A critical player in each of these processes is the p53 tumor MLN0128 concentration suppressor, which provides surveillance against cellular insults of many types and may induce G1 arrest and cellular senescence in response to tetraploidy or missegregated chromosomes.9, 10 p53 and its close relative, p73, are also linked to the mitotic spindle assembly checkpoint, as both proteins interact with kinetochore and spindle checkpoint proteins.7, 11, 12 In fact, combined loss

of p53 and p73 leads to increased polyploidy and aneuploidy in primary cultured cells9 and results in a higher incidence of tumor development in mouse liver.13 The striking tolerance of the liver for altered ploidy leads to consideration of whether a tetraploid checkpoint exists in hepatocytes. We addressed this question by analysis of checkpoint mediator p53, and characterized the synchronized

process of cellular proliferation and growth that AZD2014 occurs to regenerate the liver in response to PH in both WT and p53-null mice. Our results reveal that p53 alters levels of hepatocyte ploidy during liver regeneration and aging. Although chromosome segregation errors are common in WT hepatocytes expressing p53, these errors (e.g., abnormal mitotic figures and lagging chromosomes) are even more frequent in hepatocytes deficient for p53. Since p53′s effects may be mediated by context-specific, mitotic regulators,14 we examined whether p53 regulated expression of mediators of hepatic cell division in normal and regenerating liver. We identified Aurora kinase A (Aurka), Forkhead-box transcription factor Foxm1, regulator of cytokinesis Lats2, and Polo-like kinases (Plk2 and Plk4) as directly regulated by p53 in quiescent liver, a mitotic transcription program that is altered during liver regeneration. Thus, our findings suggest that p53 plays a role in controlling

levels of hepatic polyploidy/aneuploidy by direct transcription regulation of multiple downstream effectors. ChIP, chromatin immunoprecipitation; p53RE, p53 response element; PCR, polymerase else chain reaction; PH, partial hepatectomy; WT, wild-type. PH to remove 70% of total liver tissue, or Sham surgery was performed using isoflurane anesthesia, as described.15 5-7 C57Bl6/Sv129 F1 mice, WT or p53−/−, 2 months of age, were used for each experimental condition according to The University of Texas MD Anderson Cancer Center Institutional Animal Care and Use Committee guidelines. p53 knockout mice were sacrificed 0.5, 1, 1.5, 2, 3, 3.5, 4, or 7 days following PH and sham surgery; remnant liver tissue was harvested, flash-frozen, and processed for RNA, immunoblot, and chromatin immunoprecipitation (ChIP) analyses. Liver/body weight ratios were calculated to determine the recovery of liver mass. ChIP analyses were performed as described.

Study design characteristics.  There were a total

of 804 patients in the selected studies and the age ranged from 23 to 94 years. In 15 studies, the sex distribution was described: 385 patients were male and 321 patients were female. In all studies, imaging data were presented about the identification of patients; the reference standard was histopathologic analysis and clinical follow-up. Of all 16 studies, 10 studies28,30–34,36–38,41 enrolled patients 5-Fluoracil prospectively, five studies27,29,35,39,40 enrolled patients retrospectively, and one study26 was unknown. Eight studies27,28,30–35 enrolled patients in a consecutive manner; the others26,29,36–41 were not in a consecutive manner or unknown. There were nine studies26,27,29,31,33–37,40 in which the MRI or PET/CT reviewer was blinded to other test results and clinical data. For DWI, all of the included studies26,29,30,32,33,35,36 used the 1.5T system.

There were three studies26,30,35 in which the average lesion size was over 30 mm. In the other four studies29,32,33,36 the average lesions size was less than 30 mm. For PET/CT, contrast enhanced PET/CT was used in four studies,27,28,31,40 and noncontrast enhanced PET/CT was used in seven check details studies,27,31,34,37–39,41Table 1 presents the included datasets with the corresponding numbers of patients and reference numbers. A full list of all included articles with all relevant study characteristics and complete examination results is available on request from the authors of this article. Diagnostic accuracy

of 18 F-FDG PET and DWI.  When considering all 16 studies with data on pancreatic malignancy per patient, for PET/CT, the pooled sensitivity was 0.87 (95% CI, 0.82, 0.81) and specificity was 0.83 (95% CI, 0.71, 0.91). Overall, LR+ was 5.84 (95% CI, 4.59, 7.42) and LR− was 0.24 (95% CI, clonidine 0.17, 0.33). For DWI, the pooled sensitivity was 0.85 (95% CI, 0.74, 0.92) and specificity was 0.91 (95% CI, 0.71, 0.98). LR+ was 9.53 (95% CI, 2.41, 37.65) and LR− was 0.17 (95% CI, 0.09, 0.32). SROC curves show the overall very good, but not excellent, diagnostic performance for PET/CT and DWI is shown in Figures 2 and 3, respectively. Subgroup analysis and meta-regression analysis. I2 is an index for heterogeneity: I2 = [Q − (k − 1)]/Q × 100%, where Q is the χ2 value of heterogeneity, and k is the number of studies included. Along with P < 0.05 for heterogeneity, I2 > 50% further indicates heterogeneity between studies. The heterogeneity in the sensitivity test and specificity test was highly significant (P < 0.05 and I2 > 50%), confirming that there was strong evidence of between-study heterogeneity both for PET/CT and DWI (Table 2). Therefore, a random effect model was used for the primary meta-analysis to obtain a summary estimate for sensitivity and specificity with 95% CI. To explore the possible source of heterogeneity, subgroup analyses were applied (Table 2).

7, 8 In addition to being the envelope of infectious HBV particles, HBsAg is also found in the form of noninfectious spheres or filaments, which exceed infectious virions in number by 102 to 105.9 Serum HBsAg appears to correlate with transcriptionally active cccDNA and is considered a surrogate PLX3397 datasheet marker of infected cells.10-14 Although cccDNA is the most accurate reflection of the number of infected

hepatocytes, it can be assessed in tissue only with complex techniques that are restricted to specialized research centers. This excludes the analysis of cccDNA levels from general clinical applications. The quantitation of HBV DNA by polymerase chain

reaction is now a standard part of the diagnostic workup for CHB. A serum HBV DNA decline reflects a reduction in viral replication. In contrast, a serum HBsAg decline represents a reduction in the translation of messenger RNAs produced from transcriptionally active cccDNA or integrated sequences.14 Thus, HBsAg quantitation provides different but complementary information that may aid us in the characterization of an individual’s infection status. Several cross-sectional studies have compared HBsAg and HBV DNA levels during different phases of CHB (Table mTOR inhibitor 1). The results are encouragingly similar, even though the studies were conducted in different patient populations and, therefore, with different genotypes. Both HBsAg and HBV DNA levels vary during the natural course of the infection, and they are highest in the initial immune tolerance phase when the serum alanine aminotransferase (ALT) level is normal with no or minimal hepatitis activity. HBsAg levels become lower during the immune clearance phase and decrease slowly and progressively in those who maintain persistently normal ALT levels after hepatitis B e antigen (HBeAg) seroconversion.10 All groups have observed the lowest levels of HBsAg and HBV

DNA during this FER inactive phase, which is also characterized by the highest HBsAg/HBV DNA ratio.7, 10, 15 A Hong Kong follow-up study of 68 HBeAg-negative patients over a median period of 8 years showed a slow overall decrease in HBsAg levels, and a >1 log10 IU/mL HBsAg decline between the initial and last visits reflected improved immune control, which was associated with a higher HBsAg seroclearance rate and stronger viral suppression.10 Two European studies of inactive HBsAg carriers showed that those with subsequent HBsAg seroclearance had a significantly greater HBsAg decline than those who remained HBsAg-seropositive (0.28-0.29 versus 0.054-0.058 log10 IU/mL/year).

5) recieved initially a combination therapy of EVR with very-low dose CSA (81.8%) or tacrolimus (18.2%).

EVR treatment was started on post op day 1, 2 and 3 in 23, 8 and 2 patients, respectively. The EVR, CSA and TAC doses were adjusted to aim at a trough target level between 3-8 ng/ml, 50-80 ng/ml and 3-5 ng/ml, respectively. Other concommittant initial immu-nosuppressive therapy included basiliximab in 13 patients (39.4%), and prednisolone in all patients. Mean follow-up was 883 days. Indications for early treatment with EVR were renal dysfunction (39.4%), prophylaxis for recurrent HCC 36.4%), neurological problems (6%), other preexisting malignancies (3%) or combined ROCK inhibitor OLT/kidney transplantation (15%). During follow-up CNI was stopped in 4/33 patients (12.1%). Altogether only 2/33 patients (6%) experienced a mild episode of BPAR (BANF score 4 and 5) 20 and 80 weeks post OLT. Both patients responded well to steroids. No patient required a retransplantation. No patient developed hepatic artery thrombosis. Impaired wound healing was an uncommon complication (9%).

The 1- and 2- year patient survival rate was 90.9% and 81.8%, respectively. HCC recurred in 2/12 patients. Post-operatively 8/27 (29.6%) OLT recipients not undergoing http://www.selleckchem.com/products/pci-32765.html kidney transplantation required dialysis. At last follow-up only 1 of these patients had terminal renal insufficiency. In 8 (24.2%) patients EVR treatment was stopped after a mean treatment duration of 311.5 days for hematological side effects (9%), infections (6%), dermatological side effects (6%), polyarthral-gia

(3%). Other side effects included hypercholesterolemia (51.5%), anemia (12.1%), leukopenia (6%), edema (3%), proteinuria (9%). During follow-up incisional hernias occurred frequently (45.4%), but rarely required surgical repair (21.2%). Conclusion: Everolimus treatment start directly post operative in combination with Glutamate dehydrogenase very low-dose CNI is effective and safe post OLT resulting in a low rejection rate. Disclosures: Martina Koch – Grant/Research Support: Novartis Lutz Fischer – Advisory Committees or Review Panels: Novartis, Gilead; Grant/ Research Support: Astellas; Speaking and Teaching: Novartis Bjoern Nashan – Advisory Committees or Review Panels: Novartis, Bristol-Myer Squibb; Speaking and Teaching: Novartis, Bristol-Myer Squibb The following people have nothing to disclose: Martina Sterneck, Antonio Galante, Gesa Pamperin, Jun Li Introduction: Young people with liver disease, aged 12-25 years, are a unique population that requires special attention with respect to adherence to treatment and their subsequent transition to adult services. Reports on long-term survival following liver transplantation (LT) show decreased patient and graft survival in young adults with non-adherence (NA) as one of the main contributory factors.

This opened up the possibility of having a unique marker for the defective allele in every family segregating haemophilia A. At first, with the expensive and laborious sequencing methods available, it was

necessary to screen using techniques that could show altered behaviour in a small fragment, which was then sequenced [17]. The advent of first generation sequencing machines made it feasible to sequence an entire coding region without a screening step. It meant that we could find a mutation in one-to-two weeks. As a result of this sequencing, Epigenetics inhibitor it soon became evident that there was no plausible disease-causing mutation in about half the severely affected cases. Jane Gitschier returned to the F8 gene to show that, in such cases, there was an inversion involving either

of two copies of an intronic gene F8A located within intron 22 and an extragenic copy of F8A located 400 kb upstream [18]. The international haemophilia A database, which I started in 1991 [19] to improve understanding of the correlation this website between mutation and phenotype, went online in 1996 [20]. From a critical analysis of the mutations published up to that date, we discovered that some mutations had a highly variable phenotype and that there was a stronger risk of inhibitor development for some types of mutation than others [21]. The database has grown steadily and as of 2004 listed over 1000 unique mutations. This is set to increase massively with the next update and overhaul of the site in 2012. The most recent technical advance in detection of foetal DNA in maternal blood now allows the status of a foetus to be determined as early as week 11 of gestation [22]. In the next 50 years, genetic tools will come to dominate not only diagnosis but treatment of the haemophilias, which after all are the classic

example of genetic disorder in man. Many recent enhancements to processes Cytidine deaminase used in genetic analysis of inherited bleeding disorders are available. They are reviewed here following the pathway from patient referral to reporting of results. Computer-based laboratory information management systems (LIMS) can provide a complete system of ‘paperless’ sample management. All patient referral documentation can be scanned and stored electronically, work lists can be generated for testing to be undertaken, and results can subsequently be recorded within the LIMS. Genomic DNA can be prepared from blood and other tissues using a variety of automated extraction procedures. Bar-coding of individual samples and of the plates in which they are analysed facilitates recording storage location and ensures that the correct samples are transferred between containers during analysis. Several genetic analysis techniques are available, generally utilizing genomic DNA as template.

low = 57%, odds ratio 3.22, 90% confidence interval 1.16, 8.99, P = 0.045 by Fisher’s test). Further independent CART analysis of biomarkers for BA patients found that IL15, MCP3, MDC, IL17a and MCP1 collectively identified those likely to achieve conjugated/direct bilirubin <1 mg/dL; (AUC of 0.94, sensitivity of 86% and specificity of 93%). Conclusions: Quantification of serum cytokines, chemokines, VEGF and sICAM1 identifies a biomarker profile with discriminatory value for BA, with the potential to sub-classify BA patients and predict response to HPE. Disclosures: John C. Magee - Grant/Research Support: Novartis Jorge A. Bezerra - Grant/Research Support: Molecular Genetics

Laboratory, CHMCThe following people have nothing to disclose: James E. Squires, Kazuhiko Bessho, Lin Fei, Reena ALK targets Mourya, Pranavkumar Shivakumar Background/Aims: Recent studies from our laboratory have assigned independent and synergistic roles for Tnfα receptors, predominantly Tnf-R2 using in vitro assays evaluating cholangiocyte cell death and in vivo in a mouse model of rotavirus (RRV)-induced experimental

atresia. While Tnf-R1 binds to soluble Tnfα, Tnf-R2 preferentially recognizes transmembrane-Tnfα (Tm-Tnfα). Based on the role of Tm-Tnfα in autoimmunity and therapeutic disparity of clinically used anti-TNFα Temsirolimus mw agents, we hypothesized that Tm-Tnfα primarily modulates epithelial injury and duct inflammation in experimental biliary atresia. Methods and Results: Addressing this hypothesis, we quantified Tm-Tnfα expression on NK and CD8 T-cells, the key intrahepatic cell types regulating

atresia phenotype, at days 3, 4 and 7 post saline and RRV injections by flow cytometry. While the anti-Tnfα antibody MP6-XT22 failed to identify Tm-Tnfα, TN3-1 9 antibodies identified increased Tm-Tnfα on CD8 T-cells after RRV at days 3 and 4 (3.5-7.0 fold above controls; P < 0.01). Uniquely, NK cells expressed high and low levels of Tm-Tnfα at the initiation of epithelial injury (day 3) distinguished as Tm-Tnf-bright (44-fold above controls; P < 0.001) and Tm-Tnfα-dim (3-fold above controls; P = 0.001) and as Tm-Tnfα-dim only NK cells at day 7 (2-fold HSP90 above controls; P < 0.01). Since NK cells express Tnfα-receptors, we quantified the expression of the cognate ligand, Tm-Tnfα, on a murine cholangiocyte cell line (mCL). RRVnaϊve mCL constitutively expressed base-line Tm-Tnfα (17.0 ± 3.0%), which increased following RRV infection (36.0 ± 2.0%; P < 0.001). To precisely determine whether TmTnfα expression regulated cytotoxicity, NK cells from livers of day 3 RRV-challenged mice were used in co-culture cytotoxicity experiments with mCL in the presence or absence of TN3-19 Tnfα blocking antibodies. While day 3 RRV NK cells were highly cytotoxic (5–hrs; 15-48% at target: effector ratios of 1: 2.5-1: 25), simultaneous blocking of Tm-Tnfα on NK cells and mCL completely prevented cholangiocyte lysis. Exploring the in vivo role of Tm-Tnfα, neonatal Balb/c mice were challenged with 1.

Different from the study by Mederacke et al., where the authors did not observe any increase in LS values in patients with baseline values over 10 kPa, a cutoff value that allows predicting significant or advanced fibrosis but not cirrhosis,3 the results of the present investigation clearly indicate that LS values increase after a standardized meal in patients with chronic HCV infection at any stage of fibrotic evolution and in patients with compensated cirrhosis. The increase in LS, with return to baseline values within 120 minutes, is not just RG 7204 related to the rapid assumption

of the liquid volume but rather associated with the overall caloric intake of the meal. The meal test with postmeal portal blood flow (PBF) measurements has been suggested as a reproducible

noninvasive test to evaluate the severity of portal hypertension in cirrhosis patients. The effect of postprandial hyperemia on portal pressure has been reported 30 minutes after the onset of the meal both by direct measurement18 and by Doppler sonography19 in cirrhosis patients. Data in normal subjects and in noncirrhosis patients with CLD are scarce and obtained only by Doppler sonography,20-22 but indicate that an increase in PBF is detectable by Doppler sonography also 30 minutes after the onset of the meal. Changes in LS values following a test meal are likely a consequence of the adaptation of the hepatic microcirculation to an increased PBF8, 9 and are in overall agreement with the

observation that postprandial hyperemia is associated with a greater increase in portal pressure in cirrhosis patients. In this context, the progressive increase in postmeal delta LS values along with the fibrotic evolution of chronic HCV hepatitis could represent an indirect index of the progressive impairment of the mechanisms responsible for this adaptation, particularly sinusoidal Sulfite dehydrogenase circulation autoregulation, as a consequence of tissue fibrosis, inflammatory infiltration, and neoangiogenesis.23-25 Overall, these findings highlight an interesting potential of TE in detecting dynamic changes in LS related to both the anatomical modifications and hemodynamic alterations occurring in the progression of chronic HCV hepatitis. Accordingly, we tested whether or not the delta stiffness increase in postmeal LS values had advantages, when compared with premeal baseline LS values, in assessing the probability of liver fibrosis according to the Metavir staging system. While premeal baseline LS values were rather accurate in defining the probability of fibrosis stage and in agreement with previous observations by our group in a completely different cohort of patients with HCV-induced CLD,3 an analysis of the performance of the postmeal delta stiffness increase revealed that changes in LS values occurring after the meal test do not offer any advantage in the detection of different stages of fibrosis, whose definition becomes actually less accurate.

We performed stratification analyses on cancer type (divided into digestive system cancers and other cancers). For digestive system cancers, we further separated Asians and Caucasians. Meta regression was used to illustrate potential reasons of

between-study heterogeneity. Egger’s test and click here inverted funnel plots were utilized to provide a diagnosis of publication bias (linear regression asymmetry test65). All analyses were performed using Stata version 9.2 software (Stata, College Station, TX, USA). All statistical evaluations were made assuming a two-sided test with a significance level of 0.05, unless stated otherwise. The characteristics of the selected studies are listed in Table 1. The distribution of genotypes in the controls was consistent with the Hardy–Weinberg equilibrium for all selected studies, except for three studies for −765G>C,33,37,48 two studies for −1195G>A,19,29 and two studies for 8473T>C.46,59 When we assumed that the OR for an allelic genetic association was 1.2, only one

study achieved a statistical power greater than 80%.61 Only Pembrolizumab datasheet two studies had a detailed dominant genotype frequency, so we extracted the data only for the dominant model.18,41 The evaluation of the association between these three polymorphisms and cancer risk is presented in Table 2. Overall, the variant A allele of COX-2−1195G>A can significantly increase the risk of cancer in all of selleck chemicals the tested models (GA vs GG: OR, 1.18; 95% CI, 1.07–1.29; P = 0.267 for the heterogeneity test; AA vs GG: OR, 1.35; 95% CI, 1.14–1.60; P = 0.010 for the heterogeneity test; dominant model, GA/AA vs GG: OR, 1.29; 95% CI, 1.18–1.41; P = 0.113 for the heterogeneity test; recessive model, AA vs GG/GA: OR, 1.22; 95% CI, 1.10–1.34; P = 0.002 for the heterogeneity test). However, for COX-2−765G>C and 8473T>C, no significant associations between the polymorphisms and risk of cancer were

observed. We then evaluated the effect of the three polymorphisms by specific tumor types. As shown in Table 2and Figure 1, we found that −1195G>A can significantly increase the risk of digestive system cancers in all tested models (GA vs GG: OR, 1.23; 95% CI, 1.11–1.37; P = 0.278 for the heterogeneity test; AA vs GG: OR, 1.55; 95% CI, 1.28–1.88; P = 0.045 for the heterogeneity test; dominant model, GA/AA vs GG: OR, 1.36; 95% CI, 1.23–1.51; P = 0.149 for the heterogeneity test; recessive model, AA vs GG/GA: OR, 1.32; 95% CI, 1.16–1.51; P = 0.016 for the heterogeneity test), whereas the increased risk was not evaluated for the ‘other cancers’ group.

Methods: We conducted two phase 3 studies in treatment-naïve patients infected with HCV. In the NEUTRINO study, patients

with HCV GT 1, 4, 5, or 6 infection received open-label sofosbuvir 400 mg plus peginterferon alfa-2a 180 μg weekly and ribavirin 1000–1200 mg daily for 12 weeks. In the FISSION study, patients with HCV GT 2 or 3 infection were randomly assigned to www.selleckchem.com/products/3-methyladenine.html receive sofosbuvir 400 mg daily and ribavirin 1000–1200 mg daily for 12 weeks or peginterferon alfa-2a 180 μg weekly and ribavirin 800 mg for 24 weeks. The primary endpoint in both studies was the proportion of patients with a SVR 12 weeks after therapy. Results: In the NEUTRINO study, 327 patients (89% GT 1, 9% GT 4, <1% GT 5, and 2% GT 6) were enrolled and received study drug; 64% were male, 17% had compensated cirrhosis, and 29% carried the IL28B CC genotype. In the FISSION study, 256 patients (27% GT 2 and 71% GT 3) were randomized to receive

SOF +RBV and 243 (28% GT 2 and 72% GT 3) were randomized to receive PEG + RBV; Overall, 66% were male, 20% had compensated cirrhosis, and 43% carried the IL28B CC genotype. Rates of SVR12 are given in table.

Selleckchem Venetoclax One on-treatment breakthrough was observed in a SOF+RBV patient with documented non-adherence. No S282T was observed in patients with relapse. Sofosbuvir was generally well tolerated with lower rates of the most common find more adverse events – fatigue, headache, nausea, and insomnia – observed in patients receiving sofosbuvir and ribavirin than in those receiving peginterferon and ribavirin. Conclusions: Twelve weeks of sofosbuvir combination therapy was well tolerated and associated with high rates of SVR in treatment-naïve patients with HCV genotype 1–6 infection. Table 1. Outcomes Response NEUTRINO FISSION SOF+PEG+RBV for 12 wk SOF+RBV for 12 wk PEG+RBV for 24 wk (n = 327) (n = 253) (n = 243) VF = virologic failure; on-treatment virologic failure includes non-response and breakthrough W SIEVERT,1 M BUTI,2 K AGARWAL,3 Y HORSMANS,4 E JANCZEWSKA,5 S ZEUZEM,6 L NYBERG,7 RS BROWN JR.

A total of 13 patients (12 with haemophilia A with high-responding inhibitors and one with von Willebrand’s disease type 3) underwent a total of 19 surgical procedures under rFVIIa cover. Thirteen procedures were classified as major surgeries. Intraoperative haemostasis was achieved in the majority of patients. Only two patients required an additional dose of rFVIIa, at 30 min and 75 min, respectively, with good results. Postoperative haemostasis was considered

effective in 16 of 18 (89%) of the procedures in haemophilia learn more A patients. Treatment was considered to be ineffective in two patients because of excessive postoperative bleeding. Data from the study provide no safety concerns, and demonstrate that rFVIIa provides effective haemostatic cover in elective surgery in patients with inhibitors; research is ongoing to determine the optimal dose for such procedures. “
“Monitoring factor replacement treatment and observing concordance with clinical haemostasis is crucial in vital haemorrhages and major surgeries in haemophilic patients. We aimed to investigate the value of the thrombin generation assay (TGA) and thromboelastography (TEG) Depsipeptide clinical trial for monitoring haemostasis in haemophilic patients during factor replacement

treatment. The study group consisted of 29 patients (21 haemophilia A, 8 haemophilia B). All the patients FVIII-inhibitor were negative. A total of 35 bleeding episodes and/or surgical interventions were evaluated. aPTT, FVIII/FIX activity, TEG and TGA tests were conducted before and after factor therapy during the bleeding

episode or surgical prophylaxis of haemophilic patients. Correlations among these tests were evaluated and compared with clinical selleck chemicals responses. No correlation was found among aPTT, factor activities and clinical outcome. There were also no correlation found between TEG parameters and clinical outcome. The only significant correlation found between TGA parameters and clinical outcome was the correlation between peak thrombin. In conclusion, we found superiority of TGA-peak thrombin over other traditional tests for monitoring haemostasis in haemophilic patients in this study. “
“Magnetic resonance imaging (MRI) scores for haemophilic arthropathy are useful for evaluation of early and moderate arthropathy. The most recent additive International Prophylaxis Study Group (IPSG) MRI scale for haemophilic arthropathy includes joint effusion. However, it is unknown whether joint effusion is haemophilia specific. Correct interpretation of joint effusion is needed for outcome assessment of prophylactic therapies in haemophilia care. The aim of this study was to compare joint effusion on MRI between young adults with haemophilia and healthy controls. MRI’s of both knees and ankles of 26 haemophilic patients (104 joints) and 30 healthy active men (120 joints) were assessed. Scans in both groups were performed in 2009/2010 and 2012 respectively.