Key Word(s): 1. gastrointestinal bleeding Presenting Author: XIU QING WEI Additional Authors: JIN TAO, BIN WU Corresponding Author: XIU QING WEI Affiliations: The Third Affiliated Hospital of Sun Yat-Sen University; Third Affiliated Hospital, Sun Yat-Sen University Objective: To introduce a rare cause of upper gastrointestinal bleeding. Methods: The medical course of a rare patient with upper gastrointestinal bleeding caused by gastric cavernous hemangioma was presented in brief. Results: We report a case of a 41-year-old man who suffered from shock due to a sudden onset of hematemesis and melena. Endoscopy Metabolism inhibitor revealed a 5 cm x 1.5 cm mass mimicking a varices which is

located along with lesser curve and the gastric fundus. Abdominal contrast-enhanced CT revealed huge tumor about 10 cm x 6 cm huge mass originated from the lesser curve of the stomach with the blood supply from the left gastric artery. Based on his clinical appearance and the laboratory results, the patient was diagnosed with gastric hemangioma. In the laparotomy, the tumor was cut off and a total gastrectomy was performed. The final diagnosis

of cavernous hemangioma arising from the gastric was confirmed by postoperative pathological examination. Conclusion: Gastric cavernous hemangioma can be present as severe upper gastrointestinal bleeding. Key Word(s): 1. cavernous hemangioma; 2. upper gastrointestinal bleeding Presenting Author: ZHI E WU Additional Authors: YAN Smad inhibitor PING LIANG, JIN TAO Corresponding Author: ZHI E WU Affiliations: The Third Affiliated Hospital of Sun Yat-Sen University; Third Affiliated Hospital, Sun Yat-Sen University Objective: To summarize the nursing experience of acute upper gastrointestinal hemorrhage. Methods: 162 patients (58 from esophageal and/or gastric varices and 104 from non-varices) with acute upper gastrointestinal hemorrhage were analyzed on

nursing, Teicoplanin therapy and prognosis. Results: 3 cases were dead because of 3 times hemorrhage, 2 cases were dead because of liver failure, 2 cases were transferred to the surgery department, the other patients were successful rescued by using emergency endoscopic treatment, including sclerotherapy, ligation, titanium clips and medical treatment, and leaved hospital without re-bleeding in a long-term follow. By the same time, observing closely, taking urgent measure in a timely manner, strengthening the basic care and symptomatic care, ensuring the blood volume and taking care of patients’ psychological condition were needed to be performed in the full phase of stopping bleeding and the recovery phase. The careful nursing methods and strategies significantly improved the therapeutic treatment and prognosis of patients of acute upper gastrointestinal hemorrhage.

Key Word(s): 1. endoscopic treatment; 2. biliary pancreatitis; 3. elder; Presenting Author: WENJING SUN Additional Authors: XIAOCHUN SHENG, YAN CAO, HAIYAN LIU, CHUNHUI LAN, DONGFENG CHEN Corresponding Author: WENJING SUN Affiliations: Hospital Objective: To evaluate the guidance value of EUS and CT scan in preoperative clinical staging for diagnosis and treatment of esophageal cancer. Methods: 68 patients with esophageal cancer were randomized in a 1 : 1 ratio using a random numbers table. Patients in EUS group were examined by EUS and staged according

to the TNM staging system (2003). Patients in the other group were examined by CT scan. The EUS findings were compared with surgical pathologic findings. Results: The accuracy rates of T staging by EUS were0.0% (0/2) for Tis, 75.0% (3/4) for Tl, 75.0% (6/8) for T2, 86.7% (13/15) for T3, 80.0% (4/5) for T4, and 76.5% (26/34) for T; selleckchem those of N staging were 71.4% (5/7)

for N0, 75% (9/12) for N1, 0.0% (0/11) for N2, 0.0% (0/4) for N3, and 41.2% (14/34) for N. The accuracy rates of T staging by CT scan were 0% (0/1) for Tis, 33.3% (2/6) for T1, 28.6% (2/7) for T2, 78.6% (11/14) for T3, 83.3% (5/6) for T4 and 58.8% (20/34) for T (p = 0.005); those of N staging were77.8% (7/9) for N0, 76.9% (10/13) for N1, 66.7% (4/6) for N2, 50% (3/6) for N3 and 70.6% (24/34) for N (p = 0.005). Conclusion: The accuracy rates of EUS are higher for diagnosis selleck in esophageal cancer and preoperative T staging. The accuracy rates of CT scan are higher for the preoperative N staging. EUS combined with CT scan has great significance Tolmetin for choosing ideal therapy plan for esophageal cancer, and for estimating prognosis of esophageal cancer. Key Word(s): 1. EUS; 2. CT scan; 3. esophageal cancer; 4. clinical staging; Presenting Author: PING HE Additional Authors: ZHUO ZHAO, YUJIA LIU,

HONG XU Corresponding Author: PING HE Affiliations: The First Hospital of Jilin University.; the First Hospital of Jilin University Objective: To evaluate the method of abdominal ultrasound-guided percutaneous endoscopic gastrostomy (PEG) safety and feasibility in clinical work, to give patients the best, safest treatment. Methods: 21 in patients of the First Bethune Hospital of Jilin University carried the percutaneous endoscopic gastrostomy (PEG) through intraoperative abdomen ultrasound of the anterior abdominal wall scan of the position of the abdominal wall and stomach wall closest, looking for the best abdominal wall puncture point, to avoid injure the vessels and vital organs in the abdomen. Results: Abdominal ultrasound-guided percutaneous endoscopic gastrostomy (PEG) was performed in 21 cases, the success rate was 100%; average operation time was 21.5 minutes, the process had no bleeding, vice injury in complications; with the surveillance of 3 months to 4 years, the PEG tube patency and normal use, and no PEG late complications occurred.

Liver biopsy at 19 days after LDLT revealed mild ACR, but it resolved without any specific treatment. At 23 months after LDLT, she developed recurrent hepatitis C with mild activity and severe fibrosis on liver biopsy (METAVIR score, A1 F3). The HCV genotype was 2b and the serum HCV RNA level was 7.2 log IU/mL, as detected by a real-time polymerase chain reaction-based quantitation method. Antiviral therapy with 100 μg/week pegylated interferon-α-2b and 400 mg/day ribavirin was initiated (Fig. 2a). At that time, 50 mg/day cyclosporin and 15 mg/day prednisolone were used for immunosuppression. LBH589 supplier The prednisolone dose was reduced to 10 mg/day after 3 months

of antiviral therapy. HCV RNA was undetectable in serum; however, treatment was discontinued after 21 weeks because of severe general fatigue. The transaminase levels were reduced and maintained within the reference range from 3 weeks to the end of antiviral therapy, but worsened 2 months after the termination of the treatment to an AST level of 136 IU/L and an ALT level of 152 IU/L. The serum IgG level increased to 1719 mg/dL, from 641 mg/dL before the antiviral therapy.

She was negative for ANA and anti-LKM-1 throughout her clinical course. Liver biopsy revealed the features of AIH, including portal inflammation with plasma cell-rich lymphoid aggregates, interface hepatitis and centrilobular inflammation (Fig. 2b,c). As HCV RNA was undetectable in serum; the International AIH Group score was 14, suggesting AIH;[9] and the total score on the histological scoring system for PCH was 10,[6] the patient was diagnosed with PCH. selleckchem Methylprednisolone was started at a dose of 500 mg/day for 3 days, and then the dose was tapered from 250 mg/day on the fourth day to 62.5 mg/day on the sixth day. The treatment was terminated on the seventh day, followed by the initiation of 10 mg/day prednisolone. The transaminase levels decreased and normalized after 2 months

of steroid administration, and liver biopsy 19 months after the initiation of steroid therapy showed the remission of hepatitis. She was considered to have achieved SVR on the basis of a negative HCV RNA result at 24 weeks after the termination of antiviral therapy. IN THIS REPORT, we demonstrated the cases of two patients who developed PCH just after the termination of antiviral Amine dehydrogenase therapy for recurrent hepatitis C after LDLT. The diagnosis of PCH in the present cases is definite because both patients achieved SVR and recovered after steroid therapy. Termination of antiviral therapy likely induced PCH in these patients, as both patients had no other trigger for PCH, such as reduction of immunosuppression. At our institute, 125 HCV-infected liver transplant recipients were treated with standard interferon and/or pegylated interferon in combination with ribavirin for recurrent hepatitis C after LDLT between January 2001 and December 2012.

A combination of increased treatment efficacy and greater uptake is required to achieve major reductions in advanced liver disease and related costs. Hepatitis C virus (HCV) infection is a major public health burden in Australia. Acute HCV infection progresses to chronic infection in approximately 75% of cases,[1] and these people are at risk of progressive liver fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Around 20–30% of people with chronic HCV will develop cirrhosis, generally following at least 20–30 years infection.[2] The previously estimated large pool of chronic HCV in Australia (230 000 cases)[3] and the “aging cohort” effect in this population related

to the high incidence of injecting drug BGJ398 clinical trial use-acquired infection in the 1980s and 1990s means that the already escalating rates of HCV-related cirrhosis, liver failure, and HCC are projected to increase further over the next two decades.[4] While modeling suggests that the incidence of HCV infection is in decline from a peak of 14 000 new infections in 1999 to 9700 new infections in 2005,[4] the number of people in Australia living with

hepatitis C is expected to continue to increase for the foreseeable future. During the PI3K Inhibitor Library 2000s, combined pegylated interferon (PEG-IFN) and ribavirin (RBV) treatment was the standard of care for chronic HCV, and in Australia, this has led to a sustained virological response (SVR) in around 50% for people with HCV genotype 1 and 70% for HCV genotype 2/3.[5] However, treatment uptake remained low (2000–4000 people/year; 1–2% of the infected population), even following the removal of mandatory pretreatment liver biopsy in 2006 and broadening of inclusion criteria to include all fibrosis stages and normal alanine aminotransferase levels.[6] Several factors many contribute to low HCV treatment

rates, including toxicity of interferon-based therapy, prolonged treatment course (24–48 weeks), social marginalization of people with chronic HCV, lack of treatment infrastructure (particularly opiate pharmacotherapy, prison, community health, and primary care settings), and lack of awareness of the curative potential of treatment. Lower HCV treatment responses in those with advanced liver disease also limited the impact of antiviral therapy on disease burden. The initial phase of direct-acting antiviral (DAA) therapy, involving PEG-IFN/RBV and either telaprevir or boceprevir for chronic HCV genotype 1[7-11] commenced in Australia with government subsidization through the Pharmaceutical Benefits Scheme from April 2013 (patients provide a small monthly copayment of $AUS 7–25). However, early indications are that treatment numbers are unchanged, presumably based on the continued barriers to interferon-containing therapy and increased complexity and safety concerns with the addition of first generation protease inhibitors.

Also, alternative classifications of synesthesia have

been proposed, for example, using the self-reported localization of the concurrent perception (Dixon et al., 2004): so called ‘associators’ perceive the synesthetic sensations in their ‘mind’s eye’, whereas ‘projectors’ see synesthetic concurrents ‘outside’, for example, on the page where the inducing letter is printed. These different groups INCB024360 in vitro may well have at least partially different processes underlying their experience and should be considered separately in future studies. The current study used only complex speech-related stimuli which may engage top-down attentional processes to a greater extent than more basic stimuli. Thus, experiments with more basic stimuli could be helpful to investigate the hyperconnectivity/hyperbinding hypothesis of synesthesia. An initial effort in this direction has been made by Brang, Williams, and Ramachandran (2011)

who used simple auditory (sine tones) and visual (light points) stimulation to investigate the double-flash illusion (Shams, Kamitani, & Shimojo, 2000) in a rather small sample (n = 7). Synesthetes reported more illusionary flashes than control subjects from which the authors inferred that synesthesia is related Bcl-2 inhibitor to hyperbinding between the sensory modalities. Recently, Neufeld et al. (2012) used the same illusion in 18 synesthesia subjects. In contrast with Brang et al. (2012), a reduced number of illusions and additionally a reduced time window of the illusory double flash was revealed in synesthetes. Whether these differences can be explained by differences in the location of the synesthetic percept remains to be seen. The reduced multisensory integration of synesthetes

in this study may be explained alternatively by the increased processing effort related to increased information load induced by the synesthetic concurrent percept. Thus, the weaker performance of our synesthesia subjects Y-27632 2HCl might have been due to the fact that they had to integrate three sensory qualia instead of two (as the control subjects). Against this explanation speaks the fact that only few of our subjects reported synesthetic concurrents induced by heard voices (only three subjects in the Mc Gurk experiment and only four subjects in the speech perception experiment). To test this hypothesis we conducted the analysis again after removing the affected synesthesia subjects with no considerable changes in the result. The reduced multisensory integration of synesthetes might directly derive from their special ability. Synesthetes usually report that they have no trouble in identifying synesthetic and real parts of their perception. To keep track of which perception is synesthetic and which is ‘real’ (i.e., stimulated from the outer world), synesthetes have to separate the senses and to perform a ‘reality check’.

To determine the contribution of MFs on CCA biology, we performed cotransplantation experiments of CCA cells (i.e., Mz-ChA-1 cells) with primary MFs isolated from human liver (HLMFs)[24] in a subcutaneous (SC) xenograft model into nude mice. HLMFs in primary culture were morphologically activated

and expressed α-SMA and were negative for CD31 and HepPar1[24] (Supporting Fig. 1A,B). Mz-ChA-1 cells overexpressed EGFR, as compared to nonmalignant Romidepsin cost biliary epithelial cells (Supporting Fig. 1C). CCA cells were injected alone or in combination with HLMFs. Eight days postinjection, only mice inoculated with CCA cells and HLMFs presented palpable tumors. HLMFs boosted CCA tumor growth at any time post–cell injection with an average 4-fold increase (Fig. 1A, gray versus white bars) and an 8-fold increase in tumor weight at time of sacrifice (48 days postinjection; Fig. 1B, gray versus white bars). We also observed that the presence of HLMFs increased tumor take rate (Fig. 1C). Tumors developed in xenografted mice were histologically similar to human CCA, because they showed a prominent stromal compartment

attested by α-SMA staining. EGFR staining was exclusively detected in CCA cells (Fig. 1D). We next examined whether EGFR played a role in the enhancing

https://www.selleckchem.com/products/AZD6244.html effect of HLMFs on CCA growth by treating mice with gefitinib, a specific inhibitor of EGFR tyrosine kinase activity (Fig. 1A,B,E). From 8 days of treatment with gefitinib and until the end of the experiment (20 days of treatment), a significant growth reduction was observed in coinjected tumors, compared to vehicle-treated mice (Fig. 1A, black versus gray bars). Gefitinib decreased coinjected tumor weight with an average of 4-fold (Fig. 1B, black L-NAME HCl versus gray bars). Representative images of three tumors from each group are shown in Fig. 1E. EGFR activation, attested by its phosphorylation level status on tyrosine 1173, was detected in coinjected tumors, but not in CCA cell tumors. Gefitinib treatment abolished EGFR phosphorylation in coinjected tumors (Fig. 1F). Tumor glucose metabolism, which reflects cell viability, was examined by monitoring 18FDG (fluorodeoxyglucose) uptake with positron emission tomography (PET) imaging. A good correlation (R = 0.95) was observed between tumor volume estimated with a caliper and PET imaging (data not shown). A significant increase of 18FDG uptake (+40%), reflected by the mean of SUV (standard uptake value), was observed in coinjected tumors, as compared with CCA cell tumors (Fig.

6–2.7% of IBD patients in some series1–3. Although the underlying

pathogenesis remains unclear, a possible hypothesis involves the uncontrolled production of interferon-alpha (IFNα) as a result of TNF blockade. IFNα is an important mediator produced by dermal plasmocytoid dendritic cells in the early phase of induction of psoriasis4. Aim: To review all cases of psoriatic and psoriatiform dermatological reactions induced by anti-TNF agents in patients with IBD at a tertiary center in Australia. Method: We retrospectively identified all cases selleck products of anti-TNF-induced psoriasis or psoriasiform manifestations in IBD patients receiving treatment at Canberra Hospital. Results: A total of 10 of 270 IBD patients treated with anti-TNF therapy developed drug-induced psoriatic or psoriasiform-like reactions: 6 female, 4 male; average age of IBD diagnosis was 21 (13–28) years; average age of skin reaction was 33.2 (23–48) years. Five patients were treated with infliximab and five with adalimumab; 9 had Crohn’s disease (CD) and 1 had ulcerative selleck inhibitor colitis (UC). Three were current smokers and 2 were ex-smokers. Three patients had concomitant therapy at time of the reaction: one on prednisolone, one on mesalazine and one subject on both mesalazine and azathioprine. The time from initiation of anti-TNF agent to onset of rash was on average 9.1 (2–25)

months. The most frequent distributions were the scalp (7) and extremities (6). Five patients had a personal history of atopy and 3 had a familial history of psoriasis. Three patients Niclosamide discontinued anti-TNF treatment (2 because of the skin reaction and 1 due to autoimmune hepatitis), and the remaining

7 were maintained on anti-TNF therapy and managed with topical therapy. All 10 patients were reviewed by a dermatologist. Conclusions: Paradoxical psoriatic lesions induced by anti-TNF therapy in IBD is not uncommon. In this case series, there was no significant gender difference and the time to onset of rash was variable. The psoriatic manifestation was greater in CD than UC. The most frequent distributions were the scalp and extremities. Topical treatment of the lesions was effective in the majority of patients, allowing continued use of these biologicals and the withdrawal of these agents is seldom needed. 1. Afzali A, Wheat CL, Hu JK, Olerud JE, Lee SD. The association of psoriasiform rash with anti-tumor necrosis factor (anti-TNF) therapy in inflammatory bowel disease: A single academic center case series. J Crohns Colitis. 2014 Jun 1;8(6):480–488. 2. Rahier JF, Buche S, Peyrin-Biroulet L, Bouhnik Y, Duclos B, Louis E, et al. Severe skin lesions cause patients with inflammatory bowel disease to discontinue anti-tumor necrosis factor therapy. Clin Gastroenterol Hepatol. 2010 Dec;8(12):1048–1055. 3. Guerra I, Algaba A, Perez-Calle JL, Chaparro M, Marin-Jimenez I, Garcia-Castellanos R, et al.

Additional Supporting Information may be found in the online version of this article. “
“The retinoid X receptor a (RXRα; NR2B1), the most highly expressed RXR isoform in liver, plays a central role in regulating bile acid, cholesterol, fatty acid, steroid learn more and xenobiotic metabolism and homeostasis. Studies indicated that post-translational modification of RXRα, in particular, inflammation-induced phosphorylation of several sites, can lead to further post-translational modification (e. g., ubiquitination

and SUMOylation), as well as altered RXRa stability and subce l l ular localization. We have found that inflammation-induced reduction in RXRα nuclear quantities involves JNK-dependent phosphorylation at Ser260.Details regarding the fate, induction, localization and function of RXRα where Ser260 is phosphorylated are poorly understood, due to the lack of specific detecting reagents, cell

lines and mouse models. To begin to address these important issues, we developed and characterized an Torin 1 ic50 anti-pRXRα Ser260 antibody (p260 Ab) and verified its specificity and sensitivity with shRNA knockdown, immunoblotting and confocal immunofluorescence assays in both human and mouse models. The phosphorylation of RXRα Ser260 is significantly increased in both nuclear and cytoplasmic compartments of IL-1 β-treated Huh-7 cells and LPS-treated mouse liver, with a novel

finding of a submembrane localization at baseline which is increased in response to inflammation. Moreover, the JNK Elongation factor 2 kinase inhibitor, SP600125, inhibits IL-1 –β-induced upregulation of pRXRα Ser260 in Huh-7 cells, suggesting that JNK is a necessary upstream kinase involved in RXRα Ser260 phosphorylation. Initial explorations with confocal immunofluorescence microscopy and co-immunoprecipitation (Co-IP) assays identified submembrane phospho-RXRα interactions with the submembrane protein β-catenin. Moreover, Co-IP and immunofluorescence assays revealed that inflammation increases the interaction between phospho-RXRα and β-catenin in IL-1 β treated Huh-7 cells and LPS treated mouse livers in both cytoplasmic and subplasma membrane locales extend our knowledge of the potential biological roles played by RXRα species. We conclude that inflammatory stimuli induce JNK-dependent RXRα Serine260 phosphorylation, the interaction between p-catenin and RXRα, and the subcellular redistribution of RXRα, including heretofore novel cytoplasmic and submembrane locales. Disclosures: The following people have nothing to disclose: Hong Tang, Zhining Den, Astrid Kosters, Daniel A. Moore, Saul J.

In an attempt

to uncover the nature of the underlying deficit, some studies have manipulated the temporal characteristics of stimulus presentation. Contra- and ipsilesional stimuli with different stimulus onset asynchronies are typically used. In the present study, visual extinction was investigated in a group of left neglect patients (N=10) using a psychophysical selleck compound paradigm with different stimulus onset asynchronies of target and distractor stimuli presented in different hemifields. Contrast thresholds for a target grating were determined with the target either in isolation or in the presence of an irrelevant distractor grating. When target and distractor gratings were presented simultaneously, neglect patients showed a significant extinction effect, i.e., a significant interference from the right hemifield distractor with left hemifield selleck chemical contrast sensitivity. When the right hemifield distractor preceded the left hemifield target stimulus by 250 ms, two different patterns of results were observed in the neglect patients. Five patients showed a significant improvement compared to the simultaneous presentation condition, five other patients showed a significant increase of the extinction effect. The results suggest that different underlying mechanisms, maybe due to different lesion locations,

can cause extinction in neglect patients. “
“Earlier research has found cross-sectional attentional control deficits in manifest Huntington’s disease (HD) using neuropsychological testing combined with simultaneous P300 registration. In the current pilot-study, we investigate attentional control in pre-manifest and manifest HD over a 3-year follow-up period. Five manifest HD (MHD), 9 pre-manifest HD (PMHD), and 12 control subjects were included. Sustained attention to response task (SART) and P300 registration resulted in number of errors, reaction time (RT), and P300 amplitude and latency. Morin Hydrate RT change patterns surrounding No-go trials were

also investigated. Within-subject differences were tested using paired-samples t-tests and between-group results with ANCOVA on delta scores (follow-up – baseline scores). Manifest HD made more errors and were slower than controls and PMHD. Longitudinally, MHD showed an overall RT increase and a specific slowing on trials preceding a correct No-go trial (within-group effects). The latter was also seen in PMHD. P300 latency prolongation was found for controls on No-go and for MHD on Go trials. On specific trials surrounding both correct and incorrect No-go trials, MHD became significantly slower over time than controls and PMHD (between-group effects). Over 3-years, MHD subjects became slower on the SART and showed a prolongation of P300 latency on specific SART trials.

1). It was also introduced for ‘safety’ reasons as bleed prophylaxis after child-felt trauma (i.e. typical head trauma without bleeding signs). Prophylaxis was initiated without insertion of a Port-A-Cath after a minimal number of on-demand FVIII exposures. In patients with Everolimus research buy early joint bleeds prophylaxis was introduced at the higher frequency of 25 IU kg−1 twice a week, and in those with early severe joint or life threatening bleeds at 25–50 IU kg−1 three times a week. When required by the severity of the bleeding tendency the frequency was increased from one per week

to two per week or three per week. For tolerization (as also known from ITI programs in inhibitor patients) it seems to be important to give prophylactic FVIII doses always on the same weekday

and to avoid interrupting the prophylaxis regimen even when additional on-demand FVIII doses to manage bleeds are given. During this ‘tolerization’ period, immunological danger signals were minimized by avoiding giving first FVIII in a severe bleeding situation or during an infection, avoiding surgery during the first 20 EDs, avoiding giving vaccinations on the same day as FVIII and giving all Selleck Torin 1 vaccinations subcutaneously rather than intramuscularly. Any bleeds that did occur were treated early by giving a higher than the prophylactic dose immediately, thereby avoiding long or intensive treatment. Patients in the study group were tested for inhibitors every 3–4 EDs. Patients in the control group were treated with a standard joint-protection prophylaxis regimen of 40–50 IU kg−1 FVIII three times a week, starting at or after the first joint or other severe bleed. Please note that some of the patients in the control group (n = 8) developed their inhibitors already during on-demand therapy before they entered a standard prophylaxis program. The vaccination guidelines have been the same for both the study and the control group. Differences in inhibitor development between the study group and the historical control group were analysed by Fisher’s exact test and odds ratios (OR). The effect of potential determinants on inhibitor risk such as FVIII gene mutation

Morin Hydrate and type of product (recombinant vs. plasma-derived FVIII) was evaluated for the two groups in a logistic regression model. Differences between the two study groups of treatment-related parameters such as median EDs before prophylaxis and age at start of prophylaxis were assessed by Wilcoxon test. Fifty six of the 58 subjects studied had more than 100 EDs to FVIII therapy. Data from these were analysed for inhibitor development and both patient-related and treatment-related factors which might have affected inhibitor development. There were no significant differences between the study and control groups in any patient-related factors (Table 1), nor in the majority of treatment-related factors (Table 2). In a logistic regression model for inhibitor development with factors for study group (standard vs.