Furthermore, reduced DNA binding of FXR/RXRα caused by FXR hyperacetylation may contribute to the decreased FXR-binding sites observed in obesity (5,272, compared to 15,263 sites in healthy mice). Ibrutinib molecular weight An important, unexpected finding in these studies is that binding of agonist-activated FXR was often associated with repression of gene expression. In a large fraction (8 of 16) of genes

examined, binding of ligand-activated FXR was associated with decreased mRNA levels, which was confirmed by decreased RNAPII occupancy and reduced acetylated histone H3K9/K14 levels. More important, levels of known histone gene-repression marks as well as H3K9 and H3K27 methylation, were markedly increased at those genes that were repressed in healthy mice after exposure to the FXR agonist, GW4064, for a short 1- or 3-hour treatment. Because mRNA levels were measured after 1-hour treatment, in addition to overnight treatment with GW4064, direct effects of FXR on gene transcription were likely detected. Although our follow-up epigenetic and gene-expression studies have suggested that gene repression by FXR is common, direct comparison of FXR binding with a comprehensive global transcriptome analysis using RNA sequencing or microarray will be necessary to definitively ICG-001 manufacturer determine the extent of gene repression relative to gene activation by agonist-activated FXR. FXR is well known to repress its target genes

indirectly through the induction of SHP.11-14 These present studies suggest that FXR may also directly repress its target genes by unknown mechanisms. FXR could directly repress by binding to the

DNA as a FXR/RXRα heterodimer or as a monomer or homodimer, as previously shown in the regulation of apolipoprotein A1,29 which results in the inhibition of DNA binding of key transcription factors. In addition, FXR could directly inhibit genes by tethering to DNA-binding transcription factors and masking their interaction with coactivators and/or facilitating the interaction with corepressors. Sumoylation of peroxisome proliferator-activated receptor gamma and liver X receptor has been shown to be directly involved in the repression Selleckchem Doxorubicin of inflammatory genes by the tethering of these nuclear receptors to DNA-binding activators, such as, nuclear factor kappa light-chain enhancer of activated B cells or activator protein 1.30 We have evidence that FXR is sumoylated in mouse liver extracts (D.H.K. and J.K.K., unpublished data), and FXR was shown to inhibit inflammatory responses,9, 10 so that this is a possible mechanism for FXR gene repression. Whether FXR directly suppresses its target genes by binding to DNA or tethering to other transcription factors is an important area of future investigation. In conclusion, these studies analyze, for the first time, a genome-wide comparison of FXR-binding sites in the livers of healthy and dietary obese mice.

[37] PPAR-α

antagonism leads to hepatic lipid accumulation.[22] miR-27′s induction selleck of lipid accumulation was also reversed by the PPAR-α agonist bezafibrate (Fig. 3). Therefore, HCV-induced expression of miR-27 represents a novel mechanism by which the virus inhibits PPAR-α signaling and promotes steatosis (Fig. 6). Overexpression of individual viral proteins revealed that both core and NS4B independently activate miR-27a and miR-27b expression (Fig. 1F; Supporting Fig. S2). Both of these viral proteins have previously been reported to promote lipogenesis.[38] In the case of HCV core, its expression has previously been shown to down-regulate PPAR-α expression.[39] Separate studies demonstrated that HCV core[27] and NS4B[28] promote SREBP activity through the PI3K pathway. Our results suggest that the viral AZD2281 cell line proteins also use the PI3K pathway for activation of miR-27 expression to induce steatosis (Supporting Fig. S3). Furthermore, these results are consistent with a

model of steatosis where HCV core modulates PPAR-α expression through up-regulation of miR-27 expression. The observed repression of ANGPTL3 (Supporting Fig. S4A) may be another mechanism by which HCV-induced miR-27 expression promotes triglyceride accumulation in vivo. A previous study suggested that miR-27b inhibits ANGPTL3 expression in response to dyslipidemia to prevent lipid accumulation in circulation.[14] This is due to its role as an inhibitor of lipoprotein lipase (LPL), a key enzyme in free fatty acid uptake.[40] Decreased ANGPTL3 levels would lead to increased LPL activity and fatty acid uptake into hepatocytes, highlighting an additional mechanism contributing to miR-27′s role in HCV-induced steatosis in patients. Our results also suggest that miR-27 levels can influence the HCV viral lifecycle. At the level of replication, miR-27b appears to play an antiviral role against HCV genotype 1b replication (Fig. 4). As miR-27 is not predicted to have conserved binding sites in the HCV genome,[41] inhibition of HCV replication is most likely dependent on miR-27′s regulation of host gene expression. HCV genotype 2a appears less susceptible to miR-27-mediated

MRIP inhibition (Supporting Fig. 10), consistent with previous observations of sequence-dependent variation in HCV resistance against metabolic inhibitors.[42] Our previous work demonstrated that PPAR-α antagonism is capable of inhibiting genotype 1b HCV replication by inducing hepatic lipid accumulation and blocking the biosynthesis of new lipids required for protein lipidation.[22] This disrupts the HCV-induced cellular lipid environment required for efficient HCV replication.[22] Here we propose an analogous model where miR-27 acts like an endogenous PPAR-α antagonist, resulting in disruption of HCV replication complexes (Fig. 6). An additional antiviral mechanism in vivo for miR-27 may lie in its regulation of ANGPTL3.

Again, this may relate to allocation policy, as patients with T3 lesions are not given priority for deceased donation. It is also important

to note that the non-LDLT group did contain significantly more patients with HCV, fewer with cholestatic liver disease, and more racial diversity. Although these factors were adjusted for in the model, the power to detect differences is impacted as the numbers decrease. In addition, although this was a multicenter study the results of individual centers were not reported. A center effect has been reported to have a major impact on outcomes with liver transplantation.4 Although it is likely all centers within A2ALL are highly experienced at both living donor and deceased donor transplant, it is not known whether these results could be applied to all centers. In addition, there are marked geographic differences in MELD

threshold for access to deceased donor transplant, as check details well as in the quality of deceased donor allografts.5, 6 These differences would likely augment or mitigate the survival benefit of living donor transplant, depending on the donor service area and region of the transplant center. Finally, and most essentially, this was not a randomized trial of all patients wait-listed for liver transplantation, but rather of a selected group of patients deemed appropriate candidates for LDLT by their transplant centers. Thus, centers must still consider what is best for each and every individual patient on their wait list based on factors that may impact outcome at their center. If there is a very short anticipated wait time to DDLT based on factors such as HCC MELD exception selleck kinase inhibitor old or favorable blood type, then a survival benefit to LDLT compared to DDLT likely will not be present. For individual patients, other factors that impact the decision to proceed to LDLT beyond the

potential for a survival benefit, such as uncontrolled encephalopathy, refractory ascites, and intractable pruritus must also be carefully considered. In the future, information regarding validated quality of life outcomes following LDLT versus prolonged time on the wait list and/or DDLT would provide exceptionally helpful additional guidance to assist in discussion with patients and families regarding timing and donor options for liver transplantation. “
“In the most recent American Association for the Study of Liver Diseases hepatitis B virus (HBV) guidelines, Drs. Lok and McMahon recommend as “prudent” “to test all human immunodeficiency virus (HIV)-infected persons for both hepatitis B surface antigen (HBsAg) and antibody to hepatitis B core antigen (anti-HBc) and if either is positive, to test for HBV DNA”.1 I think that the recommendation of testing for HBV DNA in HIV-infected patients with isolated anti-HBc antibodies should be better supported by clinical evidence. HBV DNA testing is an expensive test, and unless there is a well-defined clinical benefit, it is difficult to justify it.

14, 15 X-396 Moreover, several data link PGC-1β with the LXR pathway. PGC-1β is recruited to the promoter region of CYP7a1 and ABCA1 and activates the expression of these target genes. More recently, have it has been shown that Foxa2 interacts with PGC-1β to increase serum TG by activating Mttp and Dgat2 expression.16, 17 Additionally, it has been demonstrated that PGC-1β and its target gene apolipoprotein C3 are down-regulated by nicotinic acid that mediates TG-lowering effects and is widely used for treating hypertriglyceridemia.18, 19 Finally, whole

body ablation of PGC-1β impairs hepatic lipid metabolism in response to acute high fat dietary loads, resulting in hepatic steatosis.18 Given the importance of hepatic lipid and mitochondrial LY2606368 molecular weight metabolic dysfunctions in NASH, we wondered whether the PGC-1β regulatory network could represent a potential new therapeutic target for this hepatic disease. Thus, our aim was to address the contribution of PGC-1β constitutive activation during the development of steatohepatitis and steatosis. Here, using two nutritional (methionine choline-deficient diet [MCD] and high-fat diet) models of NASH and NAFLD in hepatic transgenic mice for PGC-1β, we show that the overexpression of this coactivator ameliorates hepatic steatosis, reduces lipid overload

in the hepatocytes, and reduces the fibrotic and apoptotic phenotype. This outcome was mediated by the ability of PGC-1β to

sustain the expression of target genes of several metabolic pathways that are L-NAME HCl severely compromised during steatohepatitis. To generate pLiv.7 PGC-1β, first the hPGC-1β (3.1 kb) fragment with KpnI and XhoI restriction sites was generated by polymerase chain reaction (PCR) from pcDNA3 PGC-1β plasmid. The fragment was inserted into the KpnI and XhoI site of pLiv7, which carries the promoter, exon 1 and a fragment of exon 2 of apolipoprotein E, a protein expressed exclusively in the liver. The LivPGC-1β transgenic mice were generated by injecting into the pronuclei of the fertilized eggs of the FVB/N mice the transgene plasmid digested with SpeI. Mice carrying the transgene were identified by PCR of genomic DNA to confirm the presence of the hPGC-1β coding sequence. Stomach, liver, brain, kidney, jejunum, duodenum, ileum, and colon of transgenic mice were dissected and prepared for total RNA extraction and immunohistochemistry to evaluate the specific hepatic expression of transgene under the apolipoprotein E promoter control. For dietary protocol, wildtype and LivPGC-1β mice were randomly divided into two experimental groups and fed with MCD, high-fat diet (D12451, Research Diets), and their control diets (MCS and chow diet respectively) for 8 weeks. During the experimental period, individual body weight was recorded every 5 days.

HP was more prevalent among patients with CAD and with increasing the number

of coronary arteries with stenosis, the HP seropositivity increased so that 76.3% of patients with multiple vessel diseases (MVD) and 70% of patients with single vessel diseases (SVD) were HP seropositive versus 50% in control group and this difference was statistically significant between groups (OR=3.86, 95%CI=1.48-10; P = 0.006). Positive CAD was significantly associated with HDL level (OR=0.92, 95%CI=0.86-0.96; P = 0.01) and ESR (OR=1.07, 95%CI=1.02-1.13; P = 0.006). Also, CAD positive patients had higher CRP levels GSI-IX chemical structure than controls and it was statistically different in SVD group compared to controls (p < 0.05). HP seropositive patients had no difference with seronegative ones. Conclusion: HP infection is more prevalent in CAD positive patients and in case of proofing causal relationship, it can be considered as a reversible risk factor for CAD. Key Word(s): 1. Helicobacter pylori infection; 2. coronary artery disease; 3. risk factor Presenting Author: JAMSHID VAFAEIMANESH Additional Authors: MOHAMMAD BAGHERZADEH, MAHMOUD PARHAM Corresponding Author: JAMSHID VAFAEIMANESH Affiliations: Clinical Research Development Center, Clinical Research

Development Center Objective: Chronic complications of diabetes are one of the major causes of morbidity and mortality of this disease and MK-2206 ic50 of the most common complications, vascular events have a special role. Although prolonged hyperglycemia appears to play a key role in these events, but the precise mechanisms of these effects are Nabilone not fully understood, and recent studies have discussed about the role of inflammation.

Regarding the effect of infections in systemic inflammation and high prevalence of Helicobacter pylori (HP) in the population, the aim of this study was to investigate the association between HP infection and microvascular complications of diabetes. Methods: In this cross-sectional study 211 patients with type II diabetes have been examined. Subjects were divided into two groups (HP+ and HP-) based on HP infection (diagnosed with IgG serology), and the association between these groups and microvascular complications of diabetes including nephropathy (based on protein excretion in 24-hour urine collection), retinopathy (based on examination by an ophthalmologist) and neuropathy (diapason and monofilament examination) has been evaluated. Results: Of the 211 subjects studied, 125 (59.24%) were HP+. The mean duration of diabetes was not significantly different in both groups. In this study, we found a significant association between HP infection and diabetic neuropathy (p = 0.04), but there was no correlation between HP infection and diabetic nephropathy and retinopathy (p = 0.2 and p = 0.43, respectively). Conclusion: Infection with H. pylori increases the risk of diabetic neuropathy and is considered as a possible risk factor diabetic neuropathy. Key Word(s): 1. diabetes mellitus; 2.

To develop a clearer understanding of the pathophysiology of FH iPSC–derived hepatocytes, selleck chemicals we reprogrammed fibroblasts from JD, a 14-year-old boy with cutaneous

xanthomatosis and advanced cardiovascular disease.13 The choice to generate JD hiPSCs was considered historically relevant because Brown, Goldstein, and colleagues, in establishing the LDLR paradigm, studied JD fibroblasts extensively.10, 11 We produced several JD iPSC lines by transducing primary fibroblasts with lentiviral vectors encoding the transcription factors OCT4, SOX2, NANOG, and LIN2814 and demonstrated that they expressed characteristic markers of pluripotency (Fig. 1A). In each hiPSC line, we confirmed the retention of the JD LDLR mutations (Fig. 1B, Supporting Fig. 1), established that each had a normal karyotype (Fig. 1C), and determined that each JD hiPSC line could differentiate into derivatives of all three germ layers using teratoma assays Dabrafenib (Fig. 1D). Using a previously described protocol (Fig. 2A), which we had shown could generate functional hepatocyte-like cells (referred to here as hepatocytes),4, 9 we demonstrated that each JD hiPSC clone was capable of directed differentiation toward a hepatic fate. On day 20 of differentiation, the morphology of both control hiPSC– and JD hiPSC–derived cells was indistinguishable

and closely resembled that of hepatocytes, including the presence of PAK5 lipid vesicles, a high cytoplasmic to nuclear ratio, granular cytoplasm, and prominent nucleoli (Fig. 2B). In addition, the differentiated cells expressed hepatocyte markers, including hepatocyte nuclear factor 4a (HNF4a) and albumin (Fig. 2C). Flow cytometric analyses of hepatocytes from both control and JD hiPSCs confirmed that the cells differentiated into asialoglycoprotein receptor (ASGPR1)-positive

hepatocytes with comparable efficiency (Fig. 2D). Only cells expressing high levels of ASGPR1 were counted to avoid the possibility of counting false negatives. Finally, hepatocytes derived from control hESCs or hiPSCs as well as JD hiPSCs were found to express hepatic mRNAs at similar levels, whereas expression of each of these mRNAs was not detected in undifferentiated hESCs (Fig. 2E). Based on these data, we conclude that JD iPSCs could be directed to form cells with hepatocyte characteristics at efficiencies that were comparable to hESCs or control hiPSCs. The FH associated with JD is a consequence of compound heterozygosity at the LDLR locus. JD inherited a maternal allele containing a 5-kb deletion spanning part of exon 13 and all of exons 14 and 15 that results in the absence of functional protein.13 The inherited paternal allele contains an A>G transition within exon 17, which encodes a tyrosine>cysteine substitution at residue 807 in the LDLR cytoplasmic domain resulting in a mutant protein that can still bind LDL, but is inefficiently internalized.

Case report. A 54-year-old male with a history of myelofibrosis and no previous diagnosis of a headache disorder

presented to the emergency department with worsening severe bilateral headaches. A nonenhanced CT of the brain was performed and diffuse extra-axial nodular hyperdensities were visualized. MRI of the brain demonstrated diffuse extra-axial avidly enhancing nodular masses, dural thickening and marked susceptibility. No paravertebral masses, typical for extramedullary hematopoiesis, were present in the chest or abdomen. Although the clinical team considered a biopsy to confirm the diagnosis, we suggested a noninvasive confirmatory test. The subsequent Tc99m sulfur colloid scan corroborated the diagnosis. The patient was then referred to radiation oncology for treatment. In summary, extramedullary hematopoiesis is a hematologic compensatory disorder that rarely occurs within the CNS and may cause neurological compromise due to compression DAPT chemical structure on underlying structures. The diagnosis can be made with noninvasive imaging and treated with low dose radiation therapy. “
“Pleomorphic xanthoastrocytoma (PXA) is a brain neoplasm included Lumacaftor concentration in the astrocytic group, exceptionally manifesting with meningeal dissemination.

We described a 27-year-old patient presented with acute bilateral visual loss and papilledema with normal brain computed tomography scan, initially mimicking idiopathic intracranial hypertension (IIH). Brain and spinal cord magnetic resonance imaging (MRI) study revealed a subtle area of hyperintensity

of the gyri surrounding the left central sulcus, and contrast enhancement of the thoracic leptomeninges. Brain biopsy of the PAK6 parietal lesion revealed nonanaplastic PXA. Treatment with temozolomide was given. Yearly control MRI demonstrated new brain lesions and marked progression of leptomeningeal spinal enhancement. In spite of this, the patient has remained stable with no new symptoms. Nonanaplastic PXA may present with widespread meningeal dissemination with acute visual loss and papilledema mimicking IIH, and no clinical progression at 3 years. “
“We report the case of a 59-year-old woman who presented with several episodes of transient ischemic attack (TIA) caused by pathologically confirmed giant cell arteritis. She continued suffering from TIAs during admission despite immunosuppressant and antithrombotic therapy. Sudden neurological deterioration with paraparesis and cognitive impairment developed. A brain magnetic resonance (MR) imaging showed bilateral watershed ischemic lesions. MR angiography demonstrated severe stenosis of both intracranial internal carotid arteries (ICAs). Angioplasty and stenting on the left ICA were performed, with evident clinical improvement occurring within 24 hours. Endovascular therapy may be an alternative option to treat severe GCA with symptomatic intracranial large vessel disease not responsive to intensive conventional medical treatment.

Methods: A survey was conducted in primary and secondary

Selleckchem EPZ 6438 care patients presenting to two outpatient gastroenterology clinics in Jakarta and Padang, Indonesia, using a culturally adapted and translated version of the Rome III FGID Questionnaire that had been locally validated. Patients who were found to have organic disease during investigation were excluded. Result: A total of 142 patients (47 males and 95 females) consecutively recruited, with 50 FD, 44 IBS, and 48 both FD-IBS. Female was predominant in FD (F = 37/50, 74%; age mean 47.38, SD 17.25), IBS (F = 28/44, 63.64%; age mean 38.64, SD 14.00) and both/FD-IBS (F = 30/48, 52.5%; age mean 42.17, SD 15.48). The most bothersome complaint was abdominal pain in FD (10) and FD – IBS (23) and abdominal discomfort in IBS patients (14). In IBS-only patients, 13 had IBS-C (constipation predominant), 8 had IBS-D (diarrhea predominant), 18 had IBS-M (mixed) and 5 had IBS-U (unspecified). In patients who had both FD and IBS, 20 had IBS-C, 11 had IBS-D and 17 had IBS-M pattern. Clinically, in FD-only patients, 44% patients were diagnose as FD. In IBS-only patients, none was diagnose as IBS. In FD-IBS, only 10% diagnose as IBS, 37.5% as FD and

none as both. Previous treatment consisted of PPI 54.9%, H2RA 28.9%, check details probiotics 23.2%, gastrokinetics 18.3%, traditional herbs 17.6%, anxiolytic 16.2%, laxatives 13.4%, fibre supplement 10.6% and anti-spasmodics 5.6%. On their previous treatment 63.4% felt some improvement, 11.3% felt no change, and 1.4% felt worse. Conclusions: Overlapping diagnosis of both FD and IBS was common with abdominal pain commonly present in both disorders. This overlapping symptom

may cause mis-diagnosis in clinical setting. Key Word(s): 1. Functional dyspepsia; 2. irritable bowel syndrome; 3. overlapping diagnoses Presenting Author: MARCELLUS ABDULLAH Additional Authors: MARCELLUS ABDULLAH, KAKA RENALDI, DADANG MAKMUN, AZIZ RANI Corresponding Author: MARCELLUS ABDULLAH Affiliations: University of Indonesia Phenylethanolamine N-methyltransferase Faculty of Medicine, University of Indonesia Faculty of Medicine, University of Indonesia Faculty of Medicine, University of Indonesia Faculty of Medicine Objective: Chronic gastritis is frequent in daily practice. One of the agents that can improve gastric inflammation, mucus and mucosal healing is fucoidan. Fucoidan derived from Cladosiphon okamuranus tokida is a sulphated polysacharide algae from Japan. The aim of this study to reveal the efficacy of fucoidan in treating dyspepctic symptoms, endoscopy and histopathologic scores of gaster. Methods: This is an open study on 31 dyspeptic patients who went to polyclinic gastroenterology Ciptomangunkusumo Hospital Jakarta. The patients were given oral fucoidan 100 mg perday for 28 days.

“
“We aimed to examine the relationship of current Helicobacter

pylori infection with lipid profile and cardiovascular disease and its eradication effect. Healthy subjects, who underwent Proteases inhibitor routine checkup between October 2003 and December 2007, were followed up until June 2009. Helicobacter pylori and lipid profiles were measured both baseline and follow-up. Multiple logistic regression models for odds ratios (ORs) and 95% confidence intervals (CIs) were used to estimate the effects of H. pylori infection and its eradication, on lipids and cardiovascular disease. Current infection with H. pylori with 50.5% (6759/13383) at baseline increased low-density lipoprotein (LDL) and decreased high-density lipoprotein (HDL) than H. pylori-negative group. Successful eradication of H. pylori decreased the risk of high LDL compared with the persistent infection (OR 0.76, 95% CI 0.59–96), which was comparable to that of the persistent negative group (OR 0.82, 95% CI 0.70–0.97), and decreased the risk of low HDL (OR 0.68, 95% CI 0.49–0.96). Current infection of H. pylori increased the risk of cardiovascular disease (OR 3.27, 95% CI 1.31–8.14) at baseline,

but its eradication failed to decrease the risk at a 2-year follow-up. However, persistent negative infection decreased the risk (OR 0.57, 95% CI 0.35–0.94) comparing PI3K inhibitor to persistent positive infection at follow-up. Current infection with H. pylori had a positive association with high LDL, low HDL, and cardiovascular disease.

Successful H. pylori eradication decreased the risk of high LDL and low HDL, but did not reduce the risk of cardiovascular disease. “
“Helicobacter pylori infections are thought to eventually lead to symptoms as a result of the long-lasting interactions between the bacterium and its host. Mechanisms that allow this bacterium to cause a life-long infection involve modulation of both the immune response and host cellular processes. Last year many novel findings that improve our knowledge on how H. pylori virulence factors interact with the Oxymatrine host were reported, but because of space limitations we can only discuss a limited number of these studies. Among those are studies on the genetic variation of genes encoding outer membrane proteins and the mimicry of host antigens, factors that alter host-cell metabolism and factors that modulate the host’s immune response. While chronic Helicobacter pylori infection is usually without any symptoms, disease ranges from peptic ulcer, gastric adenocarcinoma to gastric MALT lymphoma. Although the clinical outcome of the infection is thought to be determined by host, bacterial and environmental factors, the focus of this review is on recent findings relevant to H. pylori adaptation and virulence factors. H. pylori has developed several strategies that allow it to perfectly adapt to the gastric mucosa of its human host, its only known natural niche.

As we have previously shown, LSM are very accurate at identifying patients

who underwent liver transplantation who have portal hypertension.23 This probably also explains the high accuracy of the HVPG score in the current study in which a cutoff of −0.3 identified 89% of patients with normal portal pressure (89% of certainty). In contrast, values higher than 0.15 identified 61% of patients with a risk of developing portal hypertension (92% of certainty). These results reinforce the concept of HVPG determination as a good “gold standard” for the evaluation of new noninvasive methods.13, Selleckchem LBH589 23, 38 These results support the use of noninvasive methods to monitor HCV recurrence in the transplant setting. The fibrosis and/or HVPG score at 6 months may be useful to decide the best therapeutic strategy in these patients. In patients with a HVPG score below −0.3 at 6 months after LT, follow-up with repeated LSM may be appropriate, www.selleckchem.com/products/PD-0325901.html because 80% (41 of 51) of these patients remain without significant fibrosis at 1 year. In contrast, in patients with a HVPG score higher than 0.15, antiviral treatment should be considered, because 90% (19

of 21) of these patients develop portal hypertension 1 year after LT. Nevertheless, if HCV treatment is indicated, a liver biopsy before treatment initiation is still necessary to exclude other causes of liver dysfunction.39 Despite the importance of these results, the main limitation of our study

is the number of patients included, especially in the validation group. Nevertheless, it is important to note that our data were obtained using the two current gold standards to assess disease severity: liver biopsy and HVPG measurements.13, 23, 38 In addition, an internal validation using a bootstrapping system was performed. In summary, repeated measurements of liver stiffness in HCV patients after LT allow discrimination the between rapid and slow fibrosers. Simple scores including bilirubin and LSM, or donor age and LSM at 6 months can accurately predict the risk to develop significant fibrosis or portal hypertension in these patients. This could be relevant to adopt therapeutic decisions at an early stage of HCV recurrence. Although our results need to be validated by other centers, we believe that these models might be widely used in clinical practice. We thank Concepció Bartres for performing all liver stiffness measurements during the study. M.N. received support in part by a grant from “Instituto de Salud Carlos III” (PI050230) and X.F. received support in part by a grant from “Instituto de Salud Carlos III” (PI080239). “
“Controlled attenuation parameter (CAP) has been suggested as a noninvasive method for detection and quantification of hepatic steatosis. We aim to study the diagnostic performance of CAP in nonalcoholic fatty liver disease (NAFLD) patients.