showing bile acid–dependent liver growth and regeneration.18 Serum ALT and AST levels were higher in both cholic acid–fed groups, but not different between WT and KO mice (data not shown).

However, serum total bile acid levels in cholic acid–fed KO mice were approximately five-fold higher and hepatic bile acid levels three-fold higher than in WT mice, suggesting defective ability to regulate serum and liver bile acid levels (Fig. 6C,D). Expression of the sinusoidal bile acid uptake transporters Ntcp, Slco1a1, and Slco1b2 were lower in both cholic acid–fed groups (Fig. 7A). Expression of the latter two genes was also lower in chow-fed KO mice. Expression of the basolateral efflux transporters Abcc3 (Mrp3) and Abcc4 (Mrp4) was not different, Wnt inhibitor although there was a trend toward higher 5-Fluoracil in vitro Abcc4 levels in KO mice. Among the canalicular transporters, expression of Bsep (Abcb11) was lower in cholic acid–fed KO mice, whereas Abcb4 (Mdr2) was up-regulated in both cholic acid–fed

groups (Fig. 7B). Expression levels of other sinusoidal transporters were similar between the cholic acid–fed groups. Of the bile acid regulatory genes, expression of farnesoid X receptor (FXR) was lower in both cholic acid–fed groups. However, Shp-1 expression, a downstream target of FXR, was up-regulated in both WT and KO mice on a cholic acid diet (Fig. 7C). Fgf4r levels were similar in all four groups. Expression of constitutive androstane receptor (CAR) was lower in both cholic acid–fed groups and in chow-fed KO mice. However, despite lower expression levels of CAR, KO mice had higher expression of the downstream target of CAR, Cyp2b10. This result suggests that activation of CAR, possibly by a post-transcriptional mechanism, occurs in KO mice and may represent

a Methane monooxygenase protective mechanism to down-regulate bile acid biosynthetic genes. PPARα expression was higher in both cholic acid groups whereas pregnane X receptor expression was lower in cholic acid–fed KO mice. After H&E staining, histology samples from WT mice showed mildly increased lobular inflammation on cholic acid diet (Fig. 8). On the other hand, cholic acid–fed KO mice had increased ductular reaction and greater lobular inflammation on cholic acid diet along with increased pericellular fibrosis on reticulin staining. Staining for F-actin showed that WT mice on cholic acid diet had dilated bile canaliculi, likely reflecting the choleretic effect of bile acids (Fig. 8, bottom panel). However, the interconnected lattice-like structure of canaliculi was preserved in WT livers on cholic acid diet. On the other hand, KO mice on cholic acid diet had canaliculi that were not only dilated but also tortuous and distorted (Fig. 8P). Formation and excretion of bile is one of the important functions of the liver. This task is achieved by the coordinated action of multiple proteins and cellular organelles.

The case presented

illustrates a young patient with acquired FXIII deficiency with a good clinical response to cryoprecipitate and difficulty in hemostasis monitoring utilizing clinically available assays. “
“Many risk factors for falls identified in the general population are found in patients with haemophilia. Furthermore, fall risk increases with age and patients with haemophilia are increasingly entering the over 65 age group. After a fall occurs, there are often Kinase Inhibitor Library mouse behavioural changes that have significant health consequences and further increase fall risk. Fall risk can be quickly assessed in the clinical setting with specific questions in the medical history and by a variety of performance-based screening tools. Identification of fall risk enables early intervention, thereby preventing injury and fear of physical

activity, both of which have been associated with falling and may carry an increased risk in patients with haemophilia. Review of the existing literature on assessment of fall Protein Tyrosine Kinase inhibitor risk reveals the importance of screening in the clinical setting, which is commonly done via a fall history and performance-based assessment tools. Selecting appropriate fall risk screening tools is an important step in identifying and providing optimal interventions for those at risk. Assessments of fall history, fear of falling, gait velocity, gait variability and vestibular dysfunction are suggested as screening tools for patients with haemophilia. Additional research is needed to determine the optimal screening, evaluation and treatment techniques for these patients. The longitudinal physical therapy care provided by Haemophilia Treatment Centres presents a unique opportunity for instituting measures that will reduce the incidence of falling in patients with haemophilia. “
“Factor XIII (FXIII) deficiency is a rare congenital bleeding disorder. There is a paucity of data

in MYO10 the literature about obstetrics and gynaecological problems in women affected by FXIII deficiency. The aim of this study was to examine gynaecological problems and obstetric complications and outcome in women with congenital FXIII deficiency. An electronic search was performed to identify the published literature on PUBMED, MEDLINE, EMBASE, Journals @OVID and CINAHL Plus databases using the following keywords: ‘congenital factor XIII deficiency’ AND ‘women OR Pregnancy’. A total of 39 relevant articles were found and included in this systematic review; 27 case reports and 12 case series dating from 1964 to 2012. A total of 121 women were identified. Menorrhagia (26%) was the second most common bleeding reported after umbilical bleeding. Ovulation bleeding reported in 8% of women. Among 63 women, 192 pregnancies were reported; of these, 127 (66%) resulted in a miscarriage and 65 (34%) reached viability stage. In 136 pregnancies without prophylactic therapy, 124 (91%) resulted in a miscarriage and 12(9%) progressed to viability stage.

In DDC-fed animals, an HF diet resulted in greater liver injury and up-regulation of inflammation-related genes. As a potential mechanism, K8/K18 accumulation and increased ecto-5′-nucleotidase (CD73) levels were noted. In the genetically BAY 57-1293 in vivo susceptible K8tg mice, HF diet triggered hepatocellular injury, ballooning, apoptosis, inflammation, and MDB development by way of 1) decreased expression of the major stress-inducible chaperone Hsp72 with appearance of misfolded keratins; 2) elevated levels of the transglutaminase

2 (TG2); 3) increased K8 phosphorylation at S74 with subsequent TG2-mediated crosslinking of phosphorylated K8; and 4) higher production of the MDB-modifier gene CD73. Conclusion:

Our data demonstrate that HF diet triggers aggregate formation and development of liver injury in susceptible individuals through misfolding and crosslinking of excess K8. (Hepatology 2014;60:169–178) “
“Serum ferritin was recently reported to have low diagnostic accuracy for the detection of advanced fibrosis in patients with non-alcoholic fatty liver disease (NAFLD). To corroborate these findings, we investigated the diagnostic accuracy of serum ferritin levels for detecting PD 332991 liver fibrosis in NAFLD patients utilizing a large Japanese cohort database. A total 1201 biopsy-proven NAFLD patients, seen between 2001 and 2013, were enrolled into the Japan Study Group of NAFLD. Analysis

was performed on data from this cohort comparing between serum ferritin levels and hepatic histology. Serum ferritin increased with increasing histological grade of steatosis, lobular inflammation and ballooning. Multivariate analyses revealed that sex differences, steatotic grade and fibrotic stage were independently associated with serum Reverse transcriptase ferritin levels (P < 0.0001, <0.0001, 0.0248, respectively). However, statistical analyses performed using serum ferritin levels demonstrated that the area under the receiver–operator curve for detecting fibrosis was not adequate for rigorous prediction. Several factors including sex differences, steatosis and fibrosis were found to correlate with serum ferritin levels. Therefore, serum ferritin may have low diagnostic accuracy for specifically detecting liver fibrosis in NAFLD patients due to the involvement of multiple hepatocellular processes. Non-alcoholic fatty liver disease (NAFLD) is an important cause of chronic liver injury in many countries around the world.[1] NAFLD represents a spectrum of conditions that are histologically characterized by macrovesicular hepatic steatosis and a diagnosis is made in patients who have not consumed alcohol in amounts sufficient to be considered harmful to the liver.

In addition, we analyzed the relationship between the time interval from RFA of HCC to recurrence and prognosis. Between February 2001 and September 2007, 263 consecutive Japanese patients with small HCC were referred to our hospital for treatment. None had been previously treated for HCC, up to 3 nodules, each up to 3cm in diameter, absence of portal venous thrombosis and known extrahepatic metastases, and Child–Pugh class A or B liver cirrhosis. RFA treatment was selected in consideration of the site, size and number of tumors, functional reserve of the liver, tumor marker level, and the patient’s general status. Of the total number of patients, 89 (34%) were

treated with TACE, 69 (26%) with surgical resection, nine (3%) with PEI, six (2%) with liver transplantation Fostamatinib purchase (LT) and two (1%) with intraoperative RFA. The remaining 88 (34%) patients with 116 small HCC underwent Selleck Compound Library percutaneous RFA as a first-line treatment option and were included in the study population. Patient characteristics are given in Table 1. The 54 men and 34 women (age range, 45–80 years; median, 68 years) were followed for 14–90 months (median, 36 months). All patients underwent ultrasound-guided

percutaneous RFA, at which time 73 had Child–Pugh class A and 15 had Child–Pugh class B cirrhosis. Most patients (76%, 67/88) had a single tumor, 14 (16%) had two tumors and seven (8%) had three tumors. Maximum tumor diameter ranged 1–3 cm (median, 1.8 cm). Of the 88 patients, the HCC was 2 cm or less in 61 and more than 2 cm in the remaining 27.

The RFA procedure was explained fully to all patients, and informed consent was obtained. Despite the feasibility and availability of surgery, all patients voluntarily preferred ablation Idelalisib solubility dmso under informed consent. This study protocol conformed to the ethical guidelines of the 1975 Declaration of Helsinki. Pretreatment imaging studies included abdominal ultrasonography (US), contrast-enhanced dynamic CT, and angiography combined with CT during arterial portography and hepatic arteriography. In 91 nodules, HCC was diagnosed based on the following classic imaging manifestations: (i) early enhancement at the arterial phase and hypoattenuation at the portal venous phase or at the equilibrium phase on contrast-enhanced dynamic CT; and (ii) hyperattenuation on CT during hepatic arteriography and hypoattenuation on CT during arterial portography.16–18 The remaining 25 nodules in 18 patients were diagnosed as HCC by pathological methods. All 116 nodules were percutaneously treated under US guidance, with all patients under conscious sedation with pentazocine (5–10 mg, Pentagin; Sankyo, Tokyo, Japan) and midazolam (1–4 mg, Dormicum; Astellas, Tokyo, Japan) administrated i.v. Vital signs were continuously monitored during the procedure.

In addition, we analyzed the relationship between the time interval from RFA of HCC to recurrence and prognosis. Between February 2001 and September 2007, 263 consecutive Japanese patients with small HCC were referred to our hospital for treatment. None had been previously treated for HCC, up to 3 nodules, each up to 3cm in diameter, absence of portal venous thrombosis and known extrahepatic metastases, and Child–Pugh class A or B liver cirrhosis. RFA treatment was selected in consideration of the site, size and number of tumors, functional reserve of the liver, tumor marker level, and the patient’s general status. Of the total number of patients, 89 (34%) were

treated with TACE, 69 (26%) with surgical resection, nine (3%) with PEI, six (2%) with liver transplantation ICG-001 cell line (LT) and two (1%) with intraoperative RFA. The remaining 88 (34%) patients with 116 small HCC underwent buy Alpelisib percutaneous RFA as a first-line treatment option and were included in the study population. Patient characteristics are given in Table 1. The 54 men and 34 women (age range, 45–80 years; median, 68 years) were followed for 14–90 months (median, 36 months). All patients underwent ultrasound-guided

percutaneous RFA, at which time 73 had Child–Pugh class A and 15 had Child–Pugh class B cirrhosis. Most patients (76%, 67/88) had a single tumor, 14 (16%) had two tumors and seven (8%) had three tumors. Maximum tumor diameter ranged 1–3 cm (median, 1.8 cm). Of the 88 patients, the HCC was 2 cm or less in 61 and more than 2 cm in the remaining 27.

The RFA procedure was explained fully to all patients, and informed consent was obtained. Despite the feasibility and availability of surgery, all patients voluntarily preferred ablation this website under informed consent. This study protocol conformed to the ethical guidelines of the 1975 Declaration of Helsinki. Pretreatment imaging studies included abdominal ultrasonography (US), contrast-enhanced dynamic CT, and angiography combined with CT during arterial portography and hepatic arteriography. In 91 nodules, HCC was diagnosed based on the following classic imaging manifestations: (i) early enhancement at the arterial phase and hypoattenuation at the portal venous phase or at the equilibrium phase on contrast-enhanced dynamic CT; and (ii) hyperattenuation on CT during hepatic arteriography and hypoattenuation on CT during arterial portography.16–18 The remaining 25 nodules in 18 patients were diagnosed as HCC by pathological methods. All 116 nodules were percutaneously treated under US guidance, with all patients under conscious sedation with pentazocine (5–10 mg, Pentagin; Sankyo, Tokyo, Japan) and midazolam (1–4 mg, Dormicum; Astellas, Tokyo, Japan) administrated i.v. Vital signs were continuously monitored during the procedure.

“
“(Headache

2010;50:256-263) Aim.— To estimate the proportion of individuals with migraine using triptan therapy as a function of their cardiovascular (CV) Compound Library price profile and disease severity. Methods.— As a part of the American Migraine Prevalence and Prevention study, we identified migraineurs representative of the U.S. adult population. Triptan use was estimated as a function of presence of CV disease (CVD), of CV risk factors, and by level of migraine-related disability. Results.— Our sample consists of 6102 individuals with migraine. Compared with migraineurs without risk factors for CVD, triptans were significantly less likely to be used in individuals with diabetes (11.5% vs 18.3%, OR = 0.6, 95% CI = 0.5-0.7), hypertension (14.8%, OR = 0.8, 0.7-0.9) and by smokers (12.9%, OR = 0.7, 0.6-0.8). Similar findings were seen for individuals with established CVD. As contrasted to individuals without CVD, those with myocardial infarct (8.5% vs 18.5%, OR = 0.4, 0.3-0.7), stroke (7%, OR = 0.6, 0.3-0.9) and heart surgery (9.3%, OR = 0.5, 0.4-0.7) were less likely to use triptans. Use of triptan increased as a function of disability regardless of CVD status or presence of CV risk factors. Conclusion.— Triptan use is lower in those with vs without CV risk, suggesting that doctors and/or patients fear using triptans

in individuals at risk to CVD. Furthermore, triptan use in those with established CVD increases with headache-related disability, suggesting that patients and providers balance risks and Birinapant solubility dmso Selleck Decitabine benefits. Additional and analytical data are needed on the safety of triptans in the setting of CVD risk. This study has not assessed adequacy of care. “
“Objectives.— To determine the 1-year prevalence of headache and clinical characteristics of primary headaches among school children in South Korea. Background.— Many population-based studies have estimated the 1-year prevalence of headache, migraine, and tension-type headache (TTH).

The results of those studies vary in terms of race and region. There have been few epidemiological population-based studies of headache in children and adolescents in Korea. Methods.— We conducted a cross-sectional school-based study of a randomized and proportional sample of 5360 boys and girls. All 180 sampled schools participated in this study. The questionnaires collected demographic data in addition to specific questions about headache according to the International Classification of Headache Disorder criteria, 2nd Edition. Valid questionnaires were returned by 94.1% of the sample population. Modified criteria changed the “duration” of migraine (>1 hour instead of 4 hours). Results.— The prevalence of headache among school children was 29.1% (1465/5039) in South Korea. The prevalence of headache in girls (33.4%) was significantly higher than in boys (24.4%) (P < .001). The mean age of students with headaches (14.02 ± 3.

9 mg/dL) on postoperative day five.4 This score was further validated prospectively in a series of patients after liver resection, by showing that 70% of patients who died postoperatively selleck fulfilled the “fifty-fifty criteria”.5 This score was a strong predictor of death on multivariate analysis (odds ratio = 29.4; 95% confidence interval = 4.9-167). An important limitation of this system is its availability for prediction at the earliest 5 days after surgery. A third definition predicting the degree of postoperative hepatic dysfunction6 was based on selective parameters including bilirubin,

prothrombin time, serum lactate levels, and the degree of encephalopathy. Each of these parameters was given 0-2 points, when changes were observed for at least 2 consecutive days. An appealing aspect of

this approach is that the degree of liver failure can be calculated at any time during the postoperative course. The grouping of the score into none, mild, moderate, or severe hepatic dysfunction was shown to correlate with the size of the remnant liver (Fig. 2). The size of the remnant liver is a major determinant of postoperative liver failure, and logically depends on the quality of the liver parenchyma, or in other words, the presence of underlying liver diseases. The impact of Selleck Adriamycin underlying liver conditions will be discussed below, and we will focus here on the ideal scenario of patients presenting without significant risk factors. We tried to determine the minimal amount of remnant liver mass compatible with acceptable postoperative function and Thalidomide survival through a survey including 100 international well-established liver centers

identified through the memberships to two specialized societies in the field: the IHPBA (International Hepato-Pancreatico-Biliary Association) and EHPBA (European Hepato-Pancreatico-Biliary Association).7 The results indicated that most experienced liver surgeons consider 25% (range: 15%-40%) of the remnant liver mass (RLBW: 0.5) as their limit for liver resections. Transplant surgeons, on the other hand, use significantly higher figures, with a GRWR of at least 0.8% (range: 0.6-1.2) which corresponds to 40% of the transplanted total liver volume. The lowest figure of 0.6% should be used only when the graft is implanted in a recipient without cirrhosis or with cirrhosis, but well-preserved liver function (Child A and low MELD score).8 This discrepancy between the critical liver mass needed after liver resection (∼25%) and partial OLT (∼40%) remains unclear. Part of the explanation may include exposure to cold ischemia, immunosuppressants, denervation of the graft, as well as host factors such as changes in vascular flow due to preexisting portal hypertension.

The recruitment of TNF receptor–associated factor 2 (TRAF2) mediates the proinflammatory consequences of CD154/CD40 interaction.61, 62 As IRE1 recruits TRAF2 upon activation, TRAF2 may represent a potential link between the CD40 and IRE1 signalization pathways. Our study does not exclude other mechanisms through which CD154 may

interfere with the progression of liver steatosis. These may involve deregulation of the cytokine network. Indeed, CD154 induces inflammatory cytokines, some of which play a role in lipid metabolism, such as IL-6. IL-6 alleviates liver steatosis63 and IL-6−/− mice develop mature-onset obesity and are prone to hepatic steatosis and metabolic alterations.64, 65 According to the regulatory role of CD154 on IL-6 expression, we found that CD154KO Selleck Ulixertinib mice showed impaired induction of IL-6 following the olive oil–rich diet as shown by a reduced induction of plasma IL-6 levels and liver IL-6 mRNA (Supporting Fig. 9A,B). Hence, the down-regulation of IL-6 expression may provide another mechanism to explain the steatotic phenotype of olive oil–fed CD154KO mice. ER stress also leads to IL-6 production through XBP-1 signaling59, 66 and, accordingly, in HepG2 cells expressing a dominant negative form of IRE1, TM-induced expression of IL-6 was impaired. In this context, the CD154-dependent IL-6 induction Selleck AZD5363 was preserved (Supporting Fig. 9A,B). Therefore, the control

of IL-6 expression is likely to represent another interface linking CD154, the UPR, and hepatic lipid metabolism. This observation suggests that several integrated signaling pathways are likely to account for the contribution of CD154 Ribonuclease T1 in hepatic steatosis. In conclusion, our study shows that CD154 is a mediator involved in the natural history of hepatic steatosis. CD154 appears as a new link between lipid metabolism and inflammation in the liver, supporting the idea of interdependency between inflammation and metabolic disorders.27, 32 The authors thank Chantal Combe, Jérôme Gabet, Alexandra Nicou, and Antonio Palos Pinto for technical help. Additional Supporting Information may be found in the online version of this

article. “
“See article in J. Gastroenterol. Hepatol. 2012; 27: 789–796. Nonalcoholic fatty liver disease (NAFLD) is now the most common cause of chronic liver disease worldwide. Nonalcoholic steatohepatitis (NASH) is a progressive form of NAFLD with the potential for progression to cirrhosis. The pathogenesis of NASH is incompletely understood, but may involve hyperendotoxemia1 secondary to impaired phagocytotic function of Kupffer cells (KCs)2 and consequent KC overproduction of and increased sensitivity to cytokines such as tumor necrosis factor (TNF)-α and interleukin-1β (IL-1β).3 Impaired phagocytotic function of KCs may therefore lead to higher endotoxin levels in the systemic circulation, as has been observed in patients with NASH and in animal models of NASH.

Thirty-nine and 30 patients received RFA 1 and 2-4 times, respectively. After treatments, HCC recurrence was evaluated with dynamic CT or MRI every 3-4 months. All patients gave written informed consent to participate in the study in accordance with the Helsinki declaration, and this study was approved by the regional ethics committee (Medical Ethics Committee of Kanazawa University). Blood samples were tested for hepatitis B surface antigen and hepatitis C virus (HCV) antibody using commercial immunoassays (Fuji Rebio, Tokyo, Japan). The patients with HCV antibody were tested for serum HCV RNA by real-time PCR (Roche, Tokyo, Japan), and 49 of Poziotinib 52 patients with HCV antibody were HCV RNA–positive.

HLA-based typing of PBMCs from patients and normal blood donors was performed using reverse sequence-specific oligonucleotide analysis with polymerase chain reaction (PCR-RSSO). The serum alpha-fetoprotein (AFP) level was measured via enzyme immunoassay (AxSYM AFP, Abbott Japan, Tokyo, Japan), and the pathological grading of tumor cell differentiation was assessed according to the selleck compound library general rules for the clinical and pathological study of primary liver cancer.8

The severity of liver disease was evaluated according to the criteria of Desmet et al. using biopsy specimens of liver tissue, where F4 was defined as cirrhosis.9 Fifty-five patients who participated in the present study received liver biopsy with RFA. Another 14 patients received liver biopsy 1-3 years before RFA. Eleven peptides that we

previously identified as being useful for analysis of immune response in HLA-A24–positive HCC patients were selected.10-13 Human immunodeficiency virus (HIV) envelope-derived peptide (HIVenv584)14 and cytomegalovirus (CMV) pp65-derived peptide (CMVpp65328)15 were also selected as control peptides. Peptides were synthesized at Sumitomo Pharmaceuticals Anacetrapib (Osaka, Japan). They were identified using mass spectrometry, and their purities were determined to be >90% by analytical high-performance liquid chromatography. PBMCs were isolated before and 2-4 weeks after HCC treatments as described.11 In the patients who received RFA 2-4 times, PBMCs were obtained 2-4 weeks after the final treatment. In some patients, PBMCs were also obtained 24 weeks after RFA. PBMCs were resuspended in Roswell Park Memorial Institute 1640 medium containing 80% fetal calf serum and 10% dimethyl sulfoxide and cryopreserved until use. Interferon-γ (IFN-γ) ELISPOT assays were performed as described.11 Negative controls consisted of an HIV envelope–derived peptide (HIVenv584).14 Positive controls consisted of 10 ng/mL phorbol 12-myristate 13-acetate (PMA, Sigma) or a CMVpp65-derived peptide (CMVpp65328).15 The colored spots were counted with a KS ELISpot Reader (Zeiss, Tokyo, Japan). The number of specific spots was determined by subtracting the number of spots in the absence of an antigen from the number in its presence.

19, 0.80-1.78) was not.

Conclusions: Younger (<40y) HCV LT recipients have significantly reduced graft survival, higher rates of re-LT and HCV-related death than older HCV recipients. This suggests a more aggressive natural history for HCV disease post-LT and identifies a group in need of early consideration of HCV therapy. Disclosures: Norah Terrault - Advisory Committees or Review Panels: Eisai, Biotest; Consulting: BMS, Merck; Grant/Research Support: Eisai, Biotest, Vertex, Gilead, AbbVie, Novartis, Merck The following people have nothing to disclose: Varun Saxena, Jennifer L. Dodge, John P. Roberts Background/Aims: To identify the impact of portal vein thrombosis (PVT) on post liver transplant www.selleckchem.com/products/Romidepsin-FK228.html (LT) outcomes along with other covariates and assess factors associated with complications amongst PVT patients. Methods: www.selleckchem.com/products/DAPT-GSI-IX.html Retrospective cohort study of 621 adult LT recipients (University of Alberta, London Health Sciences Centre) between 01/2002-12/2012. PVT

was identified in 147 (24%) patients and 474 (76%) non-PVT patients served as controls. Cox survival analysis was performed to determine independent associations with overall mortality. Results: Demographic factors (mean age 53, 69% male) were similar between groups. There were also no differences in mean MELD (PVT 19 vs. controls 19, p=0.9) and Child Pugh scores (10 vs. 10, p=0.9) on the day of LT. Donor factors (mean DRI:1.6 vs. 1.5, p=0.2) were similar. Using Cox multivariable survival analysis, covariates independently associated with overall mortality included Age (adjusted Hazard ratio ∼ aHR 1.02, p=0.015) and requiring ICU support pre-LT (aHR 2.17, p=0.006), but not PVT (p=0.67). 5-year survival was similar between PVT and controls (75%,p= 0.8). In comparing PVT patients who did not survive (n=32) with PVT survivors (n=115), non-survivors (n=32) were more likely to have complete thrombus occlusion (38% vs. 13%, p=0.027) and

hepatofugal flow (31% vs. 13%, p=0.08). Non-survivors were more likely require thrombectomy (69 vs. 31%, p=0.08) and develop reocclusion post-LT (16% vs. 3%, p=0.024). Anti-coagulation rates were similar between groups. Conclusion: Well-selected LT patients who had PVT prior to LT have similar post-LT outcomes with O-methylated flavonoid controls when adjusting for donor and recipient factors. Subgroups of PVT LT patients who did worse post-LT (complete thrombosis pre-LT, thrombectomy at LT and reocclusion post-LT) warrant closer evaluation in listing and management post-LT. Adjusted survival (Cox) for PVT LT recipients vs. controls (p=0.67). Disclosures: Constantine J. Karvellas – Grant/Research Support: Merck; Speaking and Teaching: Gambro The following people have nothing to disclose: Filipe S. Cardoso, Malcolm M. Wells, Fayaz A. Handoo, Lukasz Kwapisz, Mansour G. Alghanem, Norman Kneteman, Paul Marotta, Bandar Al-Judaibi Background.