2%). Among 226 newborns with severe haemophilia A in 62 HTCs, 1.82 births/HTC/year, the median age at first bleed, excluding circumcision, is 7 months. Of the 113 (53.5%) newborns who underwent INCB024360 datasheet circumcision, 62 (54.9%) bled. Despite a recommended standard of three times weekly prophylaxis, over half of surveyed HTCs do not follow these guidelines, and nearly one-third begin prophylaxis on a once weekly schedule to delay or avoid the need for central venous access. “
“Record keeping among individuals who manage haemophilia at home is an essential tool of communication between patient and Haemophilia Treatment Center (HTC). Complete records help HTCs monitor patients, their use of factor and ensure treatment learn more is optimal.

HTCs provide patients with a number of methods to track infusion practices. The study objectives were to: [1] determine the current methods of record keeping; [2] identify previous methods of record keeping; [3] understand the strengths and weaknesses associated with each method; and [4] gather suggestions for improvement. Survey methods were used to address the research objectives. Of the 83 patients in the Hamilton-Niagara region who received the survey distributed through the local HTC, 51 returned surveys were included into the analysis. Descriptive statistics were used. Results indicate individuals

with haemophilia record infusion practices using: paper diaries, excel spreadsheets, Cell press hand-held PDAs and/or the online EZ-Log Web Client. The most popular method of record keeping was EZ-Log (45.1%) followed by paper diaries (35.2%). Advantages to using paper methods include the visual tracking of information and retaining hardcopies. The disadvantage was the inconvenience of physically submitting the records monthly. Advantages to using the online EZ-Log Web Client included ease of use and improved accuracy. The primary disadvantage was technical

errors that were difficult to troubleshoot. Record keeping practices among individuals with haemophilia seem to vary according to personal preference and convenience. Respondents suggested that saving infusion history, incorporating barcode scanners or a copy and paste function could improve electronic methods. “
“In persons with haemophilia (PWH), repeated ankle haemarthroses lead to pain, loss of joint range of motion (ROM), and limitations in activity and participation in society. PWH are offered ankle arthrodesis (AA) to eliminate pain. In our experience, PWH are hesitant to proceed to AA due to concerns regarding gait anomalies, functional decline and complete loss of ROM. The aim of this study was to report outcomes in ROM, assistive device (AD)/wheelchair use, activity scale and work/school absenteeism for participants in the CDC’s Universal Data Collection surveillance project (UDC) pre- and post- AA. Males with haemophilia enrolled in the UDC with first report of AA (1998–2010) were selected.

The sensitivity of HCV virions in the cell-free supernatant from JFH-1-infected Huh7.5.1 cells to ADCML in the presence or absence of CD59 blockers (BRIC229 and rILYd4) was assessed using a protocol Selleck MG-132 modified from our previous report.6 Briefly, HCV-containing supernatant (50 μL) were preincubated with (1) BRIC229 (1.25-20 μg/mL), (2) rILYd4 (1.25-20 μg/mL), (3) irrelevant IgG control (1.25-20 μg/mL), (4) PBS, or (5) Triton X-100 at 37°C for 30 minutes. After preincubation, anti-HCV E2 pAbs or irrelevant pAbs (anti-HIV-1 gp120/160 pAbs; Abcam, Cambridge, MA) were added, followed

by exposure to either complement-competent human sera or heat-inactivated complement (CompTech, Tyler, TX) diluted in gelatin veronal buffer (GVB) (Sigma-Aldrich, St. Louis, MO). Virolysis of HCV was quantified by measuring HCV core release using the QuickTiter HCV Core ELISA Kit as per the manufacturer’s description, except

that the lysis buffer included in the ELISA kit was not used. Therefore, only HCV core released from the lysed viral particles by ADCML was quantified, whereas the core in the intact HCV virions was embedded in the outer Env, and thereby was not detected. HCV virions treated with Triton X-100 and PBS were used as 100% and blank of virolysis, respectively. The percentage of virolysis was calculated as follows: (core released by CD59 blocker − core released by PBS) / (core released by Triton X-100 − core released by PBS) × 100%. Plasma samples from six HCV-infected subjects (Pt28, Pt42, Pt49, Pt84, Pt99, and

Pt369) are described Selleck CHIR99021 in Table 1 and were directly treated with: (1) BRIC229 (20 μg/mL), (2) rILYd4 (20 μg/mL), (3) irrelevant IgG control (20 μg/mL), (4) PBS, or (5) Triton X-100 at 37°C for 1 hour. Plasma samples from another five HCV-infected subjects (Pt1 to Pt5; Table 1) were completely used for virus purification; they were not available to be included in the direct virolysis experiments. Virolysis was quantified and calculated by measuring HCV core ADP ribosylation factor protein release as described above. All samples were run in triplicate. Cells were incubated with BRIC229 or control Ab, followed by FITC-conjugated secondary Ab, and then subjected to FACS using a BD FACSCalibur (BD Biosciences). Data were analyzed using FlowJo software (Tree Star, San Carlos, CA). To measure intracellular level of CD59, PHHs or Huh7.5.1 cells were treated with PI-PLC (Sigma-Aldrich) at 0.5 units/mL at 37°C for 1 hour to remove CD59 from the surface of cells. After washing, cells were permeabilized using a Cytofix/Cytoperm Plus kit (BD PharMingen) according to the manufacturer’s instructions. Cells were incubated with BRIC229 or control Ab and followed by FITC-conjugated secondary Ab for FACS as described above. The paired two-tailed Student’s t test was used to compare the means ± standard deviation (SD). Values of P < 0.05 were judged significant.

The sensitivity of HCV virions in the cell-free supernatant from JFH-1-infected Huh7.5.1 cells to ADCML in the presence or absence of CD59 blockers (BRIC229 and rILYd4) was assessed using a protocol selleck inhibitor modified from our previous report.6 Briefly, HCV-containing supernatant (50 μL) were preincubated with (1) BRIC229 (1.25-20 μg/mL), (2) rILYd4 (1.25-20 μg/mL), (3) irrelevant IgG control (1.25-20 μg/mL), (4) PBS, or (5) Triton X-100 at 37°C for 30 minutes. After preincubation, anti-HCV E2 pAbs or irrelevant pAbs (anti-HIV-1 gp120/160 pAbs; Abcam, Cambridge, MA) were added, followed

by exposure to either complement-competent human sera or heat-inactivated complement (CompTech, Tyler, TX) diluted in gelatin veronal buffer (GVB) (Sigma-Aldrich, St. Louis, MO). Virolysis of HCV was quantified by measuring HCV core release using the QuickTiter HCV Core ELISA Kit as per the manufacturer’s description, except

that the lysis buffer included in the ELISA kit was not used. Therefore, only HCV core released from the lysed viral particles by ADCML was quantified, whereas the core in the intact HCV virions was embedded in the outer Env, and thereby was not detected. HCV virions treated with Triton X-100 and PBS were used as 100% and blank of virolysis, respectively. The percentage of virolysis was calculated as follows: (core released by CD59 blocker − core released by PBS) / (core released by Triton X-100 − core released by PBS) × 100%. Plasma samples from six HCV-infected subjects (Pt28, Pt42, Pt49, Pt84, Pt99, and

Pt369) are described selleck chemical in Table 1 and were directly treated with: (1) BRIC229 (20 μg/mL), (2) rILYd4 (20 μg/mL), (3) irrelevant IgG control (20 μg/mL), (4) PBS, or (5) Triton X-100 at 37°C for 1 hour. Plasma samples from another five HCV-infected subjects (Pt1 to Pt5; Table 1) were completely used for virus purification; they were not available to be included in the direct virolysis experiments. Virolysis was quantified and calculated by measuring HCV core PJ34 HCl protein release as described above. All samples were run in triplicate. Cells were incubated with BRIC229 or control Ab, followed by FITC-conjugated secondary Ab, and then subjected to FACS using a BD FACSCalibur (BD Biosciences). Data were analyzed using FlowJo software (Tree Star, San Carlos, CA). To measure intracellular level of CD59, PHHs or Huh7.5.1 cells were treated with PI-PLC (Sigma-Aldrich) at 0.5 units/mL at 37°C for 1 hour to remove CD59 from the surface of cells. After washing, cells were permeabilized using a Cytofix/Cytoperm Plus kit (BD PharMingen) according to the manufacturer’s instructions. Cells were incubated with BRIC229 or control Ab and followed by FITC-conjugated secondary Ab for FACS as described above. The paired two-tailed Student’s t test was used to compare the means ± standard deviation (SD). Values of P < 0.05 were judged significant.

The occurrence of side effects did not influence the efficacy of therapy and were equally distributed selleck compound among the ages. Conclusions: Data from this real life series of patients confirm the efficacy of clinical trials although the SVR seems to be of a smaller entity. Moreover the RVR is the only independent predictive factor of response regardless of cirrhosis; and the age does not seem to be a risk factor for drop out due to side effects. Based on RVR, also in cirrhotics, a shorter therapy might be considered, at least with telaprevir based therapy. Disclosures: Davide F. Precone – Consulting: Gilead, MSD; Grant/Research Support: Roche The following people have nothing to disclose: Marcello Persico, Mario

Masa-rone, Silvia Camera, Valerio Rosato,

Rocco Granata, Giovan Giuseppe Di Costanzo, Carmine Coppola, Nicola Coppola, see more Angelo Salomone Megna, Ivan Gentile, Antonio De Luna, Alessandro Federico, Ernesto Claar, Filomena Morisco Background and Objective: Telaprevir and simeprevir are potent protease inhibitors, however, treatment with telaprevir frequently induces gastrointestinal side effects, such as nausea, vomiting and anorexia, compared with simeprevir. Ghrelin is an orexigenic hormone mainly produced by stomach cells and slightly by hypothalamus. The physiological functions of ghrelin include stimulation of appetite and food intake, and modulation of gastric acid secretion and motility. Previously, we reported that hypothalamic ghrelin secretion and food intake were markedly reduced in cisplatin-treated rats 24 and 48 hr after treatment. In the present investigation, the mechanism of anorexia in patients treated with telaprevir plus pegylated interferon alfa-2b (Peg-IFN) and ribavirin, was studied in relation to plasma level of acylated ghrelin, an active orexigenic peptide. Methods: Twenty patients with HCV genotype 1b were recruited. Nine females received telaprevir plus Peg-IFN and ribavirin therapy (group TVR), and 4 males and 7 females received Aldehyde dehydrogenase simeprevir plus Peg-IFN and ribavirin therapy (group SMV). Appetite and food intake were estimated by the visual analogue scale

(VAS) score, and plasma samples after an overnight fast were collected, before, and 1 or 2 and 8 days after the initiation of the therapy. Plasma levels of acylated ghrelin, desacylated ghrelin and anorexic factors, such as leptin, serotonin, interleukin-1 β and TNF-α were measured. Results: 1) Group TVR: VAS scores of appetite and food intake significantly decreased on day 1 or 2 (5.2±3.4 and 6.6±2.7, respectively) compared with those before the therapy (10±0 and 10±0). Plasma acylated ghrelin level also significantly decreased on day 1 or 2 (7.8±5.3 fmol/ ml) compared with that before the therapy (14.6±7.3 fmol/ml). The decrease in acylated ghrelin level and the scores of appetite and food intake were attenuated on day 8 (13.1±11.4 fmol/ml, and 7.9±2.9 and 8.

With respect to each journal, the linear regression analysis showed that the increase of first female authorship was statistically significant (p= 0.016) compared to male authorship only in the Journal of Prosthetic Dentistry. The percentage of female presidents of prosthodontic organizations has been very limited. A similar trend was also observed in AEP program director positions. Conclusions: Over the past 13 years, female dentists’ participation in prosthodontics literature authorship has not increased significantly in the United States. Furthermore, female involvement in prosthodontics leadership has been limited over the past decades. “
“Purpose: The purposes of

this study were to this website describe the demographics of abstracts presented at the prosthodontics section of IADR General Sessions from 2004 to 2005, evaluate the publication rate of abstracts, and analyze the relationship between variables in abstracts and publication. Materials and Methods: Prosthodontics research section abstracts from the IADR General Session in 2004 and 2005 were evaluated for: number of authors, presentation type, origin, affiliation, topic, study design, statistics, study outcome, and funding. The publication CHIR-99021 cost rate was calculated following a PubMed search. The journal of publication, year of publication, and the length of time before

publication were analyzed. Descriptive statistics were used for the data analysis; the relationships between presentation type, study design, study outcome, statistics, funding, and publication were analyzed using logistic regression (α= 0.05). Results: From 346 abstracts, 37.0% were published. For oral presentations, 40.7% were published; 35.8% of poster presentations were published. The mean duration before publication was 26.4 months. North America had the most abstracts, and Europe had the most publications. Fixed prosthodontic research had the highest number and proportion for publication. A significant association with publication was noted for

neutral study outcomes (p= 0.018), studies with funding (p= 0.035), and abstracts from Europe (p= 0.001). Conclusions: Amino acid The majority of abstracts from the prosthodontics research section of IADR General Sessions from 2004 and 2005 remain unpublished. A significant association for publication was noted with neutral outcomes, funding, and abstracts from Europe. “
“Purpose: The purpose of this article is to examine data and results from the 2008 Survey of Prosthodontists. Survey results are used to examine current trends and characteristics of prosthodontists in private practice. Materials and Methods: Characteristics of prosthodontists and conditions of private practice are based on surveys conducted in 2002, 2005, and 2008 sponsored by the American College of Prosthodontists.

John W. Schoggins, Ph.D. “
“Encephalopathy and brain edema are serious central nervous system complications of liver failure. Recent studies using molecular probes and antibodies to cell-specific marker proteins have demonstrated check details the activation of microglial cells in the brain during liver failure and confirmed a central neuroinflammatory response. In animal models of ischemic or toxic liver injury, microglial activation and concomitantly increased expression of genes coding for proinflammatory cytokines in the brain occur early in the progression of encephalopathy and brain edema. Moreover, the prevention of these complications with mild hypothermia or N-acetylcysteine

(two treatments known to manifest both peripheral and central cytoprotective properties) averts central neuroinflammation due to liver failure. Recent studies using anti-inflammatory agents such as ibuprofen and indomethacin have shown promise for the treatment of mild encephalopathy in patients with cirrhosis, whereas treatment with minocycline, a potent inhibitor of microglial activation, attenuates the encephalopathy grade and prevents brain edema in

experimental acute liver failure. The precise nature of the signaling mechanisms between the failing liver and central neuroinflammation has yet to be fully elucidated; mechanisms involving blood-brain cytokine transfer PF-02341066 clinical trial and receptor-mediated cytokine signal transduction as well as a role for liver-related toxic metabolites such as ammonia have been proposed. The prevention of central proinflammatory processes will undoubtedly herald a new chapter in the development of agents for the prevention and

treatment Inositol oxygenase of the central nervous system complications of liver failure. (HEPATOLOGY 2011;) Hepatic encephalopathy (HE) is a serious neuropsychiatric complication of both acute liver failure (ALF) and chronic liver failure with the potential to affect heath-related quality of life, clinical management strategies, liver transplant priority, and patient survival. The neuropathological features of HE primarily include changes in the morphology and function of cells of the glial (rather than neuronal) lineage and have led to the suggestion that HE is a primary gliopathy. In particular, morphological changes in astroglial cells are characteristic of HE. Such changes include cell swelling, a characteristic cell phenotype known as Alzheimer type II astrocytosis, and concomitant alterations in the expression of genes coding for a wide range of astrocytic proteins with key roles in the control of cellular energy status, cell volume regulation, and neurotransmission.1 The causes of these alterations of astroglial integrity have generally been attributed to the toxic effects of ammonia. However, in recent years, attention has increasingly been focused on the role of proinflammatory mechanisms.

John W. Schoggins, Ph.D. “
“Encephalopathy and brain edema are serious central nervous system complications of liver failure. Recent studies using molecular probes and antibodies to cell-specific marker proteins have demonstrated Trichostatin A the activation of microglial cells in the brain during liver failure and confirmed a central neuroinflammatory response. In animal models of ischemic or toxic liver injury, microglial activation and concomitantly increased expression of genes coding for proinflammatory cytokines in the brain occur early in the progression of encephalopathy and brain edema. Moreover, the prevention of these complications with mild hypothermia or N-acetylcysteine

(two treatments known to manifest both peripheral and central cytoprotective properties) averts central neuroinflammation due to liver failure. Recent studies using anti-inflammatory agents such as ibuprofen and indomethacin have shown promise for the treatment of mild encephalopathy in patients with cirrhosis, whereas treatment with minocycline, a potent inhibitor of microglial activation, attenuates the encephalopathy grade and prevents brain edema in

experimental acute liver failure. The precise nature of the signaling mechanisms between the failing liver and central neuroinflammation has yet to be fully elucidated; mechanisms involving blood-brain cytokine transfer Metformin order and receptor-mediated cytokine signal transduction as well as a role for liver-related toxic metabolites such as ammonia have been proposed. The prevention of central proinflammatory processes will undoubtedly herald a new chapter in the development of agents for the prevention and

treatment Florfenicol of the central nervous system complications of liver failure. (HEPATOLOGY 2011;) Hepatic encephalopathy (HE) is a serious neuropsychiatric complication of both acute liver failure (ALF) and chronic liver failure with the potential to affect heath-related quality of life, clinical management strategies, liver transplant priority, and patient survival. The neuropathological features of HE primarily include changes in the morphology and function of cells of the glial (rather than neuronal) lineage and have led to the suggestion that HE is a primary gliopathy. In particular, morphological changes in astroglial cells are characteristic of HE. Such changes include cell swelling, a characteristic cell phenotype known as Alzheimer type II astrocytosis, and concomitant alterations in the expression of genes coding for a wide range of astrocytic proteins with key roles in the control of cellular energy status, cell volume regulation, and neurotransmission.1 The causes of these alterations of astroglial integrity have generally been attributed to the toxic effects of ammonia. However, in recent years, attention has increasingly been focused on the role of proinflammatory mechanisms.

10,21,22 Two of these selleck screening library studies evaluated a single treatment cycle and patients were followed for approximately 16 weeks.10,21 The other 3 studies evaluated multiple treatment cycles repeated at 120-day intervals in sequential follow-on studies.22 In 2001, 4 additional larger, exploratory, randomized, double-blind, placebo-controlled, parallel-group design studies were initiated: 2 in patients with episodic migraine and 2 in patients with CDH. All 4 studies utilized a FSFD treatment paradigm. In 2 of the studies, additional treatments were allowed in predefined head and neck muscles where patients had predominant pain. Doses evaluated in these studies ranged from 75 U

in 20 injection sites across 7 specific head

and neck muscles23,24 to 260 U in 58 injection sites across 7 specific head and neck muscles.8,25 In one of these phase 2 studies in CDH,24 the dose included 225 U, 150 U, and 75 U groups and provided insight with regard to the optimally safe and effective dosage per injection cycle. However, in this trial a dose–response was observed for tolerability, with the 225 U dose group having more AEs (eg, muscle weakness, neck pain) than the other 2 treatment groups. With regard to efficacy, the 2 higher dose groups were both different from the 75 U group, but there was no difference in efficacy between the 225 U and 150 U groups. selleck Therefore, it was determined that

the optimal total dose to maximize efficacy and tolerability was within the range of >150 U and <200 U. PREEMPT confirmed that 155-195 U of onabotulinumtoxinA is efficacious for treating patients with CM.27-29 Injection Sites and Techniques.— Dilution volume used for each 100 U vial of onabotulinumtoxinA varied across the early studies, which could have also contributed to varied findings across these studies, and this is another important factor to consider for this injectable treatment. Early exploratory studies diluted each vial with 1.33-10 mL, which resulted in onabotulinumtoxinA concentrations the that ranged from 7.5 U/0.1 mL to 0.1 U/0.1 mL.10,21,22 The occurrence of eyelid ptosis, which may be influenced by the dose and dilution administered to the frontal muscles (corrugator, procerus, and frontalis muscles), was seen in up to 17.5% patients10 injected with a total maximum dose of 57 U (75 U group) (dilution 1.33 mL/vial) to these muscles. In another study, despite a maximum dose of only 19 U in these muscles (25 U total dose group), ptosis was reported at a rate of 14.3% when using a dilution of 4 mL/vial.21 In the double-blind, placebo-controlled phase of the pivotal phase 3 PREEMPT trials, ptosis was reported at low rates (3.6% of onabotulinumtoxinA-treated and 0.3% of placebo-treated patients)27 with a total dose of 35 U to the frontalis, corrugator, and procerus muscles.

We proceed to a transjejunal puncture of the CBP guided by endoscopic ultrasound (EUS), with a 19-gauge needle. The cholangiography showed dilation of the CBP already described, with a distal stenosis. A 0,035 inches guide-wire was then passed through the needle into the CBP, but it’s constant proximal orientation prevented a rendezvous procedure. We opted by a EUS retrograde approach, with direct puncture of the CBP guided by EUS, through the papilla, with fluoroscopic control. A plastic prosthesis with 10 French and 5 centimetres

was placed, with immediate output of bile and pus. The patient evolved clinically well, and has selleck inhibitor been submitted to a cephalic duodenopancreatectomy one week later. Conclusion: In this case, we demonstrate that EUS retrograde approach to the biliary tree, through papilla, with direct puncture of the CBD with fluoroscopic control, is a feasible technique for decompressing the biliary tree when rendezvous fails. Key Word(s): 1. Pre-cut; 2. Ultrasound; 3. Surgery; 4. direct puncture; Presenting Author: ADEMAR YAMANAKA Additional Authors: CECILIAQUEIROZ SILVA, Protein Tyrosine Kinase inhibitor JAZON ALMEIDA, FABIO GUERRAZZI, LEONARDO MONICI Corresponding Author: ADEMAR YAMANAKA, JAZON ALMEIDA, FABIO GUERRAZZI, LEONARDO MONICI Affiliations: UNICAMP State University Objective: Introduction: Liver biopsy is still considered the gold standard for

the diagnosis of liver disease however is an invasive procedure with risks. Risks can be reduced when guided by ultrasound and can be practiced MRIP by residents gastroenterologists with little experience in ultrasound. Objective: To evaluate

efficacy and safety of outpatient liver biopsies guided by ultrasound (U. S. BX) in real time. Methods: Retrospective study of patients undergoing liver biopsy performed at Gastrocentro/UNICAMP/Brazil, from January/2003 to March /2013. Upon information and signing the consent form previously approved by the ethics committee of the faculty of medicine, patients received intravenous sedation with benzodiazepines before the procedure. Local anesthesia with 10% lidocaine was performed US-guided real-time and used needles type tru cut 14-gauge for biopsy. The procedure was performed by medical resident, supervised by a faculty of gastroenterology. The patient stayed at bed in the first three hours in the most comfortable position for him as to the supine position and discharged after 6 hours. Results: Total of 1244 patients (Male: 66.5%, mean age: 44.3 ± 11.0); Major indications for the procedure were: evaluation of early treatment for hepatitis C (65.2%), liver diseases diagnosis (13.2%) and post transplant evaluation (10.0%); Number of needle passes: one (76%), two (18.2%), ≥ three (5.8%), only 21.2% of patients had complications, pain being the main one (19.5%); Only 3 patients required hospitalization for observation, with good clinical outcome and discharged at the next day with hemoglobin levels sustained.

mc.vanderbilt.edu/wiki/Main/PowerSampeSize).

We calculated that the study was designed to detect a significantly increased odds ratio (OR) of 2 with a power of 80%, based on risk allele frequencies of 0.10 and type I error rates of 0.05. For the survival analysis, the study had a power of 99%, given an expected mortality rate of 30% that we expected on the basis of our previous study with comparable patients.19 Table 1 illustrates that the majority of our patients presented with ascites due to alcoholic liver cirrhosis (63%) or chronic viral hepatitis (17%). All other etiologies were less common. Most patients were Rucaparib males (72%), and the median age of all patients was 57 years (range 23–86). As expected, the majority of patients showed advanced liver disease, with 94% of the patients classifying for Child-Pugh scores B or C. The median MELD score at the time of admission was 16 (range 5–40). C-reactive protein levels at the time of paracentesis did not differ between patients with NOD2 risk alleles (29 ± 31 mg/dL) variants and those find more without (28 ± 30 mg/dL). Employing PMN cell count >250/μL as a diagnostic criterion, 14 patients (9% of the cohort) were diagnosed

with SBP on the first day of admission (index paracentesis), 16 patients (11%) in the follow-up period (median 155 days, range 1–575), and 22 patients (15%) during previous hospital stays. For the survival analysis, patients who were lost to follow-up (n = 2) were excluded and patients who received a liver transplant (n = 7) were right-censored. In total, 54 patients (36%) died. Table 2 summarizes the causes of death for these patients, with acute-on-chronic liver failure and infections representing the most common conditions. Table 3 summarizes the minor allele frequencies for the three NOD2 variants in the different groups of patients, all of which were in the range next or slightly

above previously reported frequencies in Caucasian healthy cohorts.20 No patients carried homozygous NOD2 mutations. The NOD2 genotype distributions in the total cohort were consistent with Hardy-Weinberg equilibrium (all P > 0.05). In our cohort, 19 patients carried the variant p.R702W, 10 carried p.G908R, and eight tested positive for c.3020insC (Supporting Fig.). Figure 1 demonstrates that patients who tested positive for any of the NOD2 risk alleles showed a significantly (P = 0.007, log-rank test) reduced survival in comparison to patients with wildtype genotypes at all three positions. The mean survival time in patients who carried any NOD2 risk allele was 274 days in comparison to 395 days in patients who carried wildtype genotypes. By univariate analysis, we demonstrated that carrier status for any NOD2 risk allele, male gender, MELD score, the development of SBP, and serum albumin were risk factors for death (all P < 0.05), whereas age or other risk indicators (platelet count, serum bilirubin, serum creatinine, total protein) were not (Table 4A).