Conversely, VD supplementation has been proposed as an adjunct to

Conversely, VD supplementation has been proposed as an adjunct to current standard cares for treatment of hepatitis C.[60] A clinical study found that 25(OH)D serum levels Endocrinology antagonist were significantly lower in chronic

hepatitis C (25 μg/L) than in the controls (43 μg/L).[61] Expression levels of CYP27A1 correlated with 25(OH)D levels, but they were inversely related to necroinflammation. Moreover, low VD is linked to severe fibrosis and impaired sustained virologic response (SVR) in IFN-based therapy. One clinical trial showed that adding VD to the standard IFN plus ribavirin treatment significantly increased SVR in patients with chronic hepatitis C virus (HCV) genotype 1.[62] The SVR was defined as undetectable HCV-RNA at 24 weeks post-treatment.

The increased SVR attained by VD treatment was found to be even better for patients infected with HCV genotypes 2 and 3.[63] Another clinical selleck screening library study showed that the levels of VD and of its active form were significantly lower in advanced liver disease (hepatic cirrhosis and/or carcinoma) patients.[64] Conversely, low VD is associated with inflammation, as shown by elevated IL-17 and IL-23 levels in advanced patients. Regarding the underlying molecular mechanisms, an in vitro study showed that vitamin D3 remarkably inhibits HCV production in Huh7.5 hepatoma cells.[65] These cells express VD hydroxlases and can eventually generate calcitriol. Notably, treatment with calcitriol resulted in HCV inhibition through induction of IFN-beta. Intriguingly, HCV infection increased calcitriol production by inhibiting CYP24A1, implying that viral-induced immune tolerance may favor viral chronicity. A recent study surprisingly found that 25-hydroxyvitamin D3, but not 1,25-dihydroxyvitamin D3, is capable of reducing HCV by inhibiting infectious virus assembly.[66] VDBP gene polymorphisms may also determine the VD levels. By examining HCV patients treated with a combination therapy of pegylated interferon alpha (PEG–IFN) plus ribavirin, one study found that good responses to the treatment were related to both the VD levels greater than 20 ng/mL and

the wild-type VDBP polymorphisms.[67] VDR polymorphisms have also been associated with liver diseases, such as primary biliary cirrhosis.[68, 69] A recent clinical study 上海皓元 measured the effects of 25-OH VD plasma levels and VDR polymorphisms on fibrosis progression in HCV patients. Results showed that the bAt(CCA)-haplotype was significantly associated with fibrosis progression.[70] VD deficiency or insufficiency is well recognized for the association with variety of chronic degenerative diseases, including chronic hepatitis, viral persistence, ALD, NASH, and poor responsiveness for antiviral treatment. Among its multiple functions, immune modulation/regulation by VD is essential for tissue homeostasis and health physiologic response in addition to its job in calcium adsorption.

SEMS; 2 balloon catheter; 3 malignant obstruction Presenting Au

SEMS; 2. balloon catheter; 3. malignant obstruction Presenting Author: KYEONG OK KIM Additional Authors: KOOK HYUN KIM, SI HYUNG LEE, BYUNG IK JANG, TAE NYEUN KIM Corresponding Author:

KYEONG OK KIM Affiliations: Yeungnam University College of Medicine, Yeungnam University College of Medicine, Yeungnam University College of Medicine, Yeungnam University College of Medicine Objective: Percutaneous gastrostomy can be inserted by endoscopically (PEG) or radiologically (PRG). Trichostatin A purchase The aims of the present study were to analyze and compare the clinical outcome and long term efficacy of percutaneous. Methods: We retrospectively reviewed the 138 patients who underwent percutaneous gastrostomy. The patients were classified into PEG and PRG group. The indication, complication

and tube patency were compared between groups. Results: PEG was performed in 90 patients and the other 48 patients were underwent PRG. Mean age was 60.0 ± 17.5 years and male to female ratio Temsirolimus supplier was 102: 36. The indications were mostly unable to eat (67.4%), followed by recurrent aspiration (18.1%) and esophageal stricture (10.1%). Among 48 patients in PRG group, 14 cases (29.2%) were due to the failure of scope passage. Immediate complication occurred in 5 cases. Wound infection was the most common immediate complication. One case (0.7%) of bleeding at gastrostomy site in PEG groups and one case (0.7%) of stomal leakage in PRG group were noted. Delayed complication occurred in 8.0% at 398 ± 546.9 days and insertion site infection was the most common complication. The patency was longer in PEG group (227.0 ± 50.1 days vs. 132.0 ± 32.8 MCE days, p = 0.012). The associated factors with poor patency were presence of esophageal stricture and malignancy.

Conclusion: Both PEG and PRG are relatively safe procedure. Moreover, PRG can be substituted for PEG in patients unable to pass the scope or in over-weighted patients. The presence of stricture and malignancy of esophagus were predictors of the poor tube patency. Key Word(s): 1. percutaneous endoscopic gastrostomy percutaneous radiologic gastrostomy Presenting Author: JONG SUN KIM Additional Authors: YOUNG EUN JOO, HYUN SOO KIM, SUNG BUM CHO, WAN SIK LEE Corresponding Author: JONG SUN KIM Affiliations: Chonnam National University Medical School, Chonnam National University Medical School, Chonnam National University Medical School, Chonnam National University Medical School Objective: There is no reliable evidence to support the clinical impact of prophylactic antibiotics (PA) for reducing the infectious complications after stent insertion for malignant colorectal obstruction. The aim of this study was to determine the efficacy of PA for reducing the infectious complications and the potential risk factors responsible for the infectious complications after stent insertion.

Dot blot quantification of the ToLCTWV using the replicase gene a

Dot blot quantification of the ToLCTWV using the replicase gene as a probe revealed that the recovered phenotypes accumulated a low level of ToLCTWV, and virus concentration was gradually reduced from 10 to 14 weeks postinoculation. The possible mechanisms of CP-mediated resistance are discussed. “
“Rice leaves with bacterial blight or bacterial leaf streak symptoms were collected in southern China in 2007 and 2008. Five hundred and thirty-four single-colony isolates of Xanthomonas

oryzae pv. oryzae and 827 single-colony isolates of Xanthomonas oryzae pv. oryzicola were obtained and tested on plates for sensitivity to streptomycin. Four strains (0.75%) of X. oryzae pv. oryzae

isolated from AZD4547 the same county of Province Yunnan were resistant to streptomycin, and the resistance factor (the ratio of the mean median effective concentration inhibiting growth of resistant isolates to that of sensitive isolates) was approximately 226. The resistant isolate also showed streptomycin resistance in vivo. In addition to resistant isolates, isolates of less sensitivity were also present in the population of X. oryzae pv. oryzae from Province Yunnan. However, no isolates with decreased streptomycin-sensitivity were obtained from the population Apitolisib price of X. oryzae pv. oryzicola. Mutations in the rpsL (encoding S12 protein) and rrs genes (encoding 16S rRNA) and the presence of the strA gene accounting for streptomycin resistance in other phytopathogens or animal and human pathogenic bacteria were examined on sensitive and resistant strains of X. oryzae pv. oryzae by polymerase chain reaction amplification and sequencing. Neither the presence of the strA gene nor mutations in the rpsL or rrs were found, suggesting that different resistance 上海皓元医药股份有限公司 mechanisms are involved in the resistant isolates

of X. oryzae pv. oryzae. “
“Plants evolve a strategy to survive the attacks of potential pathogens by inducing the microbial signal molecules. In this study, plant defence responses were induced in four different varieties of Arachis hypogaea (J-11, GG-20, TG-26 and TPG41) using the fungal components of Sclerotium rolfsii in the form of fungal culture filtrate (FCF) and mycelial cell wall (MCW), and the levels of defence-related signal molecule salicylic acid (SA), marker enzymes such as peroxidase (POX), phenylalanine ammonia lyase (PAL), β-1,3-glucanase and lignin were determined. There was a substantial fold increase in POX, PAL, SA, β-1,3-glucanase and lignin content in FCF- and MCW-treated plants of all varieties of groundnut when compared to that of control plants. The enzyme activities were much higher in FCF-treated plants than in MCW-treated plants. The increase in fold activity of enzymes and signal molecule varied between different varieties.

Dot blot quantification of the ToLCTWV using the replicase gene a

Dot blot quantification of the ToLCTWV using the replicase gene as a probe revealed that the recovered phenotypes accumulated a low level of ToLCTWV, and virus concentration was gradually reduced from 10 to 14 weeks postinoculation. The possible mechanisms of CP-mediated resistance are discussed. “
“Rice leaves with bacterial blight or bacterial leaf streak symptoms were collected in southern China in 2007 and 2008. Five hundred and thirty-four single-colony isolates of Xanthomonas

oryzae pv. oryzae and 827 single-colony isolates of Xanthomonas oryzae pv. oryzicola were obtained and tested on plates for sensitivity to streptomycin. Four strains (0.75%) of X. oryzae pv. oryzae

isolated from NSC 683864 ic50 the same county of Province Yunnan were resistant to streptomycin, and the resistance factor (the ratio of the mean median effective concentration inhibiting growth of resistant isolates to that of sensitive isolates) was approximately 226. The resistant isolate also showed streptomycin resistance in vivo. In addition to resistant isolates, isolates of less sensitivity were also present in the population of X. oryzae pv. oryzae from Province Yunnan. However, no isolates with decreased streptomycin-sensitivity were obtained from the population selleck screening library of X. oryzae pv. oryzicola. Mutations in the rpsL (encoding S12 protein) and rrs genes (encoding 16S rRNA) and the presence of the strA gene accounting for streptomycin resistance in other phytopathogens or animal and human pathogenic bacteria were examined on sensitive and resistant strains of X. oryzae pv. oryzae by polymerase chain reaction amplification and sequencing. Neither the presence of the strA gene nor mutations in the rpsL or rrs were found, suggesting that different resistance MCE公司 mechanisms are involved in the resistant isolates

of X. oryzae pv. oryzae. “
“Plants evolve a strategy to survive the attacks of potential pathogens by inducing the microbial signal molecules. In this study, plant defence responses were induced in four different varieties of Arachis hypogaea (J-11, GG-20, TG-26 and TPG41) using the fungal components of Sclerotium rolfsii in the form of fungal culture filtrate (FCF) and mycelial cell wall (MCW), and the levels of defence-related signal molecule salicylic acid (SA), marker enzymes such as peroxidase (POX), phenylalanine ammonia lyase (PAL), β-1,3-glucanase and lignin were determined. There was a substantial fold increase in POX, PAL, SA, β-1,3-glucanase and lignin content in FCF- and MCW-treated plants of all varieties of groundnut when compared to that of control plants. The enzyme activities were much higher in FCF-treated plants than in MCW-treated plants. The increase in fold activity of enzymes and signal molecule varied between different varieties.

Retrospective comparisons of the Swedish

Retrospective comparisons of the Swedish see more and Dutch cohorts, where different strategies have been used, indicate that a costly, high-dose regimen improves outcome, but not dramatically. A prospective comparison is now underway. Treatment, clinical outcome, clotting factor consumption and socioeconomic

parameters will be compared between the two strategies. Results are expected to provide greater insight into the long-term consequences of the different prophylactic treatment strategies. The economic justification for prophylaxis has been addressed in several studies with varying results. While the majority (implicitly) suggest that prophylaxis is not cost effective at conventional willingness to pay for additional units in health thresholds, their results vary markedly. Closer

inspection suggests that the primary reasons results differ include different definitions of prophylaxis, clotting factor price, discount rates, choice of outcome measures and time horizon. Long-term replacement therapy prophylaxis, Selleck VX770 for haemophilia has a longstanding tradition in some countries. Cohort studies have shown prophylaxis not only to be superior to treatment on demand in terms of outcome, usually measured as haemophilic arthropathy, but also of quality of life and survival. Because of the rareness of the disease, extensive international collaboration and many years of follow-up are required to perform studies of high scientific merit. Thus, these have been completed only during the last several years. Together with larger and more long-term cohort studies, we now have firm evidence for the benefits of prophylaxis. However, several questions remain such as when to start prophylaxis, dose and dosing and when or if to stop. The focus for current research has increasingly become that of identifying the best strategy for providing a reasonable economic justification of prophylaxis so that countries with fewer economic 上海皓元医药股份有限公司 resources can also afford

it. In this article, the history of prophylaxis is reviewed and a comparison of the long-term outcomes of high-dose (Swedish) and intermediate-dose (Dutch) regimens are presented. Importantly, the economic justifications for prophylaxis are also examined. (Dr Berntorp) Studies conducted in Sweden by Ramgren and Ahlberg [1,2] during the 1960s showed that persons with haemophilia (PWH) with FVIII or IX levels above 1% of normal rarely developed severe disabling arthropathy. They hypothesized that it was logical to increase the level of factor activity in severe haemophilia to at least 1% by continuous prophylaxis. In The Netherlands, another pioneering country in this field, prophylaxis was introduced in 1968 [3]. Several attempts at prevention of bleeding with prophylaxis were documented during the late 1960s and the 1970s, both in Europe and North America.

2, 6-9, 18 We present the incident rates of clinically meaningful

2, 6-9, 18 We present the incident rates of clinically meaningful outcomes for patients at three stages of advanced liver disease: advanced noncirrhotic fibrosis, compensated cirrhosis, and decompensated cirrhosis (CTP score ≥7). The observed annual rates of all-cause mortality and liver transplantation were 2.2% in patients with noncirrhotic fibrosis and 5.3% in those with cirrhosis, similar to rates reported

in European and Japanese studies. As anticipated, the rate of clinical outcomes (especially CTP score elevation and variceal hemorrhage) was higher among patients with cirrhosis at baseline than those with noncirrhotic fibrosis. Among patients with noncirrhotic fibrosis, the annual incidence of initial clinical outcomes ranged www.selleckchem.com/products/GDC-0941.html from 0.25% per year for variceal hemorrhage to 1.4% per year for CTP elevation; of note, these outcomes of end-stage liver disease (including click here HCC and liver-related death) occurred in the absence of documented cirrhosis at entry into the HALT-C Trial, although we cannot exclude the possibility that some patients may have

been understaged at entry or progressed to cirrhosis by the time an outcome developed. For patients with histological cirrhosis at entry into the HALT-C Trial, the annual incidence of clinical outcomes ranged from 0.9% per year for variceal hemorrhage to 5.0% per year for CTP score elevation. Among individual clinical outcomes, the most frequent initial decompensation event was an increase in CTP score to ≥7. Once the CTP score became elevated, the incidence

of second clinical events was indistinguishable between subjects in the fibrosis and cirrhosis strata. Thereafter, morbidity and mortality rates increased substantially, confirming the value of a rise in CTP score as an ominous prognostic sign. Findings among HALT-C Trial patients with noncirrhotic fibrosis and cirrhosis can be compared with estimates drawn from other studies. Based on the readings from three liver biopsies over ≈4 years, HALT-C Trial patients with bridging fibrosis had an annual incidence of cirrhosis of 9.9% per year, a rate that differed little medchemexpress with sex or age and that was comparable to an estimated annual incidence of 11.5% derived from a meta-analysis conducted in 2007.19 Our directly observed, empirical results differ from those in a recent modeling projection in which an approximate four-fold difference in progression to cirrhosis was assumed between younger women and older men.20 A potential explanation for the lack of an effect of sex and age on disease progression in our study may be that once advanced liver disease has developed, age and sex may no longer influence disease progression.

2-4 We previously reported that

mice transgenic for direc

2-4 We previously reported that

mice transgenic for directed expression of a dominant-negative form of transforming growth factor beta receptor type II (dnTGFβRII), under the control of the CD4 promoter lacking the CD8 silencer, spontaneously develop an autoimmune biliary ductular disease.5 This disease is associated with the spontaneous production of AMAs directed to the same mitochondrial autoantigens recognized by sera from PBC patients6 with lymphocytic liver infiltration and periportal inflammation analogous to human PBC. The murine serum cytokine profile is similar to sera of patients with PBC. These findings indicate that the dnTGFβRII mice are a useful animal model for studying the pathogenic mechanisms of human PBC. We have demonstrated that deleting the p40 chain of interleukin (IL)-12 PD-0332991 ic50 from dnTGFβRII mice produced a marked diminution in the levels of proinflammatory T helper 1 (Th1) cytokines in livers with accompanying reductions in cellular infiltrates in portal tracts and diminished bile duct damage.7 IL-12, the prototypic

member of the heterodimeric family of cytokines, consists of a p40 and a p35 subunit covalently linked by two disulfide linkages. Both p35 and p40 are components of two heterodimeric cytokines in the IL-12 family.8 In order to further examine and differentiate the role of the p35- and p40-containing members of the IL-12 cytokine family in dnTGFβRII disease, we generated an IL-12p35−/− mouse strain on the dnTGFβRII background. Our results indicate 上海皓元 that, in contrast to the IL-12p40−/− mice that were protected from liver inflammation, the IL-12p35−/− mice developed click here liver inflammation with similar severity but delayed onset compared to the parental dnTGFβRII mice. The p35−/− mice demonstrate a distinct cytokine profile, with enhanced IL-17, compared to parental dnTGFβRII and p40−/− mice. Strikingly, deletion of the IL-12p35 subunit from dnTGFβRII mice resulted in frequent development of liver fibrosis. This model is unique in that

it has a resemblance to a number of immunological and histological features of human PBC. Although we do not opine that it recapitulates PBC faithfully, we submit that it is a useful system to dissect the cellular and molecular basis of loss of tolerance and liver damage. AMA, antimitochondrial autoantibodies; dnTGFβRII, dominant-negative form of transforming growth factor beta receptor type II; MNCs, mononuclear cells; PBD, primary biliary cirrhosis; PDC-E2, pyruvate dehydrogenase E2 complex. The dnTGFβRII colony on a B6 background (B6.Cg-Tg(Cd4-TGF BR2)16Flv/J) was maintained at the University of California at Davis animal facility (Davis, CA) and bred as hemizygotes due to the severe inflammatory bowel disease of homozygotes. The dnTGFβRII mice used herein are on a B6 background. Essentially, the transgenic founder mice were backcrossed to B10.

If a family history of thrombocytopenia is present, a careful wor

If a family history of thrombocytopenia is present, a careful work-up is warranted to prevent inappropriate therapies (poorly chosen medication or splenectomy) while it is essential to compile a record of clinical complications such as bone marrow failure, oncological disorders, sensorial hearing loss, renal failure or others. For some patients, significant bleeding may only arise after surgery or trauma and a sufficient challenge to the hemostatic system. Similar bleeding patterns are found in type 1 or 2 VWD and therefore some IPDs can be wrongly diagnosed as VWD. During initial screening, particularly important is measuring the platelet count

and the mean platelet volume; while a peripheral blood smear is recommended for Selleckchem LDK378 giant platelet syndromes as electronic counters see more may underestimate platelet numbers and size

[24,27]. Measuring the Ivy bleeding time is no longer standard practice and some replace it by the platelet function analyzer (PFA-100). Laboratory investigation of platelet aggregation, ATP secretion and quantification of platelet receptors by flow cytometry are standard procedures. Often requiring specialist help, immunofluorescence (e.g. distinctive patterns for myosin-IIA in leukocytes are typical of MYH9 disease) and electron microscopy are often useful as an aid to diagnosis; while evaluating platelet adhesion and spreading on protein surfaces is informative especially if accompanied by a study of signalling pathways (phosphorylations, western blotting) [7,11,13,24,25,28]. Finally, flow chambers

and computerized analysis of thrombus formation on protein-covered surfaces (e.g. Fg, VWF, collagen) under controlled flow, procedures often validated for platelets from genetically-modified mice, will fast become applicable to human pathology [29]. Platelets are easily obtainable and citrated MCE platelet-rich plasma is mostly used to study platelet function under basal and activated conditions [3,5]. Algorithmns are being developed to permit step-by-step detection of specific pathologies. Defects in platelet adhesion, aggregation, G protein signaling, secretion and platelet production can result from mutations in platelet-specific genes leading to isolated thrombocytopathy or thrombocytopenia for which the main clinical feature is bleeding (e.g. BSS, GT, P2Y12 deficiency and other diseases as reviewed in Molecular basis of platelet disorders). In contrast, when mutations occur in widely expressed genes, patients usually develop a broader clinical phenotype with bleeding accompanied by neuropathology, endocrine dysfunction, other hematological and/or metabolic problems. Therefore, clinical investigation and platelet research go hand-in-hand to improve knowledge of broad phenotype mendelian disorders [10,30].

Using a published algorithm to find p53 consensus sites,25 we map

Using a published algorithm to find p53 consensus sites,25 we mapped potential, shared

p53 and TA-p73 (p53/p73) binding sites upstream of four TA-p73–bound genes that changed expression during the 24 to 48 hours of liver regeneration: Foxo3, Janus kinase 1 (Jak1), phosphoprotein enriched in astrocytes 15 (Pea15), and tubulin alpha 1 (Tuba1; Supporting Table 4 and Supporting Fig. 3). Binding of p53 and TA-p73 was observed for all examined genes at identified p53REs, and this confirmed that putative targets uncovered by TA-p73 ChIP/chip mTOR inhibitor may be bound by both p53 and TA-p73 in the quiescent liver in vivo (Fig. 2). Afp p53RE served as a positive control for p53/p73 binding in the quiescent liver, whereas upstream regions of albumin (Alb) and brain-specific protein 3B (Brn3B) genes served as negative controls for p53 and TA-p73 binding.4, 26 Taken together, these results suggest that p53 and TA-p73 activate or repress target genes in the quiescent liver and that regulatory activities of p53 and TA-p73 change during

liver regeneration. Among the 17 TA-p73 gene targets revealed by ChIP/chip, Foxo3 had the most significant change in expression in response to PH and strong p73 binding (Supporting Table 4). We found a p53 consensus site −3.7 kb upstream Vemurafenib of the TSS of Foxo3 as well as several other potential p53 binding sites within the second and third introns (Fig. 3A). We detected binding of both p53 and TA-p73 to the p53RE −3.7 kb upstream of Foxo3 (Fig. 3B). To confirm the specificity of p53/p73 binding to the Foxo3 p53RE, we used primers for a region that contains no p53REs (located −2.0 kb upstream of the Foxo3 TSS) and saw background levels of interaction (nonspecific region; Fig. 3A,B). TA-p73 compensates for a loss of p53 by binding to the Afp p53RE in the absence of p534 and promotes a delayed but significant 上海皓元医药股份有限公司 reduction of Afp expression in the liver by 4 months of age in p53−/− mice.26 We performed ChIP from liver tissue collected from p53−/− mice at 2 months of age and found that TA-p73 binds the p53RE of Foxo3 in the absence of p53 (Fig. 3C). Thus, both p53 and TA-p73 regulate transcription of Foxo3 in the adult mouse liver

at time zero. On the basis of known functions of FoxO3 as a tumor suppressor, we hypothesized that p53 and TA-p73 act as positive regulators of Foxo3 at the level of transcription. We determined levels of Foxo3 messenger RNA (mRNA) isolated from liver tissue collected from p53+/−, p53−/−, and p73+/− mice in comparison with WT littermates, and we observed a significant decrease in Foxo3 expression in p53−/− and p73+/− mice (Fig. 4A). Transcription of Trp73 from multiple promoters, together with alternative mRNA splicing, results in at least 28 isoforms of p73.27 We performed transient transfection of a mouse hepatoma–derived cell line (Hepa1-6)28 with plasmids that expressed transactivating TA-p73 isoforms, HA–TA-p73α and HA–TA-p73β or HA-p53.

Results: Skin biopsy of leg ulcer showed vasculitis Gastroscopy

Results: Skin biopsy of leg ulcer showed vasculitis. Gastroscopy result showed erosive gastritis and colonoscopy result showed multiple ulcer in colon. Result of biopsy of gastric showed LY2835219 cell line the presence of vasculitis which patohological anatomic result revealed signs of erythrocyte

extravacation. He was given methyl prednisolon at immunosuppresant dose, oral anticoagulant with prophylactic dose, proton pump inhibitor and acyclovir. The ulcers were resolved after one month follow up. Conclusion: We reported a 48 year old man with gastrointestinal manifestation of systemic vasculitis presented with chronic gastritis Key Word(s): 1. Systemic vasculitis; 2. Chronic gastritis; 3. Gastrointestinal; Presenting Author: XUEFENG LUO Additional Authors: XIAO LI Corresponding Author: XUEFENG LUO Affiliations: westchina hospital Objective: The purpose of this study was to evaluate the safety and efficacy of transjugular intrahepatic portosystemic shunt (TIPS) placement in the management

of portal hypertension in non-cirrhotic patients with portal cavernoma. Methods: From June 2005 to December 2011, 15 non-cirrhotic patients with portal cavernoma treated with TIPS placement via a transjugular approach alone in our hospital were followed until last clinical evaluation. There were 4 women and 11 men with a mean age Rapamycin clinical trial of 29.1 years. Technical success of TIPS placement, complications and follow-up

results were evaluated. Results: TIPS placement was successful in 11 out of 15 patients (technical success rate, 73.3%). Procedure-related complication was postprocedural hepatic encephalopathy in one patient. In patients with successful shunt placement, the portosystemic pressure gradient decreased from 25.8 ± 5.7 to 9.5 ± 4.2 mmHg (p < 0.001). TIPS dysfunction occurred in two patients during a median follow-up time of 45.2 months. Revision was not performed in one patient as there was not adequate outflow to keep the stent patent. The other patient died of massive gastrointestinal bleeding in a local hospital. The remaining nine patients all had functioning shunts until the last medchemexpress evaluation. Conclusion: TIPS is a safe and effective therapeutic option in the treatment of non-cirrhotic patients with symptomatic portal hypertension secondary to portal cavernoma. Key Word(s): 1. TIPS; 2. non-cirrhotic; 3. portal cavernoma; 4. PVT; Presenting Author: PÉTER NAGY Additional Authors: SAGA JOHANSSON, STEPHEN SWEET Corresponding Author: PÉTER NAGY Affiliations: AstraZeneca; Research Evaluation Unit, Oxford PharmaGenesis Ltd Objective: Some pharmacokinetic and pharmacodynamic studies have reported that proton pump inhibitors (PPIs), in particular omeprazole and esomeprazole, reduce the antiplatelet activity of clopidogrel by competitively inhibiting its conversion from a prodrug to an active metabolite.