1 ± 10.4 years and 62.9% were male. A total of 2,277 subjects (68.9%) had diastolic cardiac dysfunction; 1,843 were grade 1 and 434 were grade 2. More advanced diastolic dysfunction (normal, grade 1, grade 2) was associated with higher prevalence of NAFLD (OR, 2.15; 95% CI, 1.87-2.47; P<0.001). On multivariate analysis, the presence NAFLD was significantly associated with both the presence of diastolic dysfunction (odds ratio [OR], 2.02; 95% confidence interval [CI], 1.65-2.49; P<0.001) and the increased diastolic dysfunction Silmitasertib nmr grades (normal, grade 1, grade 2) (OR, 1.63; 95% CI, 1.39-1.91; P<0.001) after adjustment for age, sex, hypertension, body mass index, and serum levels

of cholesterol and triglycerides. More advanced diastolic dysfunction (normal, grade 1, grade 2) was associated with higher prevalence of NAFLD (OR, 2.15; 95% CI, 1.87-2.47; P<0.001). CONCLUSIONS: Patients with NAFLD have an increased risk for diastolic cardiac dysfunction independent of classical risk factors. Disclosures: The following people have nothing to disclose: Jeong-Hoon Lee, Donghee Kim, Goh Eun Chung, Min-Sun Kwak, Yoon Jun Kim, Jung-Hwan Yoon, Hyo-Suk Lee Background and Aims: The prevalence of non-alcoholic fatty liver Disease (NAFLD) is increasing in parallel to the epidemics

of obesity and diabetes. Although histological differences have been reported between pediatric and adult NAFLD, potential age related changes in serum transaminases 上海皓元医药股份有限公司 Bcl-2 inhibitor and liver histology remain largely unexplored. Therefore, the aim of our study was to investigate the clinical and histological characteristics of NAFLD across different age groups of adults. Methods: This was a cross sectional study of

502 biopsy proven NAFLD patients recruited from two hepatology outpatient clinics in Cleveland. Clinical data including demographics, anthropometry, medical history, biochemical and liver biopsy findings were evaluated. Comparisons of clinical characteristics and histologic changes were made among different age groups; group A(aged 18 to 44), B(aged 45 to 64) and C(aged 65 and over). Results: In this cohort of NAFLD patients, 34.9%, 56.0% and 9.1% of the cohort were distributed among group A, B, and C respectively. While the prevalence of non-alcoholic steatohepatitis (NASH) was comparable across age groups, the prevalence of advanced fibrosis increased with age; 17.7%, 31.1% and 50.0% of groups A, B and C respectively (p=0.000). Mean ALT progressively decreased with age; 87, 64, 56 U/L in group A, B, and C respectively (p=0.000) with a corresponding increase in the proportion of patients with normal ALT with age (p=0.003). In contrast, there was no difference in mean AST or proportion of patients with normal AST (p=0.939) across age. The AST: ALT ratio (AAR) progressively increased from 0.7 to 0.9 to 1.1 in group A, B and C respectively (p=0.000).

1 ± 10.4 years and 62.9% were male. A total of 2,277 subjects (68.9%) had diastolic cardiac dysfunction; 1,843 were grade 1 and 434 were grade 2. More advanced diastolic dysfunction (normal, grade 1, grade 2) was associated with higher prevalence of NAFLD (OR, 2.15; 95% CI, 1.87-2.47; P<0.001). On multivariate analysis, the presence NAFLD was significantly associated with both the presence of diastolic dysfunction (odds ratio [OR], 2.02; 95% confidence interval [CI], 1.65-2.49; P<0.001) and the increased diastolic dysfunction www.selleckchem.com/products/Trichostatin-A.html grades (normal, grade 1, grade 2) (OR, 1.63; 95% CI, 1.39-1.91; P<0.001) after adjustment for age, sex, hypertension, body mass index, and serum levels

of cholesterol and triglycerides. More advanced diastolic dysfunction (normal, grade 1, grade 2) was associated with higher prevalence of NAFLD (OR, 2.15; 95% CI, 1.87-2.47; P<0.001). CONCLUSIONS: Patients with NAFLD have an increased risk for diastolic cardiac dysfunction independent of classical risk factors. Disclosures: The following people have nothing to disclose: Jeong-Hoon Lee, Donghee Kim, Goh Eun Chung, Min-Sun Kwak, Yoon Jun Kim, Jung-Hwan Yoon, Hyo-Suk Lee Background and Aims: The prevalence of non-alcoholic fatty liver Disease (NAFLD) is increasing in parallel to the epidemics

of obesity and diabetes. Although histological differences have been reported between pediatric and adult NAFLD, potential age related changes in serum transaminases 上海皓元 LY294002 in vivo and liver histology remain largely unexplored. Therefore, the aim of our study was to investigate the clinical and histological characteristics of NAFLD across different age groups of adults. Methods: This was a cross sectional study of

502 biopsy proven NAFLD patients recruited from two hepatology outpatient clinics in Cleveland. Clinical data including demographics, anthropometry, medical history, biochemical and liver biopsy findings were evaluated. Comparisons of clinical characteristics and histologic changes were made among different age groups; group A(aged 18 to 44), B(aged 45 to 64) and C(aged 65 and over). Results: In this cohort of NAFLD patients, 34.9%, 56.0% and 9.1% of the cohort were distributed among group A, B, and C respectively. While the prevalence of non-alcoholic steatohepatitis (NASH) was comparable across age groups, the prevalence of advanced fibrosis increased with age; 17.7%, 31.1% and 50.0% of groups A, B and C respectively (p=0.000). Mean ALT progressively decreased with age; 87, 64, 56 U/L in group A, B, and C respectively (p=0.000) with a corresponding increase in the proportion of patients with normal ALT with age (p=0.003). In contrast, there was no difference in mean AST or proportion of patients with normal AST (p=0.939) across age. The AST: ALT ratio (AAR) progressively increased from 0.7 to 0.9 to 1.1 in group A, B and C respectively (p=0.000).

The success of the procedure and the complete removal of lithiasis in this first study were: in group A 97.1% and 70% , in group B 100% and 86.4%, respectively, without significant differences. Seven or ten Fr plastic stent was placed in group A 30.4% and group B 18.2%, without selleck products significant differences. Comparing only the giants stones was noted that the successful stones extraction in the first ERCP was in group A 58.6% and group B 89.3% (p = 0.019). The use of mechanical lithotripsy in group A was 44.8% and in

group B 21.4%, without significant difference. With respect to complications in group A was 5.8% (1 perforation, 2 cholangitis and 1 binding of basket) and in group B was 6.8% (2 mild pancreatitis, 1 cholangitis). There was no death in both groups following the ERCP. Conclusion: The combination of sphincterotomy and large volumes balloon dilation in the treatment of difficult stones is equally effective and safe as in sphincterotomy alone. The combination therapy was

more effective in the management of giant stone. Key Word(s): 1. choledocholithiasis; Presenting Author: HUIJER HWANG Additional Authors: RAUL MATANO, MARTIN GUIDI, JULIO DE MARIA, ESTEBAN PROMENZIO, FERNANDO Dorsomorphin chemical structure RAGONE, JUAN VISCARDI Corresponding Author: HUIJER HWANG Affiliations: El Cruce Hospital Objective: Hiliar tumors (HT) are neoplasms with a poor prognosis and most patients die within a year of diagnosis. While surgery is the standard for curative treatment, in most cases the

medchemexpress goal is palliative treatment. Endoscopic biliary drainage (EBD) and percutaneous biliary drainage (PBD) are two minimally effective invasive techniques. It is not known with certainty what is the approach of choice. Several studies have shown that EBD can be difficult in Bismuth III and IV tumors because of the high risk of post-procedure cholangitis. Aim: To report the effectiveness and complications of EBD and PBD in the palliative management of HT. Methods: Descriptive observational retrospective analysis of the management of HT in a Trainning Center of ERCP, from October 2008 to March 2012. We analyzed the following variables in the groups treated with EBD and PBD: rate of effective drain, reintervention rate, survival, complications and death associated with the procedure. Results: We included in EBD group: 40 patients and 52 procedures and in PBD group: 22 patients and 28 interventions. The final success in the first group was 85% and the second 90.9% (p = 0.788). Five patients (4 HT Bismuth IV) required combined approach. The global rate of success was 95.16%. Twelve patients of EBD group were Bismuth IV, whose effectiveness was 58.3%. Meanwhile, 11 patients of PBD group were Bismuth IV, whose effectiveness was 81.8% (p = 0.442). Overall survival in EBD group was 7.9 months, while in PBD group was 4.8 months. With respect to complications in the EBD group was 11.

1B and 4B). This finding clearly indicates that a growth-suppressive environment was generated in hyperplastic livers, preventing their further growth. On the other hand, the development of HCC in all mice given the genotoxic agent DENA prior to TCPOBOP suggests that initiated/mutated cells have escaped the growth-suppressive signals, thus clonally expanding to develop HCC. Our finding of increased YAP protein expression and its nuclear translocation this website in HCC cells suggests that dysregulation of the Hippo pathway may contribute to the

escape from the environmental growth-suppressive constraint; it is noteworthy that a strong and increased nuclear YAP staining has been observed in human tumors, including HCC.27, 30 In this study, we show that YAP nuclear translocation is accompanied by its increased activity because, in the same tumors, up-regulation of AFP and CTGF, two YAP target genes,15, 17 was observed. Taken

together, our findings suggest that YAP dysregulation could be involved in the development of DENA+TCPOBOP-induced HCC. MicroRNAs have recently emerged as important modulators of gene expression in cancer,31 including human HCC.32 Very recently, Liu et al.29 reported that miR-375 is a negative regulator of YAP; indeed, they found down-regulation PF-02341066 research buy of miR-375 in tumor tissues of HCC patients, which was accompanied by increased YAP levels. Moreover, they showed that miRNA-375 re-expression caused a severe decrease of YAP protein levels. In accordance with these results, we found a decrease of miR-375 and an increase

in YAP content in approximately 70% of mouse HCCs. Our data thus 上海皓元 provide a possible mechanism underlying the increase of YAP in chemically induced HCCs. Whether down-regulation of miR-375 is due to epigenetic modifications is presently unknown and warrants further investigation, because modulation of this microRNA could be therapeutically targeted to reactivate the growth-suppressive effect of the Hippo pathway. A better understanding of growth regulatory mechanisms may represent an important approach from a therapeutic point of view. HCC, the fifth most common malignant neoplasm and the third most frequent cause of cancer-related death worldwide, represents a major health problem.33, 34 A better definition of the molecular pathogenesis of HCC could have a significant impact on the development of new treatment strategies. The Hippo kinase cascade might have clear pathogenic implications in hepatocarcinogenesis, and its drivers might represent novel targets for molecular therapies.

1B and 4B). This finding clearly indicates that a growth-suppressive environment was generated in hyperplastic livers, preventing their further growth. On the other hand, the development of HCC in all mice given the genotoxic agent DENA prior to TCPOBOP suggests that initiated/mutated cells have escaped the growth-suppressive signals, thus clonally expanding to develop HCC. Our finding of increased YAP protein expression and its nuclear translocation see more in HCC cells suggests that dysregulation of the Hippo pathway may contribute to the

escape from the environmental growth-suppressive constraint; it is noteworthy that a strong and increased nuclear YAP staining has been observed in human tumors, including HCC.27, 30 In this study, we show that YAP nuclear translocation is accompanied by its increased activity because, in the same tumors, up-regulation of AFP and CTGF, two YAP target genes,15, 17 was observed. Taken

together, our findings suggest that YAP dysregulation could be involved in the development of DENA+TCPOBOP-induced HCC. MicroRNAs have recently emerged as important modulators of gene expression in cancer,31 including human HCC.32 Very recently, Liu et al.29 reported that miR-375 is a negative regulator of YAP; indeed, they found down-regulation Cabozantinib purchase of miR-375 in tumor tissues of HCC patients, which was accompanied by increased YAP levels. Moreover, they showed that miRNA-375 re-expression caused a severe decrease of YAP protein levels. In accordance with these results, we found a decrease of miR-375 and an increase

in YAP content in approximately 70% of mouse HCCs. Our data thus MCE provide a possible mechanism underlying the increase of YAP in chemically induced HCCs. Whether down-regulation of miR-375 is due to epigenetic modifications is presently unknown and warrants further investigation, because modulation of this microRNA could be therapeutically targeted to reactivate the growth-suppressive effect of the Hippo pathway. A better understanding of growth regulatory mechanisms may represent an important approach from a therapeutic point of view. HCC, the fifth most common malignant neoplasm and the third most frequent cause of cancer-related death worldwide, represents a major health problem.33, 34 A better definition of the molecular pathogenesis of HCC could have a significant impact on the development of new treatment strategies. The Hippo kinase cascade might have clear pathogenic implications in hepatocarcinogenesis, and its drivers might represent novel targets for molecular therapies.

Some genetic polymorphisms of TNF-α have been found to be associated with susceptibility to Hepatocellular carcinoma. We investigated TNF-α 308(G/A), TNF-α

238(G/A), TNF-α 863(C/A), TNF-α 857(C/T) and TNF-α 1031(T/C) polymorphisms for association with HCC in Korean. Methods: Patients with HCC diagnosed at CHA Bundang Medical CHIR-99021 nmr Center from June 1996 to August 2008 were enrolled. The association of TNF-α polymorphisms with HCC was analyzed in 157 HCC patients and 201 controls by the polymerase chain reaction-restriction fragment length polymorphism. Results: Any TNF-α polymorphisms was not significantly associated with HCC patients. Genotype combinations of TNF-α polymorphisms: TNF-α –1031/-857/-238 TT/CC/GA(Adjusted click here Odds ratio (AOR)=18.849,

95%CI = 2.203-161.246, P =0.007), TNF-α -1031/-308/-238 TT/GG/GA(AOR = 26.956, 95%CI = 3.071–236.584, P =0.003) TT/GA/GG(AOR = 2.712, 95%CI = 1.085–6.778, P =0.033), TNF-α -863/-308/-238 CC/GA/GG(AOR = 2.533, 95%CI = 1.007–6.371, P =0.048) CA/GG/GA(AOR = 4.242, 95%CI = 1.243–14.473, P =0.021), TNF-α -1031/-238 TT/GA(AOR = 21.576, 95%CI = 2.581–180.394, P =0.005), TNF-α -863/-238 CA/GA(AOR = 3.669, 95%CI = 1.098 – 12.253, P =0.035). TNF-α -308/-238 GA/GG(AOR = 2.283, 95%CI = 1.078–4.836, P =0.031) GA+AA/GG(AOR = 2.150, 95%CI = 1.041–4.441, P =0.039) were significantly increased in HCC patients. Haplotype: TCCGA(TNF-α –1031/-836/-857/-308/-238, AOR = 25.824, 95%CI = 1.491 – 447.223, P =0.0005), TCGA(TNF-α –1031/-857/-308/-238, AOR = 12.059, 95%CI = 2.747 – 52.950, P < 0.0001), TCA(TNF-α –1031/857/-238, AOR = 10.696, medchemexpress 95%CI = 2.428 – 47.110, P =0.0001), TGA(TNF-α –1031/-308/-238, AOR = 7.556, 95%CI = 2.173 – 26.280, P =0.0002), TA(TNF-α –1031/-238, AOR = 10.865, 95%CI = 2.473 – 47.740, P =0.0001) were found to significantly increase in HCC patients. TNF-α -1031 CC genotype had better survival

in OKUDA stage III (AOR = 5.795, 95%CI = 1.145–29.323, P =0.035) than TT genotype. Conclusion: Although a single TNF-α polymorphism was not related to HCC in this study, some genotype combinations and haplotypes of TNF-α show relation to the risk of HCC. And HCC patients of TNF-α -1031 CC genotype may have good prognosis than TT genotype in OKUDA stage III. Key Word(s): 1. HCC; 2. TNF-α; Presenting Author: QIAN BI Additional Authors: SHANHONG TANG, RUI FAN, NEERAJ AGARWAL, YONGQUAN SHI, TOMOO IWAKUMA, JIE DING Corresponding Author: TOMOO IWAKUMA, JIE DING Affiliations: Xijing Hospital of Digestive Diseases & State Key Laboratory of Cancer Biology, Fourth Military Medical University; University of Kansas Medical Center Objective: Hepatocellular carcinoma (HCC) is a rising cause of cancer-related death in the United States with a 5-year survival rate below 12%.

Some genetic polymorphisms of TNF-α have been found to be associated with susceptibility to Hepatocellular carcinoma. We investigated TNF-α 308(G/A), TNF-α

238(G/A), TNF-α 863(C/A), TNF-α 857(C/T) and TNF-α 1031(T/C) polymorphisms for association with HCC in Korean. Methods: Patients with HCC diagnosed at CHA Bundang Medical Y-27632 datasheet Center from June 1996 to August 2008 were enrolled. The association of TNF-α polymorphisms with HCC was analyzed in 157 HCC patients and 201 controls by the polymerase chain reaction-restriction fragment length polymorphism. Results: Any TNF-α polymorphisms was not significantly associated with HCC patients. Genotype combinations of TNF-α polymorphisms: TNF-α –1031/-857/-238 TT/CC/GA(Adjusted Roxadustat research buy Odds ratio (AOR)=18.849,

95%CI = 2.203-161.246, P =0.007), TNF-α -1031/-308/-238 TT/GG/GA(AOR = 26.956, 95%CI = 3.071–236.584, P =0.003) TT/GA/GG(AOR = 2.712, 95%CI = 1.085–6.778, P =0.033), TNF-α -863/-308/-238 CC/GA/GG(AOR = 2.533, 95%CI = 1.007–6.371, P =0.048) CA/GG/GA(AOR = 4.242, 95%CI = 1.243–14.473, P =0.021), TNF-α -1031/-238 TT/GA(AOR = 21.576, 95%CI = 2.581–180.394, P =0.005), TNF-α -863/-238 CA/GA(AOR = 3.669, 95%CI = 1.098 – 12.253, P =0.035). TNF-α -308/-238 GA/GG(AOR = 2.283, 95%CI = 1.078–4.836, P =0.031) GA+AA/GG(AOR = 2.150, 95%CI = 1.041–4.441, P =0.039) were significantly increased in HCC patients. Haplotype: TCCGA(TNF-α –1031/-836/-857/-308/-238, AOR = 25.824, 95%CI = 1.491 – 447.223, P =0.0005), TCGA(TNF-α –1031/-857/-308/-238, AOR = 12.059, 95%CI = 2.747 – 52.950, P < 0.0001), TCA(TNF-α –1031/857/-238, AOR = 10.696, 上海皓元 95%CI = 2.428 – 47.110, P =0.0001), TGA(TNF-α –1031/-308/-238, AOR = 7.556, 95%CI = 2.173 – 26.280, P =0.0002), TA(TNF-α –1031/-238, AOR = 10.865, 95%CI = 2.473 – 47.740, P =0.0001) were found to significantly increase in HCC patients. TNF-α -1031 CC genotype had better survival

in OKUDA stage III (AOR = 5.795, 95%CI = 1.145–29.323, P =0.035) than TT genotype. Conclusion: Although a single TNF-α polymorphism was not related to HCC in this study, some genotype combinations and haplotypes of TNF-α show relation to the risk of HCC. And HCC patients of TNF-α -1031 CC genotype may have good prognosis than TT genotype in OKUDA stage III. Key Word(s): 1. HCC; 2. TNF-α; Presenting Author: QIAN BI Additional Authors: SHANHONG TANG, RUI FAN, NEERAJ AGARWAL, YONGQUAN SHI, TOMOO IWAKUMA, JIE DING Corresponding Author: TOMOO IWAKUMA, JIE DING Affiliations: Xijing Hospital of Digestive Diseases & State Key Laboratory of Cancer Biology, Fourth Military Medical University; University of Kansas Medical Center Objective: Hepatocellular carcinoma (HCC) is a rising cause of cancer-related death in the United States with a 5-year survival rate below 12%. The leading cause of this poor prognosis is metastatic spread.

As there is no data in the literature about maximum survival, 14 years was chosen to represent the maximum

lifetime of a patient (less than 1% of patients were alive in the model at 14 years). Due to the chronic, progressive, and evolutionary nature of the disease, a Markov modeling approach was employed, following patients as they DNA Damage inhibitor passed through a series of clearly defined and mutually exclusive health states throughout their disease. The model was designed to track the health states of patients with HCC in both treatment arms. Patients received first-line treatment (sorafenib or BSC) until documentation of disease progression or until a treatment-limiting AE occurred (first-line treatment—no progression). At the point of progression, patients could either continue on first-line treatment (first-line treatment continued—post-progression) or switch to BSC (BSC—post-progression). At any point in the model, patients could die due to all-cause (general) mortality (Fig. 1). The model structure is consistent with clinical practice and other economic models developed in oncology,14–18 and was validated by clinical experts in the USA. The model used monthly cycles (30 days) to match treatment patterns, that is, patients have the possibility to move from one health state to another every month. For the analysis, the following assumptions

were made: The HCC population and the efficacy data from the SHARP trial were generalizable to the USA; Health effects are expressed as life-years (LY). Costs are given as 2007 US dollars. Results are presented as incremental LY, incremental selleck products costs, and incremental cost-effectiveness ratios (ICER) in terms of cost per LY gained. An annual discount rate of 3%19 was applied to both costs and health benefits occurring beyond the first year. The model used the effectiveness data from the SHARP trial. These

included TTP according to investigator radiological assessment, OS, sorafenib dosing, and the rate of all grade 3 and grade 4 AE. Due to the statistically and clinically significant OS benefit observed at an interim analysis in the sorafenib arm, the SHARP trial 上海皓元医药股份有限公司 was stopped at 72 weeks. Therefore, the OS and TTP results were extrapolated using survival functions that best fit the patient-level data. (Calculations were done in stata). Assuming nothing else changes in the two treatment arms except time, these estimated survival functions utilize all available data and thereby lead to the most accurate extrapolation.20 The Akaike information criteria, which measure the goodness-of-fit of an estimated statistical model,21 showed that a lognormal model provided a significantly better fit compared to a Weibull, loglogistic, exponential, or Gompertz distribution in the sorafenib subgroup, and an equally good fit as the loglogistic distribution in the BSC subgroup. Thus, lognormal distribution was chosen (Fig. 2).

Regarding TDF exposure, twelve, one and one patient(s) received TDF from the first, second and third trimester, respectively. The median duration of TDF exposure during pregnancy was 35 weeks (range: 5-39

weeks). HBV-DNA was assessed at delivery in 12 patients. Among these, 10 patients (83%) had HBV-DNA < 6 logIU/mL at delivery. Two cases of high HBV-DNA were associated with non-compliance and TDF discontinuation at week 9 of pregnancy. The median gestational age at delivery was 39 weeks (range: R788 34-40 weeks). No adverse events related to TDF and no cases of birth defects were observed. Five patients reported breastfeeding, and 3 of them breastfed while receiving TDF treatment without any consequence on the babies up to 1 year. No cases of positive HBsAg were observed in infants. Additionally, among 5 infants with anti-HBs testing, all were anti-HBs positive (84-308mIU/mL). Conclusions: In a HBV real-life cohort, TDF treatment from the first trimester of pregnancy was well tolerated. No cases of MTCT were observed. Moreover, no safety issues were reported for breastfeeding while on TDF up to 1 year. Disclosures: Nathalie Ganne-Carrie – Advisory Committees see more or Review Panels: Roche, MSD; Speaking and Teaching: BMS, Gilead Xavier Causse – Board Membership: Gilead, BMS, MSD, Janssen-Cilag; Speaking and Teaching: Roche, Gilead, BMS, Janssen-Cilag Jean-Pierre H. Zarski – Advisory

Committees or Review Panels: BMS, Gilead, Janssen Cilag, BMS, Gilead, Janssen Cilag; Consulting: Roche, Scherring Plough, Novartis, Roche, Scherring Plough, Novartis; Speaking and Teaching: Siemens Fabien Zoulim – Advisory Committees or Review Panels: Gilead; Consulting:

Roche; Grant/Research Support: Gilead, Scynexis, Roche; Speaking and Teaching: Novartis, Roche, Janssen, Bristol Myers Squibb, Gilead Isabelle Fouchard-Hubert – Speaking and Teaching: JANSSEN Olivier P. Libert – Employment: Gilead Sciences Marie Terrier- Management Position: Gilead Sciences Christiane Stern – Employment: Gilead Sciences Patrick Marcellin – Consulting: Roche, Gilead, BMS, Vertex, Novartis, Janssen-Tibotec, MSD, Boehringer, Pfizer, Abbott, Alios BioPharma; Grant/Research Support: Roche, Gilead, BMS, Novartis, Janssen-Tibotec, MSD, Alios BioPharma; Speaking and Teaching: Roche, Gilead, BMS, Vertex, Novartis, Janssen-Tibotec, medchemexpress MSD, Abbott The following people have nothing to disclose: Ghassan Riachi, Bruno Roche, Hervé Desmorat, Thierry Constant, Jean françois D. Cadranel, Denis Ouzan Background and aim; Non-invasive methods are therefore becoming increasingly important in the assessment of liver histopathology in CHB patients. One of such techniques is LSM performed with transient elastography (TE). In this study we compared pre-treatment liver histology and liver LSM results of CHB patients, and we evaluated the five-year prognostic value of LSM in CHB patients.

Regarding TDF exposure, twelve, one and one patient(s) received TDF from the first, second and third trimester, respectively. The median duration of TDF exposure during pregnancy was 35 weeks (range: 5-39

weeks). HBV-DNA was assessed at delivery in 12 patients. Among these, 10 patients (83%) had HBV-DNA < 6 logIU/mL at delivery. Two cases of high HBV-DNA were associated with non-compliance and TDF discontinuation at week 9 of pregnancy. The median gestational age at delivery was 39 weeks (range: selleck chemicals llc 34-40 weeks). No adverse events related to TDF and no cases of birth defects were observed. Five patients reported breastfeeding, and 3 of them breastfed while receiving TDF treatment without any consequence on the babies up to 1 year. No cases of positive HBsAg were observed in infants. Additionally, among 5 infants with anti-HBs testing, all were anti-HBs positive (84-308mIU/mL). Conclusions: In a HBV real-life cohort, TDF treatment from the first trimester of pregnancy was well tolerated. No cases of MTCT were observed. Moreover, no safety issues were reported for breastfeeding while on TDF up to 1 year. Disclosures: Nathalie Ganne-Carrie – Advisory Committees Palbociclib or Review Panels: Roche, MSD; Speaking and Teaching: BMS, Gilead Xavier Causse – Board Membership: Gilead, BMS, MSD, Janssen-Cilag; Speaking and Teaching: Roche, Gilead, BMS, Janssen-Cilag Jean-Pierre H. Zarski – Advisory

Committees or Review Panels: BMS, Gilead, Janssen Cilag, BMS, Gilead, Janssen Cilag; Consulting: Roche, Scherring Plough, Novartis, Roche, Scherring Plough, Novartis; Speaking and Teaching: Siemens Fabien Zoulim – Advisory Committees or Review Panels: Gilead; Consulting:

Roche; Grant/Research Support: Gilead, Scynexis, Roche; Speaking and Teaching: Novartis, Roche, Janssen, Bristol Myers Squibb, Gilead Isabelle Fouchard-Hubert – Speaking and Teaching: JANSSEN Olivier P. Libert – Employment: Gilead Sciences Marie Terrier- Management Position: Gilead Sciences Christiane Stern – Employment: Gilead Sciences Patrick Marcellin – Consulting: Roche, Gilead, BMS, Vertex, Novartis, Janssen-Tibotec, MSD, Boehringer, Pfizer, Abbott, Alios BioPharma; Grant/Research Support: Roche, Gilead, BMS, Novartis, Janssen-Tibotec, MSD, Alios BioPharma; Speaking and Teaching: Roche, Gilead, BMS, Vertex, Novartis, Janssen-Tibotec, MCE公司 MSD, Abbott The following people have nothing to disclose: Ghassan Riachi, Bruno Roche, Hervé Desmorat, Thierry Constant, Jean françois D. Cadranel, Denis Ouzan Background and aim; Non-invasive methods are therefore becoming increasingly important in the assessment of liver histopathology in CHB patients. One of such techniques is LSM performed with transient elastography (TE). In this study we compared pre-treatment liver histology and liver LSM results of CHB patients, and we evaluated the five-year prognostic value of LSM in CHB patients.