Fibrotic human liver slices remained viable for 24 hours and the gene expression of the fibrosis markers was stable up to 24 hours. As shown before, Imatinib inhibited in healthy and fibrotic rat PCLS the gene expression of Hsp47 (more than 50%) and Pcol1A1 (more than 80%), the protein expression of collagen I was inhibited by more than 40 %. In both healthy and fibrotic human PCLS imatinib did TAM Receptor inhibitor not have an effect on the gene expression

of fibrosis markers. In healthy human PCLS imatinib did not influence the protein expression of collagen I. In conclusion, clear species differences in the antifibrotic effect of imatinib were apparent. These results may explain why imatinib has not Src inhibitor reached the market as effective antifibrotic

drug. PCLS from human (fibrotic) liver tissue are a promising tool to study the efficacy of antifibrotic compounds in the early and end stage of liver fibrosis and are useful to reveal species differences in antifibrotic efficacy. Disclosures: The following people have nothing to disclose: Inge M. Westra, Dorenda Oosterhuis, Rick Mutsaers, Geny M. Groothuis, Peter Olinga Introduction. Determining the severity of liver fibrosis is important for care management in chronic liver diseases. Classical fibrosis stagings on biopsies are hampered by poor observer reproducibility. Our main aim was to develop a precise fibrosis classification based on automated morphometric diagnosis to avoid variability and increase diagnostic accuracy and precision compared to available fibrosis staging. Methods. 834 patients with chronic hepatitis C were included: 549 in the derivation population and 285 in the validation population. The pathological reference was Metavir fibrosis staging

by consensus between 2 experts. Automated morphometric analysis included the area of portoseptal fibrosis (Modern Pathology 2014) and 43 other descriptors providing scores for clinically significant fibrosis (CSF score by 5 descriptors) and cirrhosis (FM4 score by 6 descriptors). Different fibrosis classifications were derived from these scores according to published statistical merging. In the multicentric validation population, different Metavir stagings were available: this website initial local pathologists, 2 central experts and their consensus. Results. Accuracy (correctly classified patients) in the derivation population was: CSF classification (7 classes from CSF score): 94.2%; and FM4 classification (8 classes from FM4 score): 95.3%. The CSF/ FM4 classification was derived by combining the two previous classifications. We obtained 6 classes roughly reflecting the 5 Metavir stages with cirrhosis distinguished as early or definitive. CSF/FM4 classification combined the advantages of the individual classifications with an accuracy of 96.2%. The classification reproducibility was very high with intra-class correlation coefficient =0.988.

Similar to the observation among males, there was a marked decrease (46%) in the incidence of colorectal cancer in the 30–34 years group in last two decades (Table 1). The present study shows that the ASR of colorectal cancer in Hong Kong increased in the period from 1983 to 2006.

CH5424802 However, the increase was mainly among the male population. The ASR of colorectal cancer in females peaked in 1994 and declined in the past decade. The trends of colorectal cancer differ in different countries. However, the risk of colorectal cancer was higher and increasing among males, but stable or decreasing among females in most countries. In more detailed analysis of our local data, the increase was noted only in those above 60 years of age in males and those above 70 years of age in females. The rise was much higher among males than females. A gender difference and rising risk in the older, but not young population were noted also in other developed and Asian countries.6,7 The distribution of colorectal cancer was not examined in the present NVP-LDE225 study, but it was found that the decrease in colorectal cancer in women and the young population is mainly due to a decrease in colon cancer rather than rectal cancer when the data were examined again in the reviewing process. As there was a tendency towards right-sided lesions in the older population,13 and there

was an increasing proportion of colorectal cancer in the older population recently, this may explain the right-shift of colorectal neoplasm observed in a local study.14 The westernized diet, which is high in fat and low in fiber, is found to be associated with colorectal cancer in many epidemiological studies.15–19 This was further confirmed in a cohort study using cluster analysis. In the present study, a micronutrient-rich, low fat, and high-fiber food pattern was found to be associated with

lower risk of colorectal cancer.20 The Hong Kong population selleck inhibitor adopted a westernized lifestyle early in the past century with decreased intake in vegetables and fruits, but increased consumption of processed meat, fat, beer and liquor. In a local telephone study, only 15% to 21% of respondents consumed fruit at least twice a day, about 50% consumed vegetable at least twice a day and about 40% ate high fat food more than once a week.21 This may explain the overall increase in ASR locally. However, it cannot explain the decreasing risk of colorectal cancer in the younger age groups, nor the discrepancy in the ASR of men and women. Instead greater screening use in women, who are in general more health conscious, leading to greater detection and removal of neoplastic polyps may be a possible reason of the latter observation. However, concrete data are not available to support this hypothesis. Waist circumference and body mass index are associated with increased risk of colorectal cancer.

Since secondary etiologies including see more eosinophilic gastroenteritis, cardiac problems and liver diseases were excluded, the diagnosis of primary lymphangiectasia was finally made. Conclusion: The definite diagnosis of lymphangiectasia is made through endoscopic biopsy. Though primary intestinal lymphangiectasia is rare in children, this disease should be included in the differential diagnosis in patients with protein-losing enteropathy. Key Word(s): 1. lymphangiectasia; 2. protein-losing; 3.

pediatrics; 4. endoscopy; Presenting Author: BREKHNA AURANGZEB Additional Authors: YASIRBIN NISAR, ZAHEER ABBASSI, NADEEM AKHTAR, GULBIN SHAHID, STEVEN LEACH, ANDREWSTEWART DAY Corresponding Author: BREKHNA AURANGZEB Affiliations: Children’s Hospital Objective: Coeliac disease (CD) is autoimmune enteropathy and has a variety of clinical presentations ranging from classical picture of severe under nutrition with chronic diarrhea to atypical presentation of resistant anemia, short stature in different clinical settings. This study was carried out to assess the presentation patterns and nutritional status

of newly diagnosed CD in Australian and Pakistani children. Methods: All newly diagnosed CD children at Sydney Children’s Hospital, HIF inhibitor Sydney, Australia from Feb 2006 to April 2007 and the Children’s Hospital, Pakistan Institute of Medical Sciences, Islamabad, Pakistan from Nov 2008 to Nov 2012 were enrolled. History, presentation patterns, blood tests and anthropometry were done. The comparison of the groups were assessed by using chi-square

and Student t tests. Results: Twenty five Australian children and 52 Pakistani children were enrolled. There was no difference in the mean age [6.98 (SD ± 2.8) years in Pakistani cohort and 8.23 (±4.5) years in Australian cohort]. The common presenting complaints in the Pakistani cohort were diarrhea (84%), weight loss (64.5%), abdominal pain (61.3%), abdominal distension (61.3%) and vomiting (38.7%) whereas the presenting complaints in the Australian cohort were abdominal distension (100%), diarrhea (36%), abdominal pain (36%), weight loss (32%) and constipation (32%). The mean height for age and weight for age scores of Pakistani children (−2.29 and −2.80 respectively) were significantly lower than the Australian children (−0.28 and −0.21 click here respectively) (p = 0.0001 and 0.0001 respectively). Similarly, the mean hemoglobin value in the Pakistani cohort (8.47) was significantly lower than the Australian group (12.38) (p = 0.0001). Conclusion: Atypical presentation is more common in the Australian cohort whereas the Pakistani CD children are markedly undernourished and anemic at diagnosis. Public awareness of CD and availability of iron rich diet in Australia may explain these differences. Early detection of CD is important to prevent the adverse effects of under nutrition and anemia. Key Word(s): 1. coeliac disease; 2. malnutrition; 3. anemia; 4.

Primary X-tropic (92UG021) and R5-tropic (92TH007) isolates were obtained from the National Institutes of Health AIDS Research & Reference selleck chemicals Reagent Program. HIV-1 Gag–interdomain green fluorescent protein (iGFP) is an NL4-3–based HIV-1 molecular clone that carries GFP inserted internally into Gag between the MA and CA domains, and HIV-NL-GI (GFP-IRES) is an NL4-3–based HIV-1 molecular clone that carries GFP in place of the nef start codon, with nef expression

restored by inserting an internal ribosome entry site.12 Primary HSCs and LX-2 cells were plated (1-1.5 × 105 cells per well) and exposed to HIV-IIIB (X4-tropic) or HIV-BaL (R5-tropic) at a multiplicity of infection (moi) of 0.5 for 4 hours at 37°C. After viral incubation, cells were washed to remove unbound virus, and overlaid with Dulbecco’s modified Eagle’s medium (1% fetal bovine serum). Supernatants were collected up to 7 days after infection, starting at day 0 (30 minutes postwash). Infectivity was determined by

quantification of p24 antigen (HIV-1 viral capsid protein) on culture supernatant by way Belnacasan molecular weight of enzyme-linked immunosorbent assay (ELISA) according to the manufacturer’s protocol (National Cancer Institute, Frederick, MD). The detection limit of the assay is 80 pg/mL of p24. To determine whether HSC-derived supernatant contained infectious virus, supernatants from HIV-infected HSCs and primary CD4 lymphocytes as controls, were used to infect CD4 lymphocytes and TZM cells using p24 assay and Luciferase Reporter Assay, respectively. The volume of supernatant used to infect TZM cells varied, and was calculated to reach a final p24 concentration of 0.04 pg/cell. For the selleck compound experiments using primary CD4 T cells, the final p24 concentration used was 0.001 pg/cell. Luciferase activity in TZM cells, where the luciferase gene is under control of the HIV-1 promoter, was assessed in both cell-free infection studies as well as coculture studies according to the

manufacturer’s protocol (Promega, Madison, WI). For experiments using GFP constructs, primary HSCs and LX-2 cells were infected with either HIV-iGFP or HIV-NL-GI (0.4 pg/cell of p24) for 24 hours in serum-free media with or without 100 μM zidovudine (azidothymidine [AZT]; Sigma), washed to remove unbound virus, overlaid with Dulbecco’s modified Eagle’s medium (1% fetal bovine serum), and monitored daily for GFP expression under a fluorescence microscope (Nikon Eclipse TE 2000-u). For receptor-blocking experiments, primary HSCs or T lymphocytes were incubated with anti-CD4 (BD Biosciences, clone Leu 3a), anti-CXCR4 (R&D systems, clone 12G5), anti-CCR5 (R&D systems, clone 45523) or respective isotype controls (25 μg/mL) for 1 hour prior to viral challenge.

“
“Sorting nexin (SNX) family proteins are best characterized for their abilities to regulate protein trafficking during processes such as endocytosis of membrane receptors, endosomal sorting, and protein

degradation, but their in vivo functions remain largely unknown. We started to investigate the biological functions of SNXs using the zebrafish model. In this study, we demonstrated that SNX7 was essential for embryonic liver development. Hepatoblasts were specified normally, and the proliferation of these cells was not affected when SNX7 was knocked see more down by gene-specific morpholinos; however, they underwent massive apoptosis during the early budding stage. SNX7 mainly regulated the survival of cells in the embryonic liver and did not affect the viability of cells in other endoderm-derived organs. We further demonstrated that down-regulation of SNX7 by short interfering Barasertib RNAs induced apoptosis in cell culture. At the molecular

level, the cellular FLICE-like inhibitory protein (c-FLIP)/caspase 8 pathway was activated when SNX7 was down-regulated. Furthermore, overexpression of c-FLIPS was able to rescue the SNX7 knockdown-induced liver defect. SNX7 is a liver-enriched antiapoptotic protein that is indispensable for the survival of hepatoblasts during zebrafish early embryogenesis. (HEPATOLOGY 2012;55:1985–1993) Liver development begins with the specification of hepatoblasts within the anterior foregut endoderm during early embryogenesis. Previous studies in mice and chickens have demonstrated that fibroblast growth factors (FGFs) from the adjacent cardiac mesoderm learn more and bone morphogenetic protein (BMP) signals from the septum transversum mesenchyme are both required for the onset of hepatogenesis.1, 2 Other signaling pathways, including transforming growth factor beta (TGF-β)

and WNT, have also been implicated in early liver development.3, 4 After their specification, the newly formed hepatoblasts form the liver primordium, which proliferate rapidly and further differentiate into mature hepatocytes or cholangiocytes during later stages of liver development. Transcriptional factors, including hematopoietically expressed homeobox (Hhex), prospero homeobox protein 1 (Prox1), and hepatocyte nuclear factor (HNF) family members, play important roles during these processes.5, 6 Recently, teleosts, including zebrafish and medaka, have become valuable model animals for studying the mechanisms of liver development.7-9 Liver development in zebrafish can be described in three steps comparable to those in other vertebrates. First, the endodermal cells migrate to the midline and form a rod-like structure at 24 hours postfertilization (hpf).10 Two earliest hepatoblast markers, hhex and prox1, are induced by signals from the nearby mesoderm. Several such signaling molecules have been identified so far. For example, Wnt2bb, from the lateral plate mesoderm, is required for liver specification.

7) and that the the staining pattern between the two samples was similar, thus indicating good preservation

of ECM molecules in the bioscaffold. Degradation of the liver bioscaffold, showed approximately 80% loss of the original mass within the first 6 hours and complete degradation by 48 hours (Fig. 2D), indicating its susceptibility to enzymatic remodeling. The mass of control bioscaffolds incubated without collagenase remained stable. To assess the patency of the vascular channels of the decellularized liver scaffold, we infused fluorescein-labeled 250 kDa dextran particles through the portal vein (Fig. 3A). Tracking Cobimetinib mw of the particles throughout the network under low magnification fluorescent microscopy showed a defined vascular tree with multiple branching (Fig. 3B). At higher magnification, we observed fine branching structures, indicating that the architecture of small capillaries remained mostly intact and patent in the bioscaffold. No significant diffusion of dextran into areas that would correspond to liver parenchyma (Fig. 3C-F) was observed during most of the experiment. However, after 5-10 minutes of constant perfusion the whole acellular liver eventually became fluorescent,

suggesting some leakage from the vascular Poziotinib channels to the parenchymal spaces. We further analyzed the fluorescently-labeled vascular network with confocal laser microscopy to reconstruct the three-dimensional structure of the capillary network (Supporting Information Fig. 1D). We found that the bioscaffold retains a vascular network that exhibits multiple branching points with an average diameter of 15 micrometers, selleck screening library the size that would approximately be expected from capillaries.22 To further confirm the integrity of the vascular network

and to demonstrate that fluid injected into the vasculature flowed through it rather than extravasate throughout the organ, an x-ray fluoroscopic study with radio-opaque dye was performed (Supporting Information Fig. 1E,F and Supporting Information Video 1). The fluoroscopy demonstrated that the injected dye flowed, as would be expected, inside intact vascular channels, moving slowly from larger vessels to smaller capillaries. The capillary structures appeared intact, with no obvious loss of dye into extra-vesicular areas. To test the mechanical strength of the vascular network, unseeded liver bioscaffold was transplanted in the abdominal cavity of adult rats. The mechanical properties of the vasculature supported microsurgical suturing to the host’s blood vessels. Normal flow of blood throughout the acellular liver bioscaffold was maintained for up to 60 minutes in heparinized rats, without noticeable leakage (Supporting Information Fig. 2A,B). However, due to the bare lumen of the vascular network, clotting eventually stopped the blood flow. Endothelial coverage of the lumen of the vasculature is essential to prevent thrombosis and to provide proper vascular function.

15–19 SVR was previously found to be associated with longer duration of additional treatment, younger age, lower HBV DNA level at the time treatment was stopped, and genotype B.15, 17–20 However, the number of patients in these studies was smaller than in our study (under 100 vs. 178 patients). Also, the duration of treatment and additional treatment after HBeAg seroconversion were shorter than in our study (mean 13 vs. 26 months and mean 4.5 vs. 12.4 months, respectively). In our study, age and the duration of additional lamivudine treatment after HBeAg clearance or seroconversion were predictive factors for SVR. A major limitation of this multicenter, large-scale

cohort study was the use of a relatively Palbociclib insensitive HBV DNA assay. It is possible that this low sensitivity was partly responsible for the apparent

relatively low relapse rates after CR. More sensitive HBV DNA assays would be required to evaluate this issue definitively. We subanalyzed 51 patients with SVR who had been followed for more than 4 years after 2004, using a more sensitive assay (the COBAS TaqMan 48 analyzer, Roche Molecular Systems, Branchburg, NJ; with a lower limit of detection of 300 copies/mL). The mean HBV DNA level was 429 copies/mL (range, <300-1,296). The Rapamycin cost percentage of relapse could have been higher if more sensitive HBV DNA assays had been used during the study period. However, there was no virological rebound (HBV DNA level >10,000 copies/mL) in 51 patients who completed at least 12 months of additional treatment after HBeAg clearance or seroconversion. Interestingly, despite prolonged lamivudine treatment after CR, 21 of 109 (19.3%) patients experienced lamivudine-resistant mutations and virologic breakthrough. These data suggest that lamivudine could be stopped after optimal additional treatment in patients who have achieved HBeAg clearance or seroconversion. However, additional studies are needed because new antiviral agents that have low resistance and more potent antiviral efficacy could provide different

insights into prolonged therapy. In conclusion, the lamivudine-induced virologic learn more response was durable in patients under 40 years old and receiving lamivudine for more than 12 months after HBeAg clearance or seroconversion in CHB that was predominantly genotype C. Future long-term prospective and comparative data are needed to evaluate the durability of lamivudine-induced HBeAg clearance or seroconversion according to HBV genotype, given the continuing use of long-term lamivudine monotherapy in the management of CHB. The English in this document was checked by at least two professional editors, both native speakers of English. For a certificate, see: http://www.textcheck.com/certificate/8QkxbA “
“The IL28B genotype is the most important pretreatment predictor of treatment outcome in patients with chronic hepatitis C.

Results: Of 330 patients, 95 were excluded due to medical comorbidities or

low viral levels, leaving 235. Of those, 41 (17.4%) began the therapy regimen. For the remaining 194, reasons for not moving to treatment based on the chart review included: lack of patient interest (n=86), alcohol and/or illegal drug use (n=55), and loss of follow-up for tests (n=53). In multivariate logistic regression, starting treatment was associated with living with relatives but not a spouse I BET 762 (p=0.001), being employed (p=0.005), not reporting illegal drug use (p=0.017), not having depression as measured by the CES-D (p=0.034), and having higher knowledge of HCV as measured by the PEAHC (p=0.017). While race was not statistically significant in the final model, 28 out of 129 whites in the study (21.7%) and 13 of 106 African Americans (12.2%) began treatment. Conclusions: While many factors constituted barriers, our results suggest that diagnosis and treatment of depression and substance abuse as well as knowledge may play an important role in successfully initiating

HCV treatment in veterans. Additional research is needed among veterans to examine buy GSK2118436 reasons for a lack of interest in treatment and to establish methods for determining the relevance of HCV treatment for future health and well-being. Disclosures: The following people have nothing to disclose: Susan L. Zickmund, Michael K. Chapko, Barbara H. Hanusa, Ada O. Youk, Galen E. Switzer, Mary Ann Sevick, Nichole K. Bayliss, Carolyn L. Zook, David S. Obrosky, Robert A. Arnold see more Introduction:

Due to the high risk of rejection, the treatment (Tx) of hepatitis C virus (HCV) infection with interferon (IFN)-based therapies after kidney transplant (KT) is contraindicated. Most if not all KT recipients are then left untreated often without appropriate liver-specific follow-up (F/U). The introduction of IFN-free therapies has made HCV Tx for KT recipients a possibility for the first time. Aims: To implement a strategy to identify KT recipients with chronic HCV at Mount Sinai Medical Center (MSMC) and to assess their eligibility for IFN-free therapies. Methods: All HCV positive recipients who underwent KT from 01/2000 to 12/2013 at MSMC were identified retrospectively using electronic medical records. Patients were deemed eligible for IFN-free therapies (sofosbuvir and ribavirin) if they had baseline positive HCV viral load (VL), glomerular filtration rate (GFR) > 30 ml/min, and hemoglobin level > 10 g/dl. Patients with decompensated cirrhosis were excluded. Regular F/U with a GI or hepatologist was defined as having ≥ 1 appointment/year. Results: During the study period, 132 HCV positive recipients underwent KT. Among them, 36 (27%) were not alive and 29 (22%) had GFR < 30 ml/min. The remaining 67 (51%) recipients were eligible for IFN-free therapies. Among these patients, 13 (19%) had prior history of liver transplantation (LT).

In the era of directly acting antivirals the study thus highlights that targeting viral proteins may have beneficial effects

beyond mere restriction of virus propagation. “
“To demonstrate the usefulness of the computed tomography (CT) fusion imaging for the evaluation of treatment effect of radiofrequency ablation (RFA) for hepatocellular carcinoma (HCC). Eighty-five patients with 94 HCC with complete ablation judged on conventional side-by-side Talazoparib ic50 interpretation of pre-RFA and post-RFA CT at the time of RFA were included in this retrospective study. CT data was retrospectively used to create fusion images of pre-RFA and post-RFA CT using automatic rigid registration and manual correction referring to intrahepatic structures and hepatic contours around a tumor. Clinical factors including

a minimal ablative margin (MAM) measured on fusion images were examined to prove risk factors for local tumor progression (LTP). LTP was observed in 13 (13.8%) tumors with a median follow up of 21.0 months (range, 2–75). The mean MAM on the fusion image was 1.4 ± 3.1 mm and 23 tumors (24.5%) were judged to be protruding from the ablation zone. Multivariate analysis revealed that protruding from the ablation zone was the only significant factor for LTP (hazard ratio, 7.09; 95% confidential interval, 2.26–22.3; P < 0.001). Some HCC were assessed as incomplete ablation on the CT fusion images, although considered completely ablated on side-by-side images at the time of treatment, and incomplete ablation was revealed to be the only independent risk factor Tofacitinib in vitro for LTP. The CT fusion imaging enables quantitative and accurate evaluation of treatment effect of RFA. “
“We read with great interest the study by Kumar et al.,1 who reported antituberculosis therapy (ATT) as the only cause of drug-induced acute liver failure (ALF) in northern India, in contrast to antimicrobials, anticonvulsants, and paracetamol in the West2-6 and in southern India.7 Our experience with drug-induced liver injury (DILI), including injury due to ATT, from 1997 to 2008 at the Department of Gastroenterology of St. John’s

Medical College Hospital (Bangalore, India) offers something in support selleck of their findings and something at odds.7 Table 1 outlines the clinical and biochemical characteristics of all patients with DILI due to ATT. Kumar et al.1 found a mortality rate of 67% among 70 patients (mean age = 32 years) with ATT-caused ALF; most (63%) were treated empirically for tuberculosis. In support of their findings, we observed that our patients were young (mean age = 40 years) and that the mortality rate was 67% among 49 patients with ALF due to ATT and 42% among patients who were inappropriately treated for tuberculosis. Our model, using a combination of the bilirubin level [odds ratio (OR) = 1.17, confidence interval (CI) = 1.06-1.35], prothrombin time (OR = 1.13, CI = 1.06-1.24), and creatinine level (OR = 9.77, CI = 2.58-57.63), yielded a concordance of 97% for mortality.

Of the 23.4% (26/111) of patients whose thryoid dysfunction never normalised, 42% (11/26) had significant disease. The most common pattern of significant thyroid dysfunction was isolated hyperthyroidism, followed by a combination of both hyperthyroidism and hypothyroidism in the same patient at different points in time. Treatment of the dysfunction varied between watchful waiting and thyroid replacement or suppression with thyroxine or carmbimazole respectively. A Chi Squared test of independence showed no associated http://www.selleckchem.com/products/MG132.html between thyroid

disease and autoantibodies (p = 1.00); or SVR (p = 0.980). Female gender was predictive of thyroid dysfunction (OR: 2.7 p = 0.0001, 95%CI 1.6–4.5). Thyroid disease was also more likely to occur in patients with genotype 1 (OR 2.25, p = 0.014 95%CI 1.35–3.76) perhaps due to longer treatment duration. Conclusion: Those patients with pre existing thyroid disease were more likely to develop thyroid dysfunction

during antiviral therapy, even if clinically insignificant disease existed pre-treatment. Females, and patients with genotype 1 were also more likely to develop thyroid dysfunction. Ongoing thyroid dysfunction after treatment occurs not infrequency, and ongoing monitoring is warranted. The incidence of thryoid disease during HCV treatment with interferon is relatively high, and clinicians should ensure appropriate screening and treatment, if this complication occurs. E SHELTON,1 C PEI CHONG,2 L SHOCHET,2 J CHEONG,2. S ONG,1 D BOWDEN,2 A HODGE,1 V KNIGHT,1 K CHENG,3 S PASRICHA*,2 A DEV*1 1Department of Gastroenterology selleck products and Hepatology, 2Medical therapy unit (Thalassaemia Service) and 3Radiology, Monash Health, Melbourne, Australia. Background: Transfused haemoglobinopathy (TH) patients

are at significant risk of liver cirrhosis and its sequelae due to hepatic iron loading and transfusion related hepatitis C (HCV).(1) Screening for liver fibrosis in this population is inadequate using current methods – pathology, liver ultrasound and T2*MRI. Transient elastography (TE) non-invasively assesses liver stiffness and hence, risk of cirrhosis and has been see more validated in many clinical scenarios including viral hepatitis. It has been studied in small cohorts of patients with beta thalassemia.(2,3) The present study aimed to evaluate the prevalence of cirrhosis in a cohort of adult TH patients using TE. Methods: 128 TH patients were identified by enrolment at the State Thalassaemia reference centre between August – November 2012. Of these, 63 patients (males 46%, B thalassemia major 95%, HCV Ab positive 54%) prospectively underwent TE. Liver ultrasound, T2*MRI and present and historical ferritin, data were collected. Associations between risk factors and loge TE were compared by linear regression, and associations between TE thresholds (>7.9 kPa for F ≥ 2, >10.3 for F≥3, >11.9 for F = 4) versus normal, by logistic regression.