Disclosures: The following people have nothing to disclose: Lisa B. VanWagner, Marina Serper, Raymond Kang, Anton I. Skaro, Josh Levitsky, Samuel Hohmann, Donald M. Lloyd-Jones Calcineurin inhibitors (CNI) induce chronic renal dysfunction. Switching CNI to mycofenolate mofetil (MMF) monotherapy remains controversial due to an increased risk of acute rejection. To safely withdraw CNI, mycophenolic EPZ015666 concentration acid (MPA) should be monitored. Aims: 1) Define a safe MPA targeted exposure (AUC). 2) Study the benefit and efficacy

of MMF monotherapy under therapeutic drug monitoring. Methods: 1) To define a safe MPA targeted exposure, 18 stable LT recipients previously treated with MMF monotherapy, were selected. Algorithms were used to determine AUC0-12h (0, H0.5, H2, H3 and H4). 2) Patients that required CNI withdrawal were selected, and prospectively followed. Before CNI withdrawal MMF, daily doses were adjusted to reach the MPA targeted previously

determined. Angiogenesis inhibitor Data as ALT, glomerular filtration rate (GFR) using MDRD formula were prospectively collected at CNI withdrawal (baseline), M1, and each year until M72. Results: 1) A wide variability in MPA concentrations was observed at any time, with mean C0, C0.5, C2, C3 and C4 values at 2.4 (0.4 to 4.6), 15.2 (4.5 to 31.1), 5.2 (2.2 to 9.5), 3.3 (0.9 to 5.5) and 2.9 mg/L (0.6 to 5.3). For C0 MPA a greater than 10-fold range was observed. The mean estimated AUC0-12h value was 48.1 ±13 mg.h/L. MPA AUC0-12 did not correlate with MMF daily dose (r= 0.27, p=0.2). 2) From dec 2000 to dec 2013, 103 recipients (mean age 60.2±7.4 yrs) underwent MMF monotherapy after a mean of 6.3±3.9 yrs from LT. LT indication was alcoholic cirrhosis in 73% of cases, mean MPA AUC was at 49.3±17.1 and GFR was 47.8±16.9 ml/kg/ min. Follow up: 4 patients had

acute rejection and 2 required steroid bolus. Over time, patients did not have a significant change in term of: ALT (23.2±13.4 vs 25.7±16.2) see more and weight (80±18.2 to 80±19.1). Renal function improved significantly (GFR 47.7±15.7 to 53.7±19.6, p<0.001). This improvement occurred the first year of MMF monotherapy (GFR: 45.8±14.9 to 52.9±19.8 ml/kg/min; p<0.05), as shown by GFR evolution between 1 and 2 years: 50.8±17.1 vs 48.1 ±14.7 (ns), and also concerned patients with a low GFR at baseline (<60) 41.3±10 to 47.9±15.4 ml/kg/min p<0.05. GGT worsened (57.6±50.5 vs 79.6±92.5 p<0.001). Patients with elevated GGT after MMF monotherapy did not differ at baseline from other in terms of: age (60.3 vs 59.7), time after LT (6.9 vs 5.8), MPA AUC (50 vs 52) or weight (82 vs 78kg). Conclusion: In maintenance LT recipients, MMF monotherapy regimen is safe when a 45 mg.h/L AUC is targeted and improve renal function with low risk of acute rejection.

Disclosures: The following people have nothing to disclose: Lisa B. VanWagner, Marina Serper, Raymond Kang, Anton I. Skaro, Josh Levitsky, Samuel Hohmann, Donald M. Lloyd-Jones Calcineurin inhibitors (CNI) induce chronic renal dysfunction. Switching CNI to mycofenolate mofetil (MMF) monotherapy remains controversial due to an increased risk of acute rejection. To safely withdraw CNI, mycophenolic NVP-BGJ398 acid (MPA) should be monitored. Aims: 1) Define a safe MPA targeted exposure (AUC). 2) Study the benefit and efficacy

of MMF monotherapy under therapeutic drug monitoring. Methods: 1) To define a safe MPA targeted exposure, 18 stable LT recipients previously treated with MMF monotherapy, were selected. Algorithms were used to determine AUC0-12h (0, H0.5, H2, H3 and H4). 2) Patients that required CNI withdrawal were selected, and prospectively followed. Before CNI withdrawal MMF, daily doses were adjusted to reach the MPA targeted previously

determined. this website Data as ALT, glomerular filtration rate (GFR) using MDRD formula were prospectively collected at CNI withdrawal (baseline), M1, and each year until M72. Results: 1) A wide variability in MPA concentrations was observed at any time, with mean C0, C0.5, C2, C3 and C4 values at 2.4 (0.4 to 4.6), 15.2 (4.5 to 31.1), 5.2 (2.2 to 9.5), 3.3 (0.9 to 5.5) and 2.9 mg/L (0.6 to 5.3). For C0 MPA a greater than 10-fold range was observed. The mean estimated AUC0-12h value was 48.1 ±13 mg.h/L. MPA AUC0-12 did not correlate with MMF daily dose (r= 0.27, p=0.2). 2) From dec 2000 to dec 2013, 103 recipients (mean age 60.2±7.4 yrs) underwent MMF monotherapy after a mean of 6.3±3.9 yrs from LT. LT indication was alcoholic cirrhosis in 73% of cases, mean MPA AUC was at 49.3±17.1 and GFR was 47.8±16.9 ml/kg/ min. Follow up: 4 patients had

acute rejection and 2 required steroid bolus. Over time, patients did not have a significant change in term of: ALT (23.2±13.4 vs 25.7±16.2) selleck kinase inhibitor and weight (80±18.2 to 80±19.1). Renal function improved significantly (GFR 47.7±15.7 to 53.7±19.6, p<0.001). This improvement occurred the first year of MMF monotherapy (GFR: 45.8±14.9 to 52.9±19.8 ml/kg/min; p<0.05), as shown by GFR evolution between 1 and 2 years: 50.8±17.1 vs 48.1 ±14.7 (ns), and also concerned patients with a low GFR at baseline (<60) 41.3±10 to 47.9±15.4 ml/kg/min p<0.05. GGT worsened (57.6±50.5 vs 79.6±92.5 p<0.001). Patients with elevated GGT after MMF monotherapy did not differ at baseline from other in terms of: age (60.3 vs 59.7), time after LT (6.9 vs 5.8), MPA AUC (50 vs 52) or weight (82 vs 78kg). Conclusion: In maintenance LT recipients, MMF monotherapy regimen is safe when a 45 mg.h/L AUC is targeted and improve renal function with low risk of acute rejection.

In order to better assess the quality of the liver, in this review we focus on some liver-specific donor risk indices. LIVER STEATOSIS IS strongly associated with poor graft function after LT. The impact of severe steatosis on allograft survival appears greater than other donor factors, including CDK activation the calculated DRI.[1] Moreover, clinicopathological studies have demonstrated an inverse correlation between steatosis and graft survival.[9] Steatosis is typically characterized qualitatively and quantitatively. Fatty infiltration is separated into two categories, macrosteatosis and microsteatosis. Macrosteatosis is characterized by a single, bulky fat vacuole

in hepatocytes, displacing the

nucleus to the edge of the cell. In microsteatosis, the cytoplasm of the hepatocytes contains tiny lipid vesicles without nuclear dislocation. Microsteatosis seems GDC-0980 clinical trial to have a low impact on the postoperative liver function. Macrosteatosis and microsteatosis most often present simultaneously at different degrees in the liver.[10] The quantitative evaluation is traditionally based on percentages of visualized hepatocytes containing fat vacuoles within the cytoplasm, classified as mild (<30%), moderate (30–60%) or severe (>60%).[11-13] Livers with more than 40–50% macrosteatosis should not be used.[14] In all such selleck products cases, the procurement surgeon has to make the definitive decision. A percutaneous liver biopsy performed at the bedside, before organ procurement, may help prevent unnecessary donor laparotomy. In addition, livers with severe steatosis from donation after

cardiac death donors, combined with a prolonged cold ischemic time have a high risk for developing early allograft dysfunction which is correlated with shorter graft survival. Therefore, severe steatosis livers should only be considered for LT in selected recipients without the presence of additional risk factors.[15] Although hepatic steatosis is a widely accepted risk factor for postoperative complications after LT, studies have been inconsistent regarding the relevant amount of fat or type of fat. All those observations lead to controversies in the field. Some studies showed that liver grafts containing moderate degrees of microsteatosis significantly increase the rate of organ failure after LT,[16] while other groups recommended the use of microsteatotic grafts, regardless of the total amount, to safely expand the donor pool.[17] The main reason for the inconsistent outcome is the estimation of steatosis using frozen section liver biopsy which is both difficult and subjective.[18, 19] Quantification of hepatic steatosis in histological sections is strongly observer-dependent, not reproducible. El-Badry et al.

In order to better assess the quality of the liver, in this review we focus on some liver-specific donor risk indices. LIVER STEATOSIS IS strongly associated with poor graft function after LT. The impact of severe steatosis on allograft survival appears greater than other donor factors, including PD-1/PD-L1 cancer the calculated DRI.[1] Moreover, clinicopathological studies have demonstrated an inverse correlation between steatosis and graft survival.[9] Steatosis is typically characterized qualitatively and quantitatively. Fatty infiltration is separated into two categories, macrosteatosis and microsteatosis. Macrosteatosis is characterized by a single, bulky fat vacuole

in hepatocytes, displacing the

nucleus to the edge of the cell. In microsteatosis, the cytoplasm of the hepatocytes contains tiny lipid vesicles without nuclear dislocation. Microsteatosis seems TSA HDAC nmr to have a low impact on the postoperative liver function. Macrosteatosis and microsteatosis most often present simultaneously at different degrees in the liver.[10] The quantitative evaluation is traditionally based on percentages of visualized hepatocytes containing fat vacuoles within the cytoplasm, classified as mild (<30%), moderate (30–60%) or severe (>60%).[11-13] Livers with more than 40–50% macrosteatosis should not be used.[14] In all such selleck kinase inhibitor cases, the procurement surgeon has to make the definitive decision. A percutaneous liver biopsy performed at the bedside, before organ procurement, may help prevent unnecessary donor laparotomy. In addition, livers with severe steatosis from donation after

cardiac death donors, combined with a prolonged cold ischemic time have a high risk for developing early allograft dysfunction which is correlated with shorter graft survival. Therefore, severe steatosis livers should only be considered for LT in selected recipients without the presence of additional risk factors.[15] Although hepatic steatosis is a widely accepted risk factor for postoperative complications after LT, studies have been inconsistent regarding the relevant amount of fat or type of fat. All those observations lead to controversies in the field. Some studies showed that liver grafts containing moderate degrees of microsteatosis significantly increase the rate of organ failure after LT,[16] while other groups recommended the use of microsteatotic grafts, regardless of the total amount, to safely expand the donor pool.[17] The main reason for the inconsistent outcome is the estimation of steatosis using frozen section liver biopsy which is both difficult and subjective.[18, 19] Quantification of hepatic steatosis in histological sections is strongly observer-dependent, not reproducible. El-Badry et al.

Long-term lamivudine treatment is associated with the emergence of lamivudine-resistant mutants, which has occasionally find more been associated with severe, and even fatal, flares of hepatitis.21 In this study, the patients with lamivudine treatment were followed up for only 12 weeks. We did not detect any clinical evidence of drug-resistant mutants during the 3-month lamivudine treatment in the survivors. The method of PCR-RFLP

is incapable of detection of YMDD mutants under 1 × 104 copies/mL, which limits its sensitivity. The adverse effects of YMDD mutations may be overcome by the addition of adefovir dipivoxil. In conclusion, our study suggests that lamivudine treatment can significantly decrease the mortality of patients with a MELD score of 20–30, but have no effect on patients with a MELD score higher than 30. For ACLF patients with this website a MELD score of 20–30, a low pretreatment viral load and rapid decline of HBV DNA load are good predictors for the survival of patients with lamivudine treatment. A significant weakness in the present study is the use of a retrospective control cohort leading

to a possible sources of bias. Our report suggests the need for a prospective, randomized, double-blind, placebo-controlled trial of lamivudine in patients with ACLF. “
“Genotype 3 of the hepatitis C virus (HCV) has been long considered an easy-to-treat infection, with higher cure rates (∼70%) than other viral genotypes with the standard combination of pegylated interferon-α and ribavirin. However, the relative insensitivity of this genotype to most protease inhibitors and the recent unexpected data on decreased effectiveness of sofosbuvir have raised questions on how to achieve universal cure, a goal that seems reasonable

for other genotypes. In addition, increasing clinical and experimental data show that HCV genotype 3 may be associated not only with severe steatosis, but also with accelerated fibrosis progression rate and increased oncogenesis. Conclusion: Currently available data suggest that we should increase our efforts to understand the virology and pathogenesis click here of HCV genotype 3, aiming at better and more potent, genotype-targeted treatments. (Hepatology 2014;59:2403–2412) “
“Aim:  To evaluate the association between liver stiffness measured by transient elastography (FibroScan) and the efficacy of long-term nucleoside analog (NA) treatment for patients with chronic hepatitis B. Methods:  Study 1: Forty-four chronic HBV patients had liver stiffness measured by FibroScan and underwent liver biopsy. Study 2: Group A: 22 patients started NA treatment at entry and FibroScan was done annually for 3 years. Group B: 23 patients started NA treatment prior to pretreatment FibroScan measurement, and FibroScan was done for from 3 to 5 years after the start of NA treatment.

3). Bacterial translocation of organisms from the gut in patients R788 cell line with cirrhosis and portal hypertension results in chronic endotoxemia.42 This culminates in a local milieu of proinflammatory cytokines/chemokines, which can up-regulate the adhesion receptor CD11b/CD18 (MAC-1 and complement 3b receptor),

and activate neutrophils through Toll-like receptors (TLR) and chemokine receptors (CXCR1 and CXCR2). Stadlbauer et al.43 demonstrated increased expression of TLR-2, TLR-4, and TLR-9 and decreased expression of CXCR1 and CXCR2 in normal neutrophils incubated with plasma from patients with alcoholic hepatitis. This was associated with phagocytic dysfunction and increased spontaneous OB, endotoxemia, and energy depletion, which was prevented by incubation with albumin, an endotoxin scavenger. Inhibition of TLR-2, TLR-4, and TLR-9 prevented an increase in spontaneous OB and Crizotinib cost CXCR1/CXR2 expression but did not improve phagocytosis. Ex vivo removal of endotoxin from the plasma of patients with alcoholic hepatitis and cirrhosis decreased neutrophil spontaneous OB and improved phagocytosis.24 In chronic endotoxemia, the adaptive immune system plays a key role in limiting overzealous neutrophil activation by decreasing survival mediated by T regulatory cells.44 Therefore,

the interaction of neutrophils and T regulatory cells in cirrhosis and hyperammonemia warrants further investigation. The rapid recruitment of activated neutrophils to the liver in patients with alcoholic hepatitis/liver injury, and click here data that supports the development of organ failure in sepsis (both conditions commonly being associated with encephalopathy) results from an inappropriately vigorous response of neutrophils to an inflammatory stimulus.

Therefore, in the context of a patient with cirrhosis, hyperammonemia and chronic endotoxemia, where it has already been shown that neutrophils are pre-primed and have a reduced ability to eliminate bacteria, then it would be logical to suppose that there will be enhanced endothelial–neutrophil interaction within the cerebral microcirculation. This would result in neutrophil adhesion, migration across the blood–brain barrier and the production of chemokines, proinflammatory cytokines, proteases, ROS, and transcription of inflammatory target genes (Fig. 3). It is within this inflammatory milieu that the cerebral effects of ammonia (with or without superimposed infection) will have their greatest impact. Furthermore, astroglial activation promotes neutrophil recruitment by the production of neutrophil-specific chemokines.45 Historically, treatments for HE have been based upon the hypothesis that the colon is the primary source of ammonia and have included dietary protein restriction, the use of nonabsorbable disaccharides and nonabsorbable antibiotics.

3). Bacterial translocation of organisms from the gut in patients click here with cirrhosis and portal hypertension results in chronic endotoxemia.42 This culminates in a local milieu of proinflammatory cytokines/chemokines, which can up-regulate the adhesion receptor CD11b/CD18 (MAC-1 and complement 3b receptor),

and activate neutrophils through Toll-like receptors (TLR) and chemokine receptors (CXCR1 and CXCR2). Stadlbauer et al.43 demonstrated increased expression of TLR-2, TLR-4, and TLR-9 and decreased expression of CXCR1 and CXCR2 in normal neutrophils incubated with plasma from patients with alcoholic hepatitis. This was associated with phagocytic dysfunction and increased spontaneous OB, endotoxemia, and energy depletion, which was prevented by incubation with albumin, an endotoxin scavenger. Inhibition of TLR-2, TLR-4, and TLR-9 prevented an increase in spontaneous OB and selleck inhibitor CXCR1/CXR2 expression but did not improve phagocytosis. Ex vivo removal of endotoxin from the plasma of patients with alcoholic hepatitis and cirrhosis decreased neutrophil spontaneous OB and improved phagocytosis.24 In chronic endotoxemia, the adaptive immune system plays a key role in limiting overzealous neutrophil activation by decreasing survival mediated by T regulatory cells.44 Therefore,

the interaction of neutrophils and T regulatory cells in cirrhosis and hyperammonemia warrants further investigation. The rapid recruitment of activated neutrophils to the liver in patients with alcoholic hepatitis/liver injury, and learn more data that supports the development of organ failure in sepsis (both conditions commonly being associated with encephalopathy) results from an inappropriately vigorous response of neutrophils to an inflammatory stimulus.

Therefore, in the context of a patient with cirrhosis, hyperammonemia and chronic endotoxemia, where it has already been shown that neutrophils are pre-primed and have a reduced ability to eliminate bacteria, then it would be logical to suppose that there will be enhanced endothelial–neutrophil interaction within the cerebral microcirculation. This would result in neutrophil adhesion, migration across the blood–brain barrier and the production of chemokines, proinflammatory cytokines, proteases, ROS, and transcription of inflammatory target genes (Fig. 3). It is within this inflammatory milieu that the cerebral effects of ammonia (with or without superimposed infection) will have their greatest impact. Furthermore, astroglial activation promotes neutrophil recruitment by the production of neutrophil-specific chemokines.45 Historically, treatments for HE have been based upon the hypothesis that the colon is the primary source of ammonia and have included dietary protein restriction, the use of nonabsorbable disaccharides and nonabsorbable antibiotics.

When compared to matched controls

without AKI, ascites (78.7% versus (vs.) 52.0%), non-white race (16.3% vs. 7.9%) and absence of malignancy (89.6% vs. 82.7%) were more commonly seen among the cases. In the overall comparison with the controls, the frequency of NSBB use was higher among the cases, albeit insignificantly (46.0% vs. 37.6%, p=0.09). In the univariate proportional hazard regression analysis, female sex, non-caucasian, malignancy, autoimmune etiology, high MELD and MELD-Na at baseline, and ascites were significantly associated with development of AKI. In multivariable analyses, the impact of NSBB on AKI incidence was different according to the presence of ascites: STI571 in vivo NSBB use in patients with ascites was significantly associated with development of AKI (hazard ratio [HR], 2.79; 95% confidence interval [CI], 1.40-5.54), while in patients without ascites, NSBB was protective (HR, 0.19; 95% CI, 0.06-0.60), after adjusting for MELD-Na at baseline, sex, race, etiology of cirrhosis and presence of liver cancer. Conclusions: The use of NSBB increased the risk of AKI in cirrhotic patients with ascites, which likely contributes to increased mortality. Disclosures: W. Ray Kim – Consulting: Bristol Myers Squibb, Gilead Sciences Patrick S. Kamath – Advisory Committees or Review

Pembrolizumab in vitro Panels: Sequana Medical The following people have nothing to disclose: Sang Gyune Kim, Joseph J. Larson, Walter K. Kremers Probiotics may not be efficacious in altering clinically relevant outcomes in cirrhotic patients with hepatic encephalopathy (HE). This study assessed the efficacy of a probiotic preparation in the prevention

of HE recurrence (primary outcome), and reduction in click here hospitalizations, improvement in the severity of liver disease and in proinflammatory markers, and improvement in health-related quality of life (HRQOL) (secondary outcomes) in patients with liver cirrhosis. In a randomized, double-blind, placebo-controlled trial using computer generated number allocation, conducted at a tertiary care hospital in India, patients with liver cirrhosis who had recovered from an episode of HE during the previous month were assigned to receive either a probiotic preparation (VSL#3®; CD Pharma India Pvt. Ltd, New Delhi, India) at a dose of 900 billion bacteria daily (n=66), or placebo (n=64) for 6 months. There was a trend toward reduction in the mean-time to HE recurrence [123 (95% confidence interval [CI], 108–138) vs 105 (89– 120) days] in probiotic-treated versus placebo-treated patients (P=0.10). The hazard ratio (HR) for the risk of a breakthrough episode in the probiotic group was 0.65 (95% CI, 0.38-1.11; P=0.10) versus the placebo group. Hospitalizations were significantly less common in the probiotic group versus placebo group for overall complications of liver cirrhosis [24.2% vs 45.3%, HR 0.52 (95% CI, 0.28–0.95); respectively; P=0.034] and for those involving HE [19.7% vs 42.2%, respectively; HR 0.45 (95% CI, 0.23–0.87; P=0.02)].

Data were censored at the patient’s last follow-up visit or at 7.5 years after a patient began peginterferon and ribavirin treatment, whichever occurred first. Variables with a P value <0.05 on univariate

analysis and variables reported previously to be associated with outcomes were entered Adriamycin into multivariate analyses for each of the five clinical outcomes. One multivariate model was created for each of the five outcomes, and the adjusted cumulative incidence rates for each of the five outcomes were calculated by adjusting for risk factors that were significant on multivariate analyses. Adjusted cumulative rates were compared at the means of the covariates for each group. http://www.selleckchem.com/products/ensartinib-x-396.html Routine blood tests used to assess disease severity in patients with chronic hepatitis C were compared at three time points: (1) baseline (entry into the lead-in phase of the HALT-C Trial), (2) approximately 18 months after baseline (Week 72 visit for SVR patients; Month 18 visit for BT/R and NR patients), and (3) approximately 72-84 months after baseline (amended

protocol study visit for SVR patients; Month 72 visit for BT/R and NR patients). Paired t tests were used to compare means of baseline and follow-up laboratory tests between different time points in each group. Data were obtained on 140 (78%) of the 180 HALT-C Trial patients who achieved SVR. Thirty patients could not be located, and 10 declined to participate. The 40 patients who did not participate did not differ from the 140 who did at baseline or at Week 72 in demographic characteristics, baseline Ishak fibrosis score, or routine blood tests. Specifically, at Week 72 no difference was found between the SVR nonparticipants (n = 40) and participants (n = 140) for key predictors of clinical outcome such as age (49.8 ± 8.02 years versus 50.0 ± 6.12 years for nonparticipants and participants, respectively; P = 0.87), albumin (4.3 ± 0.4 versus 4.2 ± 0.4 g/dL; selleck inhibitor P = 0.26), platelet count (191 ± 56 versus 191 ± 59 × 1000/mm3; P = 0.97), AFP (3.3 ± 1.5 versus 3.3 ± 1.7 ng/mL; P = 0.88) or

alkaline phosphatase (72 ± 20 versus 78 ± 20 IU/mL; P = 0.27). Three of the 140 SVR patients had died, and copies of death certificates for two of the three were obtained. Of the 137 surviving participants, 70 were seen in clinic whereas 67 were evaluated by telephone interviews supplemented by examination of external medical records. None of the 30 patients with SVR who could not be located were listed as deceased in the online SSDI. Baseline demographic data as well as clinical and laboratory data on the SVR group and the two comparison groups (BT/R and NR) are shown in Table 1. The three groups differed significantly in race/ethnicity, presence of cirrhosis, hepatitis C genotype, and laboratory values associated with advanced liver disease.

Data were censored at the patient’s last follow-up visit or at 7.5 years after a patient began peginterferon and ribavirin treatment, whichever occurred first. Variables with a P value <0.05 on univariate

analysis and variables reported previously to be associated with outcomes were entered BVD-523 into multivariate analyses for each of the five clinical outcomes. One multivariate model was created for each of the five outcomes, and the adjusted cumulative incidence rates for each of the five outcomes were calculated by adjusting for risk factors that were significant on multivariate analyses. Adjusted cumulative rates were compared at the means of the covariates for each group. BAY 57-1293 mw Routine blood tests used to assess disease severity in patients with chronic hepatitis C were compared at three time points: (1) baseline (entry into the lead-in phase of the HALT-C Trial), (2) approximately 18 months after baseline (Week 72 visit for SVR patients; Month 18 visit for BT/R and NR patients), and (3) approximately 72-84 months after baseline (amended

protocol study visit for SVR patients; Month 72 visit for BT/R and NR patients). Paired t tests were used to compare means of baseline and follow-up laboratory tests between different time points in each group. Data were obtained on 140 (78%) of the 180 HALT-C Trial patients who achieved SVR. Thirty patients could not be located, and 10 declined to participate. The 40 patients who did not participate did not differ from the 140 who did at baseline or at Week 72 in demographic characteristics, baseline Ishak fibrosis score, or routine blood tests. Specifically, at Week 72 no difference was found between the SVR nonparticipants (n = 40) and participants (n = 140) for key predictors of clinical outcome such as age (49.8 ± 8.02 years versus 50.0 ± 6.12 years for nonparticipants and participants, respectively; P = 0.87), albumin (4.3 ± 0.4 versus 4.2 ± 0.4 g/dL; click here P = 0.26), platelet count (191 ± 56 versus 191 ± 59 × 1000/mm3; P = 0.97), AFP (3.3 ± 1.5 versus 3.3 ± 1.7 ng/mL; P = 0.88) or

alkaline phosphatase (72 ± 20 versus 78 ± 20 IU/mL; P = 0.27). Three of the 140 SVR patients had died, and copies of death certificates for two of the three were obtained. Of the 137 surviving participants, 70 were seen in clinic whereas 67 were evaluated by telephone interviews supplemented by examination of external medical records. None of the 30 patients with SVR who could not be located were listed as deceased in the online SSDI. Baseline demographic data as well as clinical and laboratory data on the SVR group and the two comparison groups (BT/R and NR) are shown in Table 1. The three groups differed significantly in race/ethnicity, presence of cirrhosis, hepatitis C genotype, and laboratory values associated with advanced liver disease.