antigen (

(HEPATOLOGY 2011;) The detection of hepatitis B surface antigen (HBsAg) in serum was pivotal to the 5-Fluoracil ic50 discovery of hepatitis B virus (HBV) more than 4 decades

ago and remains the cornerstone of diagnosis today.1-3 HBsAg seroclearance is considered to be the closest thing to a cure for chronic hepatitis B (CHB): it reflects immunological control of the infection and confers an excellent prognosis in the absence of preexisting cirrhosis or concurrent infections with other viruses.2-6 Not surprisingly, HBsAg seroclearance has attracted considerable attention in both natural history studies and therapeutic trials. The incidence of spontaneous HBsAg seroclearance is low, especially in younger patients. Interferon (IFN) therapy appears to be able to enhance the rate of HBsAg seroclearance from 0.72% (controls) to 2.25% per year in European

patients and from 0.07% to 0.43% per year in Asian patients.6 A greater understanding of the factors influencing HBsAg levels might enable us to improve this still further. Recently, a Ceritinib cell line wealth of new data on HBsAg quantitation has emerged, and it is becoming apparent that information on HBsAg levels can add to our understanding of both the natural history of the disease and its response to therapy. This is a good time to review and discuss issues concerning the clinical utility of HBsAg quantitation and the ways in which this may help us with patient management in the future. ALT, alanine aminotransferase; anti-HBe, antibody to hepatitis B e antigen; cccDNA, covalently closed circular DNA; CHB, chronic hepatitis B; ETV, entecavir; HBeAg, hepatitis B e antigen; HBsAg,

hepatitis B surface antigen; HBV, hepatitis B virus; HCV, hepatitis C virus; IFN, interferon; LAM, lamivudine; LdT, telbivudine; NA, nucleos(t)ide analogue; NPV, negative predictive value; PEG-IFN, pegylated interferon; PPV, positive predictive value; TDF, tenofovir. Our understanding of the pathogenesis and natural history of CHB has been facilitated by technological advances that have improved the sensitivity of both serological assays for quantifying antigens (including HBsAg) and polymerase chain reaction assays selleck kinase inhibitor for measuring HBV DNA. Several independent groups have compared HBsAg and HBV DNA levels during different phases of the disease, and their findings have been rather consistent. To put these findings into context, we must consider the HBsAg production pathway and the ways in which this is related to serum HBV DNA levels and intrahepatic covalently closed circular DNA (cccDNA). HBsAg is produced by more than one pathway (Fig. 1): the translation of transcriptionally active cccDNA molecules, which serve as a template for replication, and the translation of viral genes transcribed from integrated HBV DNA sequences in the host genome.

We prospectively enrolled HCV-positive patients with congenital b

We prospectively enrolled HCV-positive patients with congenital bleeding disorders with or without HIV coinfection. Liver function tests and platelet counts were determined and TE was performed. Aspartate aminotransferase-to-platelet

ratio index (APRI) and a simple index called FIB-4 were calculated and results were correlated with TE. A total number of 174 patients were included (23% HCV, 36% HIV/HCV coinfected, selleck products 33% with cleared HCV and 8% with ongoing HIV but cleared HCV). TE correlated significantly with APRI and FIB-4 (r = 0.60; P < 0.001 and r = 0.54; P < 0.001 respectively). This correlation was pronounced in patients with ongoing HCV infection (r = 0.67; P < 0.001 and r = 0.60; P < 0.001). Prediction of advanced fibrosis resulted in concordance rates >80% with combinations of TE plus APRI and APRI plus FIB-4. HIV/HCV coinfected patients did not present with advanced fibrosis stages when compared with HCV-monoinfected patients. Combinations of

two non-invasive markers may significantly reduce the number of liver biopsies in patients with bleeding disorders and advanced liver fibrosis. Furthermore, our data support previous studies that observed a favourable outcome in patients with HIV/HCV and a preserved immune function in times of highly active selleck antibody antiretroviral therapy. “
“Summary.  selleck kinase inhibitor We studied two families in which the probands had severe bleeding

tendency and showed low plasma levels of coagulation factor V (FV) antigen and activity. Sequence analysis of the FV gene on proband 1 demonstrated a novel G16088C homozygous missense mutation in exon 3 resulting in an Asp 68 to His substitution and on proband 2, a C69969T homozygous missense mutation in exon 23 leading to Gly2079Val. The parents of both families were each heterozygous for the corresponding FV gene defect. During their second pregnancy, the two families requested prenatal diagnosis. Chorionic villi were analysed at 12 weeks of gestation and cord blood samples were tested at 22 weeks. Microsatellite analysis performed in family 1 showed that the foetus sample was not contaminated by maternal tissue. The foetus 1 was found to be heterozygous for the familiar G16088C mutation with lower FV activity in the cord blood; the foetus 2 was a normal one. The diagnosis was confirmed after the birth. This is the first report of prenatal diagnosis for FV deficiency. “
“Summary.  Building our global family by reaching out to women, children and youth and those in sub-Saharan Africa to achieve Treatment for All. The World Federation of Hemophilia (WFH) has committed to recognizing and incorporating the critical and important challenges that are faced by women with bleeding disorders within our global family.

Various kinds of mutations of ATP7B cause Wilson disease Wilson

Various kinds of mutations of ATP7B cause Wilson disease. Wilson disease is a rare genetic disease that can be treated pharmacologically. Recognition and prompt diagnosis are very important, because Wilson disease is fatal if left untreated. In Pirfenidone this review, I summarize the pathogenesis and management of Wilson disease. “
“Background and Aims:  The adjuvant effects of probiotic-containing yogurt on second-line triple therapy

for Helicobacter pylori (H. pylori) infection have not been evaluated. Methods:  A total of 337 patients with persistent H. pylori infection, after first-line triple therapy, were randomly assigned to receive either triple therapy with (yogurt group, n = 151) or without (control group, n = 186) Will yogurt. Triple therapy consisted of 400 mg moxifloxacin q.d., 1000 mg amoxicillin b.i.d., and 20 mg esomeprazole b.i.d. for 14 days. Will yogurt contains Lactobacillus acidophilus, Lactobacillus casei, Bifidobacterium longum, and Streptococcus thermophilus. H. pylori eradication was evaluated by the 13C-urea breath test, histology, or the rapid urease test. Results:  The eradication rates by intention-to-treat analysis were 66.7% and 68.9% in the control and yogurt groups, respectively (P = 0.667). The eradication rates by per-protocol

selleck analysis were 78.5% and 86% in the control and the yogurt groups, respectively (P = 0.110). The adverse event rates were 25.3% and 28.5% in the control group and yogurt group, respectively (P = 0.508). Conclusions:  The addition of yogurt containing probiotics to moxifloxacin-containing second-line treatment neither improved H. pylori eradication rates nor reduced the adverse events of treatment. “
“Liver cirrhosis is a predominant risk factor for hepatocellular carcinoma (HCC). However, the mechanism underlying the progression

from cirrhosis to HCC remains unclear. Herein we report the concurrent increase of liver progenitor cells (LPCs) and transforming growth factor-β (TGF-β) in diethylnitrosamine (DEN)-induced rat hepatocarcinogenesis and cirrhotic livers of HCC patients. Using several experimental approaches, including 2-acetylaminofluorene/partial selleck kinase inhibitor hepatectomy (2-AAF/PHx) and 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)-elicited murine liver regeneration, we found that activation of LPCs in the absence of TGF-β induction was insufficient to trigger hepatocarcinogenesis. Moreover, a small fraction of LPCs was detected to coexpress tumor initiating cell (T-IC) markers during rat hepatocarcinogenesis and in human HCCs, and TGF-β levels were positively correlated with T-IC marker expression, which indicates a role of TGF-β in T-IC generation. Rat pluripotent LPC-like WB-F344 cells were exposed to low doses of TGF-β for 18 weeks imitating the enhanced TGF-β expression in cirrhotic liver.

However, aminotransferase vary with

However, aminotransferase vary with Small molecule library cell line confounding factors (age, sex, body mass index (BMI), alcoholism, diabetes, etc). Normal aminotransferase does not rule out advanced liver disease. Currently used normal cut-offs were determined in pre-hepatitis C and non-alcoholic fatty liver disease era. Recently, different cut-off of aminotransferase for adult males(30 IU/l) and females(19 IU/l) is suggested. In India, we use normal range of

aminotransferase directly borrowed from western data or as directed on commercial kits. There are no guidelines for cut-off of aminotransferase in pediatric population. This study was planned to determine aminotransferase in asymptomatic healthy school children (AHSC) with normal BMI and no confounding factors. Methods: This prospective study was done during 2012 in 17 schools of Anand, western India. Total 3368 AHSC(5-18 yrs) agreed for clinical evaluation (history, examination and anthropometry), laboratory testing ICG-001 order (ALT, AST, HBsAg, antiHCV, glucose, creatinine, cholesterol, bilirubin and

complete blood counts) and abdominal ultrasonography. Only AHSC with normal BMI(2716) were further analyzed. Confounding factors like hepatitis B (1), fatty liver disease(16), diabetes(2), dyslipidemia(24), elevated ALT&gt40 IU/l(42), elevated AST&gt40 IU/l(38), thallassemia (4), elevated bilirubin&gt1.5 mg/dl(9), and malaria(1) were also excluded from 2716 AHSC. In remaining AHSC (2615), mean age, BMI, ALT and AST values were analyzed. Results: In study population of 2615 AHSC with normal BMI and no confounding factors, mean age was 10.5±3.50 years, mean BMI=15.6±2.28 kg/m2, mean ALT=15.4±5.49 IU/l,

mean AST=20.9±5.25 IU/l. In males, mean age was 10.5±3.68 selleck years, mean BMI=15.8±2.48 kg/m2, mean ALT=15.2±5.40 IU/l and mean AST=20.6±5.03 IU/l. In females, mean age was 10.5±3.38 years, mean BMI=15.5±2.14 kg/m2, mean ALT=15.5±5.55 IU/l and mean AST=21.1±5.38 IU/l. Conclusion: There is need to reevaluate cutoffs for ALT and AST in pediatric population. Key Word(s): 1. aminotransferase ; 2. body mass index; 3. school children; 4. gender; Presenting Author: NIKHIL PATEL Additional Authors: DEEPAK AMARAPURKAR, SANJAY PATEL, JAYESH BHATT, RITESH PRAJAPATI, PAYAL PATEL, SULABH SOLANKI, JIGNESH SHAH Corresponding Author: NIKHIL PATEL Affiliations: nil Objective: Pediatric liver diseases pose risk of morbidity and mortality, which is modified with early detection-treatment. In hospital-based pediatric studies, viral, Wilson’s disease, infantile cholestasis and cryptogenic etiologies predominate. Epidemiological studies are lacking in India. This prospective study was planned to define prevalence and etiology of liver disease in asymptomatic healthy school children (AHSC). Methods: This prospective study was done during 2012 in 17 schools of Anand. 10000 students participated by filling a questionnaire.

Rockey – Consulting: Ono; Grant/Research Support: Sucampo, Sucamp

Rockey – Consulting: Ono; Grant/Research Support: Sucampo, Sucampo, Hyperion, Actelion William M. Lee – Consulting: Eli Lilly, Novartis; Grant/Research Support: Gilead, Roche, Vertex, BI, Anadys, BMS, merck; Speaking and Teaching: Merck The following people have nothing to disclose: Lafaine Grant, Jiezhun Gu, Saleh Alqahtani Background: Recently, cholangiocarcinoma cases have epidemically developed among offset color proof-printing workers check details of a printing company in Japan. In this series, DNA damage of biliary epithelial cells due to inhalation of organic solvents including 1, 2-dichloropropane and/or dichloromethane (DCM) is supposed to be associated with the carcinogenic

process. The metabolism of DCM proceeds through two pathways; a cytochrome P450 (CYP) 2E1 dependent pathway and a Thetaclass glutathione S-transferase (GST) T1-1-catalyzed pathway, where the latter has been implicated in carcinogenicity. Aim: This study was performed to examine the carcinogenic process of cholangiocarcinoma cases developing among workers of the printing company. Methods: Immunostaining of GST T1-1, CYP2E1, and gamma-H2AX was performed using formalinfixed, paraffin-embedded tissue sections of the cholangiocarcinoma cases of the printing company (n = 5). For comparison, tissue sections of cholangiocarcinoma associated with hepatolithiasis (n =16) as well as

normal livers (n =10) were used. All cholangiocarcinoma cases were surgically resected, and were histologically associated with biliary intraepithelial neoplasia click here (BilIN). Gamma-H2AX was used as a marker of DNA double strand break. Results: The immunohistochemical Lumacaftor supplier expression of GST T1-1 was observed in biliary epithelial cells of normal biliary tract and hepatocytes. The expression

of GST T1-1 was also observed in the foci of BilIN and invasive adenocarcinoma for all cholangiocarcinoma cases used. The immunohistochemical expression of CYP2E1 was observed in hepatocytes of normal livers, while normal biliary epithelial cells as well as BilIN and cholangiocarcinoma were typically negative. Gamma-H2AX was detected in foci of invasive adenocarcinoma in 4 of 5 cholangiocarcinoma cases of the printing company, and 3 cases further showed occasional expression of gamma-H2AX in non-neoplastic biliary epithelial cells as well as BilIN. In the cases of cholangiocarcinoma associated with hepatolithiasis, 7 of 16 cases showed the expression of gamma-H2AX in the invasive foci, whereas non-neoplastic biliary epithelial cells and BilIN were typically negative. Conclusions: These results suggest that the inhalation of organic solvents may act as a carcinogen for biliary epithelial cells by causing DNA damage through the GST T1-1-catalyzed pathway, and provide evidence that supports the causal relation between organic solvent inhalation and cholangiocarcinoma development in the patients.

Clinical outcomes were predefined in the HALT-C Trial protocol an

Clinical outcomes were predefined in the HALT-C Trial protocol and included death due to any cause, liver-related death, HCC, and hepatic decompensation (ascites, hepatic encephalopathy, variceal hemorrhage, or spontaneous bacterial peritonitis); we also collected data on liver transplantation. Two definitions

of HCC were adopted in the HALT-C Trial: “definite” HCC and “presumed” HCC. Definite HCC was defined by histologic confirmation or a new, ≥2-cm mass lesion on imaging with AFP levels increasing to >1000 ng/mL. Presumed HCC was defined as a new mass lesion on ultrasound in the absence of histology and AFP < 1000 ng/mL selleck in conjunction with one of the following characteristics: (1) two liver imaging studies showing a mass lesion with characteristics of HCC, (2) progressively enlarging lesion on ultrasound and leading to death, or (3) one additional imaging study showing a mass lesion with characteristics of HCC that either increased in size over time or was accompanied by increasing AFP levels.11 An outcome committee, whose

members consisted of a rotating panel of three clinical site investigators blinded to study participant and clinical site, reviewed and adjudicated the validity of each clinical outcome. For the current analysis, we assessed overall mortality (i.e., death from any cause) or liver transplantation, and liver-related morbidity and mortality. Death from any cause or liver transplantation was defined this website as any patient who died (of any cause) or had undergone liver transplantation. The four categories of liver-related morbidity and mortality were: (1) Any liver-related clinical outcome: all patients in whom decompensated liver disease (ascites, variceal bleeding, hepatic encephalopathy, or spontaneous bacterial peritonitis) or HCC (presumed or definite) developed, or who had undergone liver transplantation, or died from conditions related to liver disease. For the calculation of

the cumulative selleck chemical incidence of any liver-related outcomes, patients were censored at the time when the first outcome developed. (2) Decompensated liver disease: all patients whose first clinical outcome was decompensated liver disease. (3) HCC: all patients in whom, at any time during the study, definite or presumed HCC developed. (4) Liver-related death or liver transplantation: any patient who died as the result of a liver-related cause, based on the opinion of the clinical site principal investigator, or who had undergone liver transplantation. Statistical analyses were performed at the Data Coordinating Center (New England Research Institute, Watertown, MA) with SAS software, release 9.1 (SAS Institute Inc., Cary, NC). The chi-squared and analysis of variance tests were used to determine categorical and continuous variables that were significantly different between the SVR group and the two comparison groups (NR and BT/R).