Key Word(s): 1. bowel obstruction; 2. diagnosis; 3. biomarkers; 4. physical examination; Presenting Author: JOHNSON MARIAANTONY Corresponding Author: JOHNSON MARIAANTONY Affiliations: Dr.

www.selleckchem.com/products/lee011.html MGR Medical Unversity Objective: Obstructive jaundice due to Bile Duct Tumor Thrombi is an uncommon presenting feature of Hepatocellular Carcinoma (HCC) reported in about 2–9% (Okuda &Nakashima series) and 12% (Hong Kong study group) of cases respectively. Only a few studies have examined the outcome of hepatectomy in this subset of patients. Aim: To evaluate the outcome of hepatectomy for non- fibrolamellar- type HCC with obstructive jaundice due to bile duct tumor thrombi in non-cirrhotic liver. Methods: From 1995 to 2007, out of 156 HCC patients, 19 (12.1%) with

non-fibrolmellar- type HCC with obstructive jaundice due to bile duct tumor thrombi in non-cirrhotic BMS-354825 datasheet liver, who underwent hepatectomy were retrospectively analyzed. HBsAg, Anti HCV Ab and AFP were positive in 3 (15.7%), one (5.2%), and 13 (68.4%) cases respectively. The operative procedures included, right hepatectomy with thrombectomy through choledochotomy and T-tube drainage (n = 8), extended right hepatectomy combined with extrahepatic bile duct excision (n = 3), left hepatectomy (n = 6), extended left hepatectomy (n = 1) and left lateral segmentectomy (n = 1). Results: The diameter of primary Non-specific serine/threonine protein kinase tumor ranged from 5 to 13 cm. Biliary tumor thrombi were located in the right and left hepatic ducts in two, free floating in the common bile duct in 9, and extended across the confluence of the right and left hepatic ducts in 8 patients respectively according to Satoh’s classification. Portal vein invasion were found in 4 patients (right branch n = 1, left branch n = 1, right posterior branch n = 1, right branch to stem n = 1). Postoperative morbidity was 31.5% (n = 6), which included bile leak in 4 (21.05%) patients. One patient died of postoperative liver failure (mortality rate 5.2%). The tumor recurrence rates were intrahepatic in 68.4%, extrahepatic in 21.0% and both intrahepatic and extrahepatic in

10.5%. The 1-; 3- and 5-year survival rates were 78.9%, 47.3% and 10.5% respectively with a median survival time of 24.8 months. Conclusion: Presence of bile duct tumor thrombi in HCC patients should not be considered as advanced disease or inoperable lesion. When technically feasible, a formal hepatic resection is the first-line treatment option in a subset of HCC patients with obstructive jaundice due to bile duct tumor thrombi in non-cirrhotic liver with significantly large-sized tumors. It can achieve better quality of life with significant improvement in both disease-free and overall survival. Key Word(s): 1. HCC; 2. Non-cirrhotic liver; 3. Tumor thrombi; 4. Hepa; Presenting Author: JOHNSON MARIAANTONY Corresponding Author: JOHNSON MARIAANTONY Affiliations: Dr.

Key Word(s): 1. bowel obstruction; 2. diagnosis; 3. biomarkers; 4. physical examination; Presenting Author: JOHNSON MARIAANTONY Corresponding Author: JOHNSON MARIAANTONY Affiliations: Dr.

BVD-523 in vivo MGR Medical Unversity Objective: Obstructive jaundice due to Bile Duct Tumor Thrombi is an uncommon presenting feature of Hepatocellular Carcinoma (HCC) reported in about 2–9% (Okuda &Nakashima series) and 12% (Hong Kong study group) of cases respectively. Only a few studies have examined the outcome of hepatectomy in this subset of patients. Aim: To evaluate the outcome of hepatectomy for non- fibrolamellar- type HCC with obstructive jaundice due to bile duct tumor thrombi in non-cirrhotic liver. Methods: From 1995 to 2007, out of 156 HCC patients, 19 (12.1%) with

non-fibrolmellar- type HCC with obstructive jaundice due to bile duct tumor thrombi in non-cirrhotic Sorafenib nmr liver, who underwent hepatectomy were retrospectively analyzed. HBsAg, Anti HCV Ab and AFP were positive in 3 (15.7%), one (5.2%), and 13 (68.4%) cases respectively. The operative procedures included, right hepatectomy with thrombectomy through choledochotomy and T-tube drainage (n = 8), extended right hepatectomy combined with extrahepatic bile duct excision (n = 3), left hepatectomy (n = 6), extended left hepatectomy (n = 1) and left lateral segmentectomy (n = 1). Results: The diameter of primary Buspirone HCl tumor ranged from 5 to 13 cm. Biliary tumor thrombi were located in the right and left hepatic ducts in two, free floating in the common bile duct in 9, and extended across the confluence of the right and left hepatic ducts in 8 patients respectively according to Satoh’s classification. Portal vein invasion were found in 4 patients (right branch n = 1, left branch n = 1, right posterior branch n = 1, right branch to stem n = 1). Postoperative morbidity was 31.5% (n = 6), which included bile leak in 4 (21.05%) patients. One patient died of postoperative liver failure (mortality rate 5.2%). The tumor recurrence rates were intrahepatic in 68.4%, extrahepatic in 21.0% and both intrahepatic and extrahepatic in

10.5%. The 1-; 3- and 5-year survival rates were 78.9%, 47.3% and 10.5% respectively with a median survival time of 24.8 months. Conclusion: Presence of bile duct tumor thrombi in HCC patients should not be considered as advanced disease or inoperable lesion. When technically feasible, a formal hepatic resection is the first-line treatment option in a subset of HCC patients with obstructive jaundice due to bile duct tumor thrombi in non-cirrhotic liver with significantly large-sized tumors. It can achieve better quality of life with significant improvement in both disease-free and overall survival. Key Word(s): 1. HCC; 2. Non-cirrhotic liver; 3. Tumor thrombi; 4. Hepa; Presenting Author: JOHNSON MARIAANTONY Corresponding Author: JOHNSON MARIAANTONY Affiliations: Dr.

Over the subsequent weeks the patient spontaneously recovered and was completely asymptomatic. Cholestasis with normal gamma glutamyl transferase is a key feature of functional deficiencies in the gene ATP8B1, encoding a P-type ATPase1 or ABCB11, which encodes the bile salt export pump (BSEP), a liver specific adenosine triphosphate (ATP)-binding cassette transporter.2 Depending on their www.selleckchem.com/products/BAY-73-4506.html localization, mutations in ABCB11 may result in promoter changes affecting transcription or new splice acceptor sites leading to nonsense mediated decay of the messenger RNA.3 As a result the protein can be quantitatively or functionally insufficient. Sequence analysis

in this patient revealed a heterozygote ABCB11 mutation c.221T>C. This nucleotide change results in an amino acid change p.Ile74Arg in the first transmembrane domain of the ABCB11 protein. Immunohistochemical staining of the liver biopsy showed a normal (canalicular) expression of BSEP (Fig. 1, Panel 4). However, there was a gradual decrease from zone 1 to zone 3 of the liver lobule with a very low

expression of BSEP in the zone around the central vein (Fig. 1, Panel 4, arrow). In contrast, we observed in a control patient a homogeneous distribution of BSEP throughout the liver parenchyma, including the pericentral area (Fig. 1, Panel 5, arrow). Two years later the patient continued to show marginally elevated levels of serum bile acids (33 μmol/L) and alkaline phosphatase (110 U/L), indicating the persistence

of a mild cholestasis. ABCB11 deficiency has been described in association with numerous MAPK inhibitor mutations and represents a clinical continuum from very mild to progressive forms of cholestasis, including Liothyronine Sodium benign recurrent intrahepatic cholestasis type 2, intrahepatic cholestasis of pregnancy, and progressive familial cholestasis 2. This patient had biliary stones, a distinguishing feature of ABCB11 deficiency, probably due to the low bile salt concentration secondary to impaired BSEP function. The attack of cholestasis in this patient was preceded by nausea and vomiting for a few days. Episodes of minor infections or drugs taken shortly before the cholestatic event are considered possible trigger factors in patients carrying mutations in the ABCB11 gene and may explain the intermittent character of intrahepatic cholestasis.4 In our case sequence analysis revealed only one heterozygous single nucleotide mutation, but we cannot exclude the possibility that other mutations have been missed. The immunohistochemical findings suggest that the mutation identified here may predispose patients to cholestasis through a regulatory mechanism of BSEP not at the canalicular, but at the lobular level. Further investigation will be needed to confirm these findings and to understand the role of BSEP in the different liver lobule zones.

Ten healthy adults (eight men, two women; age, 48 ± 17 years) with no blood biochemical abnormalities were included as a control group. Between November and December 2005, 60 patients (33 men, 27 women; age, 63 ± 12 years) with HCV-associated CLD, including 13 patients enrolled in the former study, were included in a study designed to assess the correlation between plasma stromal derived factor-1α (SDF-1α) concentrations

and CLD stage. Additionally, seven patients with HCV-associated LC, who had adequate liver function and underwent splenectomy between February 2005 and May 2007 (three men, four women; age, 55 ± 9 years), were enrolled in this study. Blood samples were collected preoperatively, at 1 week after surgery and at 1–3 months after surgery. Spleen samples were obtained from another three LC patients, who learn more underwent splenectomy within 1 year. Written informed consent

was obtained from all patients and healthy volunteers. The study protocol was approved by the Human Studies Subcommittee of Mie University Graduate School of Medicine (approval no. 287) and conformed to EGFR targets the ethical guidelines of the Declaration of Helsinki, 1975. Peripheral blood samples were drawn from patients with HCV-associated CLD and from healthy volunteers. Erythrocytes were lysed using ACK lysis buffer, and the remaining cells were washed twice with Ca2+/Mg2+-free phosphate-buffered saline (PBS; Gibco, Grand Island, NY, USA) and resuspended in PBS containing 0.1% de-ionized fraction V bovine serum albumin (BSA; Sigma-Aldrich, St. Louis, MO, USA). We used

the remaining cells as PB total nucleated cells (TNC) for flow cytometry. PB mononuclear cells (MNC) were prepared by density gradient centrifugation over Ficoll-Paque PLUS (GE Healthcare Bio-Sciences, Uppsala, Sweden) and were used for the CFU-C assay. Peripheral blood TNC were stained with fluorescein isothiocyanate (FITC)-conjugated antihuman CD34 (Becton Dickinson Immunocytometry Systems, San Jose, CA, USA) and phycoerythrin (PE)-conjugated antihuman CD90 (Becton Dickinson Pharmingen, San Diego, CA, USA) or PE-conjugated antihuman CD117 (Becton Dickinson Pharmingen). Relevant isotype-matched control antibodies were included in the staining to exclude non-specific binding. After adding 1 μg/mL of ioxilan propidium iodide (Sigma-Aldrich) to eliminate dead cells from the analysis, the cells were washed and resuspended in PBS containing 0.1% BSA. At least 200 000 events in live leukocyte populations were acquired by flow cytometry (FACSCalibur; BD Biosciences, San Jose, CA, USA) and were analyzed using CellQuest software (BD Biosciences). The number of CD34+ cells in living PB-TNC was determined using a CD34-FITC versus side-scatter dot plot. In some samples, PB-TNC were double stained with FITC-conjugated anti-human CD34 antibody and allophycocyanin-conjugated anti-human CD45 antibody (BioLegend, San Diego, CA, USA).

6/10 (95% CI 6.92–8.28). In the high dose group 86.4% were satisfied with treatment with an

mean satisfaction score of 8.5/10(95% CI 7.3–9.50). When asked if they would consider repeat botulinum toxin A treatment if needed 81.0% (47/58) of the low dose group stated they would, compared to 86% (19/22) in the high dose group. The average reported number of repeat treatment sessions prior to contemplating surgical intervention was 1.4 (95% CI 1.2–1.7, range 0–3) in the low dose group compared to 1.5 (95% CI 1.2–1.8, range 0–3) in the high dose group. Efficacy was better when treated with high dose botulinum toxin A. Significantly fewer patients had recurrent symptoms of CAF in the high dose group (27.3% vs. 53.4%, P = 0.04) and there was a statistically significant reduction in the rate of surgical BVD-523 mw management of CAF following high dose botulinum toxin A treatment (4.5% vs. 8.6%, P < 0.05). Conclusion: This study reveals that high dose botulinum toxin A has a similar safety profile to low dose treatment; there is no significant increase in bleeding or incontinence. Pain from CAF is shown to be significantly improved following high dose treatment. High dose botulinum toxin A also demonstrates a significant reduction in the recurrence

of CAF disease and surgical intervention rate is significantly less. The rate of post procedure complication with high dose botulinum toxin A (80–100 IU) demonstrated in this study is less than current published data of surgical intervention for CAF. The majority of patients treated with

botulinum toxin A for CAF are willing CDK inhibitor to have repeat treatment for recurrent episodes prior to planning surgical intervention. This indicates Bcl-w the importance of chemical sphincterotomy in CAF disease. CJ SHUTTLEWORTH,1 M HALLAND,2 K BRISCOE3 1Basic Physician Trainee, St George Hospital, Sydney, Australia, 2Department of Gastroenterology, Mayo Clinic, Rochester Mn, 3North Coast Cancer Institute, Coffs Harbour, Australia Introduction and Cases: Carcinoid is typically considered a sporadic disease and little is known about its hereditary forms. There is growing evidence that familial Carcinoid exists outside its classical association with syndromes of Multiple Endocrine Neoplasia (MEN). Novel oncogenes have been identified associated with autosomal dominant forms of Ileal Carcinoid, leading to the emergence of “Familial Ileal Endocrine Carcinoma” (FIEC). 1. Here we present the case of two brothers recently diagnosed with small bowel Carcinoid as well as a systematic review of the literature. Case One: Mr. AB, a 51 year old man, presented in 2012 with a four year history of increasing abdominal pain and minimal diarrhoea without flushing. He was one of ten siblings and interestingly one of his brothers had died from an unknown abdominal malignancy several years prior.

Median duration of ETC treatment was 38 months (6-66). Cumulative CVR rates in NA-naïve and experienced patients were 69% vs. 54% at 12th month and 84% vs. 68% at 24th month, 92% vs. 86% at 36th month, respectively (Fig.1, log-rank, p=0.32). 3 patients (10.3%) in NA-experienced group and 4 patients in NA-naïve group (2.2%) required a switch to tenofovir (TDF) due to sub-optimal response to ETC (p=0.061) and 1 NA-naïve patient developed ETC resistance (L180M, M204V, S202G). Multi-variate

logistic regression analysis showed that HBeAg positiv-ity (OR: 6.3, 95% CI 1.16-34.3, p=0.033) and previous LAM experience (OR: 5.8, 95% CI 1.15-29.2, p=0.033) were independent predictors for a requirement LDE225 to switch to TDF. Conclusion: ETC has a potent antiviral efficacy in patients with CHB. The antiviral efficacy of ETC is not influenced by prior treatment with NAs if LAM resistance is excluded at baseline. However, HBV-DNA kinetics should be carefully monitored in patients with HBeAg-positive CHB and previous LAM experience. Disclosures: The following people have nothing to

disclose: Bulent Baran, CB-839 purchase Ozlem Mutluay Soyer, Asli Cifcibasi Ormeci, Suut Gokturk, Sami Evirgen, Filiz Akyuz, Cetin Karaca, Kadir Demir, Fatih Besisik, Derya Onel, Mine Gulluoglu, Selim Badur, Sabahattin Kaymakoglu Background: Chronic hepatitis B (CHB) disproportionately affects Asian-Americans in the US. TDF has been demonstrated potent antiviral in clinical trials, but real-life data in Asian-Americans are lacking. We prospectively followed patients on TDF for 144 weeks and assessed outcomes. Methods: Asian-American patients with CHB from multiple community-based practices were prospectively enrolled and treated with TDF (300 mg/day) in a single arm study for 48 weeks. After week 48, patients had the option to continue TDF up to week 144, or opt out of further observation. The primary efficacy endpoint was hepatitis B virus (HBV) DNA < 29 IU/mL at week 48 Clomifene and 144. Secondary endpoints were safety and tolerability, serologic and biochemical

responses, liver fibrosis by FibroTest at week 48, and the development of drug resistant mutations. Results: Ninety patients were enrolled with baseline values in Table 1. At week 48, seventy four patients (82% overall; 70% HBeAg-positive and 100% HBeAg-negative) had HBV DNA <29 IU/mL. 12% (6/52) HBeAg+ patients achieved HBeAg loss/seroconversion. The percentage of patients with alanine aminotransferase (ALT) in the normal range increased from 26% at baseline to 66% at week 48. The percentage of patients with F0 fibrosis by FibroTest increased from 48% to 51%, and those with F4 fibrosis decreased from 4% to 1 %. At week 48, 31 /90 patients (19 HBeAg+) opted to continue on TDF with assessment at 12 week intervals up to week 144. Two patients with HBV viremia did not participate beyond week 48. At week 144, 84% (26/31) patients had HBV DNA <29 IU/mL; No viremic patient (n=5) had genotypic mutation on Sanger sequencing (2/5 TDF non-adherence); 67.

Together, these findings may lead to novel therapies for liver injury. Additional Supporting Information may be found in the online version of this article. “
“Tripodi A, Mannucci PM. The coagulopathy of chronic liver disease. N Engl J Med 2011;365:147-156. (Reprinted with permission.) The reassessment of hemostasis in patients with chronic liver disease challenges the dogma that the

major coagulopathy in these patients leads consistently to bleeding. Other changes that accompany chronic liver disease may restore the balance of anticoagulant and procoagulant effects. In certain circumstances, the risk of thrombotic events may be greater than the risk of hemorrhage. We speculate that drugs that are often regarded as contraindicated in patients with chronic selleck antibody inhibitor liver disease may instead prove beneficial and should be tested in

appropriate clinical trials. For any provider who cares for patients with liver disease, whether directly or in a supportive or procedural capacity, bleeding from one site or another has likely left an indelible, and often dour, clinical impression. This feeling is especially amplified when the bleeding originates from one’s own puncture or biopsy site. The prothrombin time (PT) and international Selisistat clinical trial normalized ration (INR) are reliable measures of coagulation in warfarin-treated patients. It stands to good reason that direct extrapolation and application of PT/INR to cirrhosis patients should provide a practical measure of bleeding risk and serve as a reliable

guide for therapy and prevention of bleeding. However, for those who have practiced this concept for many years, the emergence of a contrary body of literature may be difficult to digest. Sorafenib purchase Nonetheless, it is currently evident that the hemostatic system in liver disease patients is far more complex than the PT/INR. Indeed, these patients may be relatively hypercoagulable, in spite of prolongation of the PT/INR. These paradoxical relationships have recently been summarized in an important article from two key investigators in this field, Armando Tripodi and Pier Mannuccio Mannucci. 1 Investigations over the recent past have redefined the “balance” of the coagulation cascade in cirrhosis patients as a more sensitive state of equilibrium, where perturbations can result in either a hypo- or hypercoagulation clinical event. From a simplified perspective (Fig. 1), coagulation in the cell-based model of hemostasis originates at a site of vascular breach from activation of tissue factor and factor VII on the phospholipid membrane of a platelet (or adventitial cell). This, in turn, leads to assembly of activated factors X and V (prothrombinase complex), which results in a “priming” amount of thrombin (factor II) and initiation of fibrin production from fibrinogen.

Tadpoles with a large starting size remained the largest ones through the entire larval development, and attained metamorphosis earlier. Food with a high-protein content reduced mortality and increased the growth and development rate; the choice of food may be important in captive-breeding/headstarting programmes. We did not detect effects of the interaction between provisioning and type of food on tadpole performance. Our study confirms the importance of egg provisioning in amphibians,

showing that it can affect multiple traits, and that their effects can last through the entire larval development. “
“To examine the mechanism of sperm storage in Idiosepius paradoxus, here we describe aspects of the mating behavior of I. paradoxus and the morphology of the spermatozoa and the seminal Wnt antagonist receptacle after copulation. The seminal receptacle Selleck Rucaparib is located in the ventral portion of the buccal membrane surrounding the buccal mass, and opens inside the buccal membrane. It branches into approximately six sacs, similar in appearance to a bunch of bananas, and its wall consists of cuboidal ciliated epithelial cells (with oval nuclei) surrounded by a connective tissue. Multiple vacuoles are distributed in the bottom region of each sac. These

histological and morphological characteristics differ from previous reports for loliginid squids and cuttlefish. In all except one receptacle observed in this study, sperm were stored near the bottom of each sac, and each sperm was facing the sac bottom. We observed spermatozoa in the entrance of the seminal receptacle in only one squid. from These results suggest that spermatozoa were actively moving,

and that sperm actively swam to the seminal receptacle. The volume of sperm in the seminal receptacles of the squid that had copulated eight times was the same as that in the squid that had copulated 29 times, which suggests that the seminal receptacle was filled after approximately eight copulation events. A squid that had copulated nine times retained a significant number of sperm in the seminal receptacle after spawning, suggesting that all of the sperm in the receptacle was not depleted after one spawning event. “
“Reliable data on jaguar population densities are needed to propose appropriate conservation and management strategies, and camera trapping may be effective for estimating the population density of secretive large cats. I determined the population density of jaguars in the Chamela-Cuixmala Biosphere Reserve along the coast of Jalisco, Mexico, through camera trapping and capture–recapture analysis during the dry season of March to June 2008. I applied the half mean maximum distance moved (1/2MMDM) to calculate the radius of the effectively sampled area, and compared this with estimates of the effectively sampled area based on existing data on mean home range of jaguars at the study site.

In the previous issue of the Journal, Horsfall et al.[8] report data that show a markedly reduced overall risk of death from all causes in persons with GS than those without this condition. Their study with a “cohort” design included 4266 “patients” with GS and 21 968 matched controls from a primary-care database in the United Kingdom, who had been “followed-up” for a median of 9 years. Their data showed that all-cause mortality in the GS cohort was almost half

that of the control group. This effect remained largely unchanged after adjustment for various comorbidities. The stark difference observed would make one envy the people with GS. However, it also begs an important question—is this difference real? This is not the first study LY294002 clinical trial to show that GS patients are endowed with health benefits. Several previous studies have looked at the

relationship of GS with the risk of cardiovascular diseases (CVD), including coronary artery disease,[9] peripheral arterial disease,[10] and ischemic stroke.[11] Whereas the initial studies on the health effects of GS looked at the relationship of CVD with serum bilirubin levels, subsequent studies have assessed the relationship of these diseases with UGT1A1 alleles associated with increased serum bilirubin levels. Of these studies, several have shown a protective effect of high bilirubin Staurosporine in vitro levels or of the genetic changes associated with GS on various CVDs.[9, 12, 13] The most convincing evidence supporting an inverse relationship between the GS genotype and the risk of CVD in healthy people came from the Framingham Offspring Cohort Study.[9] In

this cohort study of 1780 unrelated individuals, homozygous carriers of UGT1A1*28 allele had higher serum bilirubin levels and nearly one third the risk of CVD and ischemic heart disease during a 24-year follow-up than those with either one or no such allele; in addition, the risk of myocardial infarction was reduced to nearly half, though this did not reach statistical significance. Further, an analysis of 13 214 adult participants in the National Health and Nutrition Examination Survey 1999 to 2004 Oxalosuccinic acid in the United States showed reduced stroke prevalence and improved stroke outcomes in persons with a higher serum total bilirubin level.[11] In another large cohort study, patients undergoing chronic hemodialysis and serum bilirubin levels in the upper tertile had an adjusted hazard ratio of 0.32 for cardiovascular events (CVEs) and 0.48 for all-cause mortality during a 12-year follow-up than those with bilirubin in the lower tertile; further, in this study, individuals homozygous for UGT1A1*28 variant had approximately one-tenth the risk for CVEs and one-fourth the risk for all-cause mortality than in those with the major allelic form of the gene.[13] Carotid artery intima-media thickness, a marker of atherosclerosis, has also been found to be inversely related to serum bilirubin levels.

FXIII deficient patients benefit from a plasma concentrate with a long-lasting efficacy and safety record. A phase III clinical trial has recently been completed with a recombinant FXIII which has been proven to be safe and effective in preventing bleeding episodes in patients with congenital FXIII-A subunit deficiency [27]. In future, patients with RBD could take advantage of the many bioengineering as well as alternative strategies (aptamers, RNAi, inhibition

of TFPI, etc.), which are under development for persons with haemophilia [28]. Midori Shima has received honoraria as a consultant for his Selleckchem NVP-LDE225 active participation in advisory boards of Chugai Pharmaceutical Company, The Chemo-Sero-Therapeutic Research Institute, Bayer, Baxter, Biogen Idec, CSL Behring, Pfizer, Novo Nordisk. He has received research grants from Bayer, Baxter, Pfizer, Novo Nordisk, Chugai Pharmaceutical Company, Japan Blood Products Organization. Cedric Hermans has received honoraria as a consultant or for his active

participation in advisory selleck compound boards organized by Baxter, Bayer, Pfizer, CAF-DCF, SOBI, Ipsen, LFB, CSL Behring, Novo Nordisk, and Octapharma. He has received research grants or lecture chairs from Baxter, Bayer, Pfizer, CAF-DCF, CSL Behring, Novo Nordisk, Octapharma, and Ipsen. P de Moerloose has received honoraria as a consultant or for his active participation in advisory boards organized by Baxter, Bayer and LFB and has received research grants

or lecture chairs from Baxter, Bayer, CSL Behring, LFB and Novo Nordisk. “
“To compare the use of 740 Mbq (20 mCi) of 153Sm and 185 Mbq (5mCi) of 90Y, both labelling hydroxyapatite (HA), for knee synovectomy in haemophilic patients, 1 year after the intervention. Thirty three men (36 knees) were studied, divided into two groups: 1 – treatment using 740 Mbq of 153Sm-HA: 20 knees of 18 patients, with mean age of 21.4 ± 13.3 years (ranging from 7 to 56 years) and mean Pettersson score of 5.3; 2 – treatment using 185 Mbq of 90Y-HA: 16 knees of 15 patients, with mean age of 26.3 ± 10.3 (ranging from 7 to 51 years) and Carbohydrate mean Pettersson score of 6.3. The following criteria were adopted for the evaluation before and 1 year after synovectomy: reduction in haemarthrosis episodes and pain using a visual analogue scale, as well as improved joint mobility. The occurrence of adverse events in the treatment was also considered. The chi-square, Wilcoxon and Mann–Whitney tests were used with P ≤ 0.05 set as significant. The occurrence of haemarthrosis declined by 65.7% with the use of 153Sm-HA and 82.6% for 90Y-HA, with no statistical difference between the groups (P = 0.632); pain reduction was 42.5% in group 1 and 30.7% in group 2, once again with no statistical difference (P = 0.637). Improvement in joint mobility was not significant for both groups.