For controls we analyzed 60 consecutive HCC patients without previous Angiogenesis chemical TIPS implantation. These patients were matched 1:1 for age (±5 years), sex, etiology of liver disease, and Child-Pugh score at the time of HCC diagnosis. In all, 51/60 patients (85.0%) in the TIPS group and 42/60 patients (70.0%) in the non-TIPS group died within the observation time. Tumor stages were assessed using the established Barcelona Clinic Liver Cancer (BCLC) classification. In both groups the

majority of patients presented with BCLC stage A (48.3% and 44.3%) and BCLC stage B (30.0% and 35.7%) without statistically significant differences (P = 0.966). TIPS patients had a median OS of 17.0 months (95% confidence interval [CI]: 10.21; 23.79) compared to 24.0 months (95% CI: 9.39; 38.61) of non-TIPS patients (P = 0.040, Fig. 1A). A multivariate Cox regression model identified multifocal hepatic tumor manifestation (hazard ratio [HR] 2.13, P = 0.012), TIPS (HR 1.74; P = 0.040), Child-Pugh B (HR 1.98; P = 0.008), and C (HR: 3.30; P = 0.004), alpha-fetoprotein (AFP) >20 ng/mL (HR: 1.94; P = 0.008), and metastasis (HR 5.20; P = 0.001) as significant independent negative predictors of OS. Moreover, we analyzed firstline treatment in TIPS and non-TIPS patients. A majority of

patients with TIPS were treated by best supportive care Bcl-2 inhibitor (BSC) and did not receive any HCC-specific treatment compared to patients in the non-TIPS group (26.8% versus 6.2%). Interestingly, 28 (46.6%) TIPS patients were treated with TAC compared to 49 (81.6%) non-TIPS patients who had been treated with TACE (P = 0.002, Fig. 1B). None of the TIPS patients developed click here severe hepatotoxicity as a possible reason for impaired OS. No statistical differences concerning surgical approaches, percutaneous therapies (radiofrequency ablation [RFA]) and sorafenib application, were found. In conclusion, our findings indicate that TIPS patients have

limited therapeutic possibilities concerning HCC-specific therapies, resulting in impaired OS. Especially, transarterial chemotherapies are less often administered in patients with TIPS. Therapy strategies in TIPS patients with HCC should be reassessed, since treatment options are expanded: (super)selective TACE[2] yttrium-90 radioembolization[3] or percutaneous ethanol injection in combination with TACE[4] might be alternative approaches. Therefore, prospective studies are needed to determine the effectiveness and the safety of therapeutic approaches using embolization in patients with TIPS and HCC and to establish treatment guidelines for HCC in these patients. Eva Knüppel, M.D.1* “
“IL-22 acts on epithelia, hepatocytes and pancreatic cells and stimulates innate immunity, tissue protection and repair. IL-22 may also cause inflammation and abnormal cell proliferation.

More important, our study also shows that HuR regulates HSC activation, which likely results in the reduced fibrosis observed in vivo after HuR silencing. HSC activation is highly regulated, with hundreds of genes up- and down-regulated.5 Modulation of mRNA stability and translation rates plays an important role in the regulation of gene expression during liver fibrosis development and hepatic stellate activation.1 Here, we show that HSC activation in vitro and in vivo after BDL is accompanied by an increase in HuR. HuR silencing significantly reduces the expression of HSC activation markers. Importantly, we observed that HuR mediates the response of two of the principal mediators of HSC activation (PDGF and TGF-β).30,

31 These data, together with the finding that HSC from human samples of hepatic cirrhosis expressed HuR, suggest Anti-infection Compound Library molecular weight that HuR has a significant role in fibrosis development after liver injury by controlling HSC activation itself, in addition to Tamoxifen nmr liver damage and inflammation. HuR regulates PDGF-induced proliferation and migration, controlling the expression of several genes involved in these processes. PDGF binding to its receptor leads to the sequential activation of RAF photo-oncogene serine/threonine-protein kinase, MEK, and ERK1/2. ERK

signaling is involved in PDGF-stimulated mitogenesis, migration, and chemotaxis. PI3K also mediates PDGF-induced proliferation, migration, and chemotaxis, at least in part, through ERK-independent pathways.30 Here, we demonstrated that ERK1/2, but not PI3K, regulates the cytoplasmic translocation of HuR. PDGF also induces LKB1 (Ser428) phosphorylation through ERK activation.22 LKB1 has been classically described as a tumor suppressor,32 but seems to have the this website opposite role in the liver, controlling HuR nucleocytoplasmic shuttling and proliferation in HGF-stimulated hepatocytes and during apoptosis in hepatoma cell lines.8, 9 Here, we also identified LKB1 as a downstream target of ERK1/2 in PDGF-stimulated HSCs, and silencing LKB1 significantly reduced PDGF-induced migration and proliferation. These functions of LKB1 are possibly mediated by HuR activity,

because LKB1 regulates the nucleocytoplasmic shuttling of HuR and both regulate the expression of a common set of mRNAs. It is known that LKB1 phosphorylates and regulates AMPK; however, we observed that PDGF-induced HuR cytosolic localization was independent of AMPK activity. This observation is in agreement with previous work describing that AMPK exerts antiproliferative properties in HSCs,23, 24 as well as with studies in melanoma cells, which show that LKB1 can be active without affecting AMPK activity.22 Previous studies have shown that PI3K and ERK are activated in HSCs in vivo after liver injury.33, 34 Here, we found that, similarly, LKB1 (Ser428) phosphorylation is also expressed in vivo in activated HSCs in two animal models of hepatic fibrosis (i.e.

This study evaluated long term adverse clinical outcomes for CHC patients stratified by all Metavir fibrosis stages. Methods: Clinical outcomes were determined using population

based data linkage methodology for 984 CHC compensated patients who had a liver biopsy performed from 1992 to 2012. This included 833 with ongoing infection and 151 with a sustained virological response (SVR). Results: 198 (20.1%) of patients had F0, 458 (46.5%) Opaganib in vitro had F1, 145 (14.7%) had F2, 98 (10%) had F3 and 85 (8.6%) had F4 fibrosis. During 11,226 person-years of follow-up, 31 (3.2%) patients developed hepatocellular carcinoma (HCC), 61 (6.2%) developed liver decompensation and 49 (5.0%) had liver transplantation or liver related death (LRD). In the 833 patients with ongoing CHC there was no significant difference in LRD for those with F0, F1 or F2 fibrosis with an 18 year survival probability >94%. Age adjusted hazard ratio (HR) Talazoparib cell line of LRD for F3 compared to F0-F2 was 4.24(P = 0.003),

with no significant difference in the first 13 year follow up. The 15 year liver complication (HCC and liver decompensation) free survival for F0, F1 and F2 was 100%, 96% and 94% respectively. Age adjusted HR of liver complication free survival for F3 compared to F0-F2 was 3.22 (P = 0.001), with no significant difference during the first seven years of follow up. F4 (cirrhosis) had

significantly higher risk of LRD, liver decompensation and HCC development than F3 (p < 0.001). selleck screening library 151 patients had a SVR after HCV treatment and the mean time between biopsy and treatment was 1.8 years. Mean follow up after the SVR was 12 years. Of this group 25 (12.6%) patients had F0, 75 (16.4%) had F1, 21 (14.5%) had F2, 18 (18.4%) had F3 and 12 (14.1%) had F4. Compared with the group with ongoing HCV infection there was a significant benefit of SVR in F4 patients with HR of 0.15 (95% CI, 0.02–1.17) for LRD and HR of 0.19 (95% CI, 0.05–0.81) for liver complications. There was no improvement in end points for F0, F1, F2 or F3 patients. Conclusion: CHC patients with ongoing infection and F0, F1 or F2 had few liver complications after 15 years follow up. Those with F3 and F4 had significantly increased HR for LRD and liver complications. However for F3 patients the increase in LRD occurred after 13 years and for liver complications after seven years.

L selectin was blocked and hepatocellular damage after IRI was assessed to mechanistically define the role of the adhesion molecule. Results: Mice fed a HFD diet showed significant increase in body weight (42±1.2, vs. 24.6±0.6 grams; p<0.0001) and presence of hepatic steatosis by ORO stain. Splenocytes from HFD mice undergoing IRI demonstrated significant increase in CD4+ T cell activation markers, such as PD1

(p<0.0009), CD69(p<0.01), and CD62L(p<0.001), in addition to higher INCB024360 levels of serum ALT and significant increase in hepatocellular necrosis. The T cell proliferation marker Ki67 (p<0.0089), was significantly higher in HFD IRI as compared to lean IRI. Expression levels of L-selectin (p<0.03) but not P or E-selectin were elevated in HFD IRI. Increased cytokines such as IFNγ, IL-1a, IL-10, IL-6 and IL-17, suggested a pro-inflammatory milieu in HFD IRI. Blockade of L-selectin, lead to a significant attenuation of hepatocellular injury. Conclusion: A steatotic liver undergoing IRI is associated with elevation of adhesion molecule L-se-lectin along with activation and proliferation of CD4+ T cells, and a pro-inflammatory

cytokine milieu. Blocking the adhesion molecule L-selectin leads to mitigation of hepatocellular injury, thus offering an important and clinically relevant therapeutic intervention in the increasingly prevalent clinical condition of IRI of fatty liver www.selleckchem.com/products/gsk1120212-jtp-74057.html disease. Disclosures: The following people have nothing to disclose: Vasantha L. Kolachala, Abramowsky Carlos, Ming Shen, Alayna Feng, Allan D. Kirk,

Nitika A. Gupta “
“From the mid-1950s, it was observed that liver injury by a variety of toxins greatly sensitized the host to the effects of administered lipopolysaccharide. In the nutritional cirrhosis of choline deficiency, and in acute toxic injury as well, the need for the presence of enteric endotoxin was demonstrated. The universality of this association was striking for almost all agents associated selleck inhibitor with liver injury. In addition, the presence of endotoxemia in human liver disease was documented in the 1970s, when the hypothesis was first proposed, and correlated with the severity of the disease. Despite imposing evidence of the critical role of enteric endotoxin in liver injury, it did not excite much interest in investigators until the 1980s. With the ability to study effects of alcohol in newer delivery systems, and an increased understanding of the role of Kupffer cells in the process, the original hypothesis has been accepted. This historical review details the progress of this novel concept of disease initiation and suggests future directions to bring potential therapies to the bedside. (HEPATOLOGY 2010.) Continuing work over the past several decades has further solidified the importance of intestinal endotoxins as critical cofactors in toxic liver injury by a number of agents.

We

prescribed bismuth subnitrate four times daily, as used in the literature, and within the approved dose in Japan (up to 2 g) MK0683 for diarrhea. To ensure an appropriate dose of PPI, knowledge of the CYP2C19 genotype is important.3,13–15,18 Because the present patient had an EM genotype, we prescribed PPI four times daily. Thus we designed a new quadruple therapy regimen, which may be called either a tailor-made modified classical quadruple therapy or a modified high-dose PPI + AMPC dual therapy supplemented with bismuth and MINO. In this patient we used LPZ, but RPZ might be also effective. The result was satisfactory. The patient had successful eradication without any adverse events. A follow-up study also showed continued

negative results at 1 year after the therapy. A 14-day, tailor-made, modified classical Anti-infection Compound Library cell assay (or modified high-dose PPI + AMPC) quadruple therapy may be one of the choices for patients with multiple-antibiotic-resistant H. pylori infection or multiple eradication failures. It is unknown that MINO and bismuth subnitrate have additive effects on the high-dose PPI + AMPC dual therapy. Further trials with more patients are needed to confirm the effectiveness of the novel therapy. Most of this study was performed by the principal author, SN. The second author, HI, participated in the clinical affairs in Inoue Clinic before referring the patient to Social Insurance Shiga Hospital. The other authors, TI and YM, coordinated bacterial culture and drug information, respectively. None of the authors has a conflict of interest with any corporation or organization. “
“Fifty percent of people treated with radiotherapy are long-term survivors. Acute radiation injury to the gastrointestinal (GI) tract is common, particularly esophagitis and diarrhea, but usually resolves after

treatment is completed. Significant late effects of radiotherapy occur in 5–15% and are due to abnormal vasculature and fibrosis. This results in stricturing and bleeding. The most troublesome symptoms after pelvic radiotherapy are urgency, frequency, and tenesmus. Bleeding can be treated with endoscopic thermal methods, check details formaldehyde, sucralfate or hyperbaric oxygen. Chemical damage to the GI tract is uncommon. Oral ingestion of chemicals, particularly lye-based cleaners, causes severe esophagitis and strictures. Chemical colitis is often iatrogenic. There are no specific treatments and colectomy may be required if the injury is severe. “
“Immunoglobulin G4 (IgG4)-associated cholangitis (IAC) is a manifestation of the recently discovered idiopathic IgG4-related disease. The majority of patients have elevated serum IgG4 levels and/or IgG4-positive B-cell and plasma cell infiltrates in the affected tissue. We hypothesized that clonally expanded, class-switched IgG4-positive B cells and plasma cells could be causal to these poorly understood phenomena.

PJC improved the diagnostic utility of EUS-FNA for pancreatic tumor. Endoscopic ultrasonography (EUS) is a widely accepted modality for detecting pancreatobiliary diseases, determining the depth of gastrointestinal malignancies, and, often, for visualizing lesions more precisely than other imaging modalities. Endoscopic ultrasound-guided fine-needle aspiration biopsy (EUS-FNA) has enhanced the diagnostic

capabilities of EUS by providing additional pathological findings.[1] More than 20 years have passed since the use of EUS-FNA was demonstrated selleck for pancreatic disease,[2] and now, this technique is popular worldwide. However, EUS cannot detect minimally invasive carcinoma, and EUS-FNA cannot be performed for intraductal papillary mucinous carcinoma (IPMC) because of concerns about needle tract seeding.[3, 4] Since the introduction of endoscopic retrograde cholangiopancreatography (ERCP), pancreatic juice cytology (PJC) has yielded sensitivities for pancreatic cancer that have ranged from 33% to 67%.[5, buy HM781-36B 6] Recently, Uehara et al. have shown the usefulness of PJC for pancreatic cancer.[7] However, whether PJC strengthens the diagnostic power of EUS-FNA for pancreatic masses remains unclear. In the present study, the

diagnostic ability of EUS-FNA and/or PJC in pancreatic disease was examined. A total of 161 patients (103 men, 58 women; age range, 24–86 years; mean age, 67.0 years) with pancreatic disease was enrolled (Table 1). Of these, 90 patients (54 men, 36 women; age range, 24–86 years; mean age, 65.1 years) had malignant disease, and 71 patients (49 men, 22 women; age range, 28–82 years; mean age, 69.5 years) had benign disease. All patients who underwent EUS-FNA and/or PJC between April 2009 and March 2012 were reviewed. Ten patients were repeated during follow up in some patients

(Table 1). The true number of patients who underwent EUS-FNA, PJC, and both of them are 124, 89, and 36. Patients were referred for EUS-FNA and/or PJC based selleck kinase inhibitor on the need to evaluate them for malignancy. Cytodiagnosis of the specimen was performed by Papanicolaou’s method; rapid cytopathologic diagnosis was not used. Informed consent was obtained from all patients. Eight patients were excluded from EUS-FNA, but not from PJC, if they had thrombocytopenia or uncontrolled coagulopathy. EUS-FNA was not performed for cases of intraductal papillary mucinous neoplasm (IPMN) and IPMC, as it is contraindicated in Japan in such cases. EUS-FNA and PJC were performed in an inpatient endoscopy suite as previously described.[7-11] EUS-FNA was performed using a 7.5-MHz, convex, linear array echoendoscope (GF-UCT240; Olympus Optical Co. Ltd, Tokyo, Japan), a 22-G needle (NA-200H-8022, Olympus), and a 25-G needle (ECHO-25 Cook Medical Inc, Winston-Salem, NC, USA, M00550020; Boston Scientific Corporation, Natick, MA, USA). PJC was performed using a lateral-viewing endoscope (JF260V; Olympus), a cannula (M00535700; Boston Scientific Corporation), and a 0.

His achievements, along with his relationship with many famous gastroenterologists, opened the door at Harvard Medical School and American Gastroenterological Association (AGA) for Japanese researchers. Professor Daniel Podolsky was then Chief of the GI unit of Massachusetts’ General Hospital in the

Harvard Medical School at that time, later becoming President of the AGA, and is now President of the University of Texas, Southwestern Medical Center. Podolsky helped Mamoru personally, as well as, through him, becoming a good friend of the Japanese Society of the Gastroenterology (JSGE). In April 2000, Dr Watanabe accepted the position of Professor and Chairman, Department of Gastroenterology and Hepatology at Tokyo Medical and Dental University, where he currently selleck kinase inhibitor serves. He also leads two other clinical gastroenterology divisions, the Department of Endoscopy and the Advanced Clinical Center for Inflammatory Bowel Disease. At Tokyo Medical and Dental University, his work continues to have a tremendous impact and he and his team have met numerous challenges both in the research field and in clinical care. Dr Watanabe has used his expertise to mentor many co-investigators in clinical sciences and trials,

to advance basic research and the principles of evidence-based medicine. His extraordinary professional standards always provide inspiration to all those with whom he works. This has built up the Division of Gastroenterology at Tokyo Medical and Dental University with talented faculty members and gastroenterologists, comprising an unprecedented AT9283 ic50 intellectual environment. It is no surprise that his currently leading department has become an extremely popular

GI center for training and research among Japanese schools and institutes. Mamoru Watanabe’s research interests are in immune-modulating therapy for IBD, cellular and molecular biological aspects of IBD, mucosal immunology, molecular biological aspects of inflammation-related carcinogenesis, and regeneration and differentiation of intestinal epithelial cells. Most recently, he has turned his attention to intestinal epithelial stem cell biology. An see more early discovery was the recognition that interleukin (IL)-7 is an essential factor for the pathogenesis of IBD, being responsible for the persistence of chronic T cell-mediated colitis. Mamoru has shown that IL-7 is constitutively produced by intestinal goblet cells. He is the first scientist who found the critical role of IL-7 in mucosal immunology and this ground-breaking paper was published in the Journal of Clinical Investigation in 1995.[1] IL-7 transgenic mice develop colitis that mimics the histopathological characteristics of human IBD (J Exp Med 1998).[2] CD4+ T cells that express high levels of IL-7Rα reside in inflamed lamina propria (LP) (Journal of Immunology [JI] 2003, JI 2011) and IL-7–/– mice do not develop colitis (JI 2007).

7E). Taken together these results indicate that the PPARγ-independent antiproliferative effect of TZD is mediated by NMP through a mechanism involving p53. Our study shows that chronic administration

of two different TZD, significantly inhibit tumor formation in a HBV-related mouse model check details of hepatocarcinogenesis. This effect was correlated by in vivo and in vitro inhibition of hepatocyte proliferation and induction of apoptosis with negligible effects on the degenerative and the inflammatory responses. On the contrary, the non-TZD PPARγ agonist GW1929 had no effect on tumor formation and hepatocyte proliferation although this drug is able to induce PPARγ transactivation and target gene expression in mouse hepatocytes. This suggests that PPARγ activation is unlikely involved in the antitumor effect of TZD in mouse liver. Previous in vitro evidences suggest that the antiproliferative effect of TZD is independent of PPARγ activation; indeed, troglitazone induced growth arrest by inhibition of translation initiation in PPARγ−/− embryonic stem cells.22 Similarly, we found that in hepatocytes isolated from HBV transgenic mice, the growth inhibitory effect of TZD is dissociated from the ability of these drugs to promote PPARγ transactivation. In fact, ectopic expression of DN-PPARγ was unable to revert the growth inhibitory effect of TZD. selleck chemical Although PPARγ is clearly recognized as master regulator of lineage-specific

cell differentiation that differs according to the cellular type,23 the correlation between PPARγ activation and programmed cell death induced by TZD is doubted. In pancreatic cancer cells, TZD-induced PPAR-dependent growth

arrest is primarily mediated by cell differentiation without proapoptotic effects.24 Conversely, TZD analogues, which have a double bond adjoining the terminal thiazolidinedione ring that is responsible for the abrogation of the PPARγ ligand property, retain the ability to induce apoptosis with click here a potency equal to that of their parental TZD in cancer cell lines,25 suggesting that mechanisms involved in TZD-induced differentiation differ from those mediating apoptosis. The dissociation of TZD effects on apoptosis from their original pharmacological activity (i.e., PPARγ activation), is in line with the observation that sensitivity of cancer cells to TZD-induced growth inhibition does not correlate with the PPARγ expression levels, and there exists a three orders of magnitude discrepancy between the concentration required to produce antitumor effects and that needed to modify insulin action.26 The PPARγ-independent proapoptotic effect of TZD was confirmed in triple transgenic animals Tg(HBV)CreKOγ in which Cre specifically deletes PPARγ in hepatocytes. In this experimental model, genetic deficiency of PPARγ does not modify the process of hepatic carcinogenesis and tumor development when compared to parental HBV transgenic mice.

(HEPATOLOGY 2011;) The liver is the central organ responsible for the selective uptake, metabolism, and excretion Angiogenesis inhibitor of drugs, xenobiotics, and environmental toxins. This essential function predisposes the liver to drug toxicity and is the primary reason for the failure of pharmaceutical agents during drug development. Hepatic drug toxicity is the most common cause of acute fulminant hepatic failure, accounting for more than 50% of cases.1 More than a thousand drugs and herbal remedies have been reported to cause a variety of different liver disorders. However, specific diagnostic markers for drug-induced liver

injury (DILI) are lacking, and convincing cause-and-effect evidence exists for few cases.2 Indeed, establishing causality has been a major hindrance in the understanding

of DILI.3, 4 Cholestatic & mixed cholestatic and hepatocellular injury are two of the most severe manifestations of drug-induced liver disease (DILD),5 and account for close to half of all hepatic drug toxicity in some epidemiologic reports.6 There is increasing evidence that drugs that are excreted by the liver into bile are prime candidates for producing cholestatic liver disease in the susceptible patient.7 Several forms of cholestatic liver injury can be produced by drugs, and these can present acutely or in the form of chronic liver disease. Drug-induced cholestasis may mimic other intrahepatic EPZ-6438 manufacturer and extrahepatic cholestatic diseases. Not recognizing a drug as a triggering factor for cholestasis prolongs exposure to the toxic agent, which may lead to worse liver injury and unnecessary diagnostic and therapeutic

interventions. Acute and chronic cholestatic liver injury results from dysfunction of the mechanisms of bile formation. However, drug-induced cholestasis can present with asymptomatic disease where the only clinical manifestation is an elevation in alkaline phosphatase (AP). Moreover, the target of injury can vary from a mixed hepatocellular cholestatic injury, to impairment of canalicular bile flow resulting in pure intrahepatic cholestasis, or to an “obstructive” drug-induced cholangiopathy where the initial site of injury is located at various levels of the bile duct epithelium.8-10 The incidence and associated health see more care costs secondary to drug-induced cholestasis are not available, in part because most drugs commonly cause asymptomatic cholestasis associated with mild abnormalities in the serum liver profile. A Danish study of 110 cases of DILI from 1978 to 1987 reported a 17% prevalence of acute cholestatic injury.11 In the United States, the prevalence of drug-induced cholestasis was reported to be 20% in the elderly population. However, on examination, not all of these cases included patients with cholestasis.12 Approximately 2%-5% of hospitalized cases with jaundice are caused by drugs but cholestasis is expressed in only some of these patients.

Three successive

liver stiffness measurements (LSM) were performed at different sites on the liver. Two-validated algorithms were used to improve evaluation of fibrosis by non-invasive methods. Fifty-seven hepatitis C-infected haemophilia patients were evaluated by FT and FS. Acquisition of LSMs was not feasible in two patients: obesity – one, surgical scars – one. Fibrosis stage ≥F2, ≥F3 or =F4 were estimated in about a half, about high throughput screening compounds a third and in 15–20% of the evaluated patients by FS and FT respectively. The corresponding concordance rates and κ score for fibrosis stage ≥F2, ≥F3 or =F4 between FT and FS were 62%, 69%, 85% and 0.24, 0.32, 0.44 respectively. Using the two aforementioned algorithms, additional 14 patients could be reliably estimated for fibrosis stage ≥F2. High proportion hepatitis C-infected haemophilia patients were estimated with significant or advanced stages of liver fibrosis using both tests. Nevertheless, the agreement between modalities was only fair and improved with more advanced stages of fibrosis. Practical algorithms for the accuracy of FT and FS may improve reliable evaluation of fibrosis in this population. “
“Summary.  The clinical relevance of subtle changes on magnetic resonance imaging (MRI) for evaluating haemophilia treatment is unknown. To determine the relationship of findings on MRI with joint

function and bleeding in joints with apparently Pritelivir price very mild arthropathy, a prospective study was performed. Knees and ankles of 26 patients, 13–26 years, were scanned. Two blinded radiologists scored the MRI (IPSG consensus score) and the radiography [Pettersson score (PS)].

Clinical function (HJHS) was scored by one physiotherapist. Life-time number of bleeds was collected from patient files. Of 104 joints scanned, three were excluded because of previous arthrodesis or trauma. Remaining 101 MRI scores correlated weakly with clinical function (r = 0.27, P = 0.01) and less with lifetime number of bleeds (r = 0.16, P = 0.14). 上海皓元 MRI scores were 0 in 58 joints, including 27 with major bleeds. In three joints of patients playing intensive sports MRI showed minor changes (MRI score = 1) in the absence of bleeds. Agreement was reasonable between PS and MRI score (r = 0.41, P < 0.01). In 30% of joints, MRI detected abnormalities in soft-tissue and cartilage, while PS was 0 points. No evidence of occult haemorrhages was found. Instead, we found no abnormalities on MRI in 43 joints with a history of repeated joint bleeding. Haemosiderin seemed associated with the time between assessment and last bleed; joints that had suffered a bleed long before MRI had hardly haemosiderin, while those with a recent bleed showed haemosiderin, suggesting joint damage may be reversible. Abnormalities detected by MRI, but not by PS were minor and their clinical implications are not yet clear. "
“Summary.