The Malmö protocol combines high-dose FVIII and immunosuppressive therapies and has shown success in 10/16 (62.5%) of patients. The Van Creveld protocol, which uses low-dose FVIII (25–50 IU kg−1 every second day) in patients with an inhibitor titre <10 Bethesda units (BU)

at the start of therapy, has demonstrated success in 21/24 (87.5%) patients. In routine clinical practice, treatment often involves variations of these three main ITI protocols. To date, there is no clear understanding of how ITI works although several hypothetical mechanisms have been proposed. These include the development of anti-idiotypic antibodies [5, 6], depletion of memory ACP-196 supplier B cells [7], or generation of FVIII-specific regulatory T cells [8, 9]. Based on ITI protocols currently in use, it is known that the FVIII/IX complex

is the only essential component. At present, there are no biomarkers that can be utilized to assist in understanding the mechanistic process of ITI. Thus, current knowledge stems mainly Selleckchem CCI-779 from clinical observations and analyses of retrospective data. Data generated during the 1990s from a global perspective indicated that ITI is significantly influenced by the maximum historical titre (higher titres are associated with poorer outcomes), the pretitre at the start of ITI, the time between diagnosis and treatment (the shorter the better), treatment age (the younger the better) and FVIII dose [10]. The protocol for the subsequent

prospective International ITI study (in good-risk patients) considered these historical observations, and recruited children (aged NADPH-cytochrome-c2 reductase <8 years at the time of randomization; peak historical titre ≥5 and ≤200 BU mL−1; starting titre ≤10 BU mL−1 before randomization) as soon as possible after inhibitor detection [11]. Since the mid-1970s, 91 patients with inhibitors have been treated at the Bonn Centre according to the Bonn protocol which uses plasma-derived (pd) FVIII/von Willebrand factor (VWF) for ITI in patients at any age. Of these, 68 and 23 patients were classified as high and low responders respectively. All patients were treated by the same physician using a standardized protocol. The overall success rate of ITI was 78%, with a failure rate of 15% and with some treatments either ongoing (3%) or withdrawn (4%). Considering only high responders with available data, the success rate was 71% (42/59 patients). Interestingly, patient age at the start of therapy or time from diagnosis to the start of ITI did not influence the success rate in high responders, reflecting the fact that many patients were adults. By multivariate analysis, maximum inhibitor titre was the only independent variable that significantly affected the high-responder success rate.

A low initial inhibitor titre and a short interval between the appearance of the inhibitor and the start of therapy seem to be positive predictive factors. The problems of infectious complications and therapy-related mortality were addressed, but

data are scanty. In a randomized prospective multicentre trial [26], 31 patients with newly diagnosed acquired haemophilia were treated with prednisone 1 mg kg day−1 for 3 weeks; 20 non-responders were randomized: four patients Trametinib cost with prednisone (1 mg kg day−1); six patients with cyclophosphamide 2 mg kg day−1; 10 patients with prednisone + cyclophosphamide for additional 6 weeks. The inhibitor disappeared in three patients (75%) treated with prednisone and in eight patients (50%) treated with cyclophosphamide or cyclophosphamide + prednisone. No information on the follow-up was given. In the Italian study [3], 65 of 90 patients were evaluable for the immunosuppressive therapy. Three patients died

before starting treatment, one because of bleeding and two for reasons of the underlying disease. Eight patients with a low inhibitor titre (<10 BU) did not receive immunosuppressive therapy; three of them died because of bleeding complications. Information relevant to the response to the immunosuppressive therapy was missing in 14 patients. Results of the initial immunosuppressive therapy: complete remission 46 (70.7%), partial remission 13 (20%), failure 6 (9.3%). Four patients in partial remission Pregnenolone achieved a complete remission after discontinuation of treatment. selleck products The other patients including the failures received alternative treatments (Table 4). Patients with low (<10 BU) or high (>10 BU) inhibitor titre did not differ in the rate of complete remission (30 and 22 patients respectively). Eleven patients (21.1%) relapsed; eight were rescued with additional therapy, one patient died because of bleeding and two achieved

a spontaneous complete remission. Rituximab, an anti-CD 20 monoclonal antibody, has been used as salvage therapy. Sperr et al. compared Rituximab and prednisone + cyclophosphamide in 42 and 44 patients respectively reported in various studies in the literatures [27]. Results were similar: complete remission (CR) rate 78.6% and 84.1% without difference between patients who had (75%) or had not received previous treatment with other immunosuppressive drugs. The median treatment duration to CR was 8.3 and 6.3 weeks and the probability of CR at 2 years 66% and 94% with a plateau in the Kaplan–Mayer curve. The authors concluded that the use of Rituximab should be limited to failure of first/second line therapy. Few patients were treated with cyclosporine A or 2-chlorodeoxyadenosine. Immune tolerance is an accepted and effective treatment of haemophilic patients with inhibitor, but has been rarely applied in acquired haemophilia.

For 4 weeks, along with access to HFD, one group received indomethacin (n = 5 rats, 1 mg/day) every 24hours, and the second group (n = 5 rats) was fed with HFD; a control group (6 rats) was fed with standard chow diet (SCD) for 12 weeks. We observed that indomethacin significantly revert fatty liver disease (Fig. 1). EGFR antibody inhibitor The most remarkable effects of COX inhibition by indomethacin in the HFD group in comparison with the SCD group were: a 230% increase of liver expression of CPTA1 mRNA, a 100% increase of liver abundance of PCK1 mRNA (phosphoenolpyruvate carboxykinase, the main control point for the regulation of gluconeogenesis),

and an increase of 84% ofPPARα mRNA (peroxisome proliferator-activated receptor alpha,a transcription factor that controls the expression of genes encodingfatty acid oxidation enzymes and mitochondrial fatty acid oxidation) (Fig. 1). As far as we know, we show for the first time that indomethacin is able to increase liver CPT1A mRNA. We can not explain the exact mechanism by which the Talazoparib nmr drug influences liver CPT1A expression, although an inhibitory effect of

a COX product on the gene expression is an obvious option, but we agree with Orellana-Gavalda etal. that liver CPT1A is a prime target to increase beta-oxidation of hepatic long-chain fatty acids. Other explanations are probable. Indomethacin was regarded as a dual PPARγ/PPARα ligand.3 In addition, the 5′-flanking region of COX2 has several potential transcription regulatory sequences, including CCAAT/enhancer binding protein motif (a gene that specifically regulates hepatic gluconeogenesis and lipogenesis4) and two nuclear factor-κB sites (a key modulator of liver injury in NAFLD). Hence, these observations may explain the beneficial effects of indomethacin on NAFLD. In summary, our results represent proof of principle that

pharmacological COX inhibition may provide a novel approach for reversing fatty liver by modulating the liver CPT1A mRNA expression. These results also add some clues about the potential role of the inducible COX2 and its proinflammatory prostaglandin products in metabolic disorders, including NAFLD. Maria S. Rosselli M.Sc.*, Adriana L. Burgueño Ph.D.†, Carlos J. Pirola Ph.D.†, Silvia Sookoian M.D., Ph.D.*, * Department of Clinical and Molecular Hepatology, udad Autónoma before de Buenos Aires, Buenos Aires Argentina, † Department of Molecular Genetics and Biology of Complex Diseases, Institute of Medical Research “Alfredo Lanari” Instituto de Investigaciones Médicas, University of Buenos Aires–National Council of Scientific and Technological Research (CONICET), Ciudad Autónoma de Buenos Aires, Buenos Aires Argentina. “
“A 65 year-old male cadavaric renal transplant (CRT) recipient maintained on mycophenolate mofetil (MMF), tacrolimus, and low-dose prednisone for 7 years presented with a 10-month history of diarrhea and a 60-pound weight loss.

Also, most studies were relatively under-powered and did not meet or publish CONSORT criteria for clinical trials. Despite these limitations, it can be summarized that (1) the use of vitamin E is associated with a decrease in aminotransferases in subjects with NASH, (2) studies where histologic endpoints were evaluated indicate that vitamin E causes improvement in steatosis, inflammation, and ballooning and resolution of steatohepatitis in adults with NASH, and (3) vitamin E has no effect on hepatic fibrosis. Although two meta-analyses8,

129 failed to observe significant histological benefits with vitamin E in patients with NASH, these analyses were conducted before PIVENS122 and TONIC130 trials were published. In the largest clinical trial (PIVENS)122 reported to date, the pure form of rrr α-tocopherol was orally administered at a dose of 800 IU/day for 96 weeks. The primary endpoint as stated previously was achieved in a significantly greater number of participants receiving vitamin E compared to placebo (42% vs. 19%, P< 0.001, number needed to treat= 4.4). One concern with vitamin E is the controversial issue of whether it increases all-cause mortality. Some meta-analyses have reported an increase in all-cause mortality with high dose vitamin E,131, 132 but others failed to confirm such an association.133-135 A recently published RCT showed that vitamin E administered at a dose of 400 IU/day

increased the risk of prostate cancer in relatively healthy men (absolute increase of 1.6 per 1000 person years of vitamin E use).136 Recommendation 21. Vitamin E (α-tocopherol) administered at daily dose of 800 IU/day improves liver histology in non-diabetic adults with biopsy-proven NASH and therefore it should be considered as a first-line pharmacotherapy for this patient population. (Strength -1, Quality – B) 22. Until further data supporting its effectiveness become available, vitamin E is not recommended to treat NASH in diabetic patients, NAFLD without most liver biopsy,

NASH cirrhosis, or cryptogenic cirrhosis (Strength – 1, Quality – C) Several studies126, 137-140 investigated UDCA (conventional and high doses) to improve aminotransferases and steatosis in patients with NAFLD and liver histology in patients with NASH. All but one study139 have been proof-of-concept studies with small numbers of participants and/or surrogate endpoints. Notably, a single large multicenter RCT convincingly showed that UDCA offers no histological benefit over placebo in patients with NASH.139 Omega-3 fatty acids, currently approved in the United States to treat hypertriglyceridemia, have been investigated to treat NAFLD both in animal models and in humans.141 A recent review by Masterton et al.,142 of published literature GW-572016 related to omega-3 fatty acids in NAFLD, found experimental evidence to support their use but the interpretation of human studies was limited by small sample size and methodological flaws.

Period 2 was immediately followed by Period 3, in which check details subjects received 200 mg MK-5172 QD coadministered with 600 mg QD oral doses of RIF for 14 days. Results: Coadminis-tration of MK-5172 with RIF was safe and well-tolerated. A single IV dose of RIF increased the MK-5172 AUC0-24, Cmax, and C24, with geometric mean ratios (GMRs, MK-5172+RIF/MK-5172) [90% confidence intervals (CIs)] of 12.61 [10.83, 14.67], 10.94 [8.92, 13.43], and 1.77 [1.40, 2.24], respectively. A single dose of oral

RIF increased the MK-5172 steady-state AUC0-24, Cmax, and C24 with GMRs (MK-5172+RIF/MK-5172) [90% CIs] of 8.35 [7.38, 9.45], 6.52 [5.16, 8.24], and 1.62 [1.32, 1.98], respectively. Multiple oral doses of RIF did not statistically impact the MK-5172 steady-state AUC0-24 or Cmax with GMRs (MK-5172+RIF/MK-5172) [90% CI] of 0.93 [0.75, 1.17] and 1.16 [0.82, 1.65], respectively, but decreased the MK-5172 C24h with a GMR [90% CI] of selleck 0.15 [0.11, 0.20]. Conclusions: There was a significant increase in MK-5172

PK when MK-5172 is coadministered with a single IV or oral dose of RIF, which may be primarily attributed to inhibition of OATP by RIF. There was no significant effect of oral 600 mg QD RIF on MK-5172 AUC and Cmax, but a significant decrease in C24h, likely due to a net-effect of OATP inhibition and CYP3A4/P-gp induction by multiple oral RIF doses. These results suggest that MK-5172 is an OATP substrate and confirm that MK-5172 is a CYP3A4/P-gp substrate.

Disclosures: Luzelena Caro – Employment: Merck & Co., Inc. Jennifer E. Talaty – Employment: Merck, Sharp, & Dohme Zifang Guo – Employment: Merck & Co., Inc. Kristin Butterfield – Employment: Merck, Sharp & Dohme Thomayant Prueksaritanont – Employment: Merck Sharp & Dohme Corp Scott Rasmussen – Employment: Celerion, Inc Iain P. Fraser – Employment: Merck & Co.; Stock Shareholder: Merck & Co. Wendy W. Yeh – Employment: Merck & Co. Joan R. Butterton – Employment: Merck Sharp & Dohme Corp.; Stock find more Shareholder: Merck Sharp & Dohme Corp. “
“The Korean College of Helicobacter and Upper Gastrointestinal Research first developed guidelines for the diagnosis and treatment of Helicobacter pylori (H. pylori) infection in 1998, and revised guidelines were proposed in 2009 by the same group. Although the revised guidelines were based on a comprehensive review of published articles and the consensus of expert opinions, the revised guidelines were not developed using an evidence-based process. The new guidelines presented in this study include specific changes regarding indication and treatment of H. pylori infection in Korea, and were developed through the adaptation process using an evidence-based approach. After systematic review of the literature, six guidelines were selected using the Appraisal of Guidelines for Research and Evaluation (AGREE) II process. A total of 21 statements were proposed with the grading system and revised using the modified Delphi method.

After the diagnosis of an internus obturator muscle haematoma in Patient 2 (P2) in November 2011, we performed an exhaustive research of such a case in our patient database including severe and moderate inherited haemophilia A (n = 260; about 20% with actual or past medical history of inhibitor) and B (n = 63; about 2% with actual or past medical history of inhibitor). A second patient (P1), displaying the same diagnosis than P2, was identified in November 1987; both patients exhibited an inhibitor to FVIII at the time of the bleeding event. Ultrasonography (US),

Computed Tomography (CT) and Magnetic Resonance Imaging (MRI) were performed, respectively, at first or secondly according to their availability and their results. The radiologic Sirolimus concentration criteria of haematoma of the obturator internus muscle corresponded to the definition proposed by Ali et al. as an ‘asymmetry in size or focal blood attenuation in the substance of the muscle’ [4], notably in the CT pictures. The two patients (P1 and P2) had no other medical history than an inherited haemophilia A. P1 has

been lately diagnosed with a sporadic moderate haemophilia (FVIII, 2–3%) at 7 years of age because of a traumatic right thigh haematoma that had required local treatment only. At 11-year old, he was firstly infused with plasmatic FVIII concentrate (16 days exposure) to cover a surgery for appendicular peritonitis. selleck Within the following

2 months spontaneous muscular and joint bleedings (left iliopsosas, right knee, left Selleckchem AZD3965 calf, left forearm) occurred concomitantly to a low level inhibitor of FVIII (FVIII < 1%; inhibitor, 1–2 Bethesda Unit (BU)). P2 has been diagnosed with a sporadic severe haemophilia (FVIII < 1%; non-sens Ser568X mutation) at 8 months of age because of multiple ecchymoses and muscle haematomas. A persisting high-titre inhibitor occurred rapidly at 12 months old under on-demand treatment with recombinant FVIII therapy (6 days exposure; history peak titre, 53 BU). Successive immune tolerance and recombinant activated FVII (rFVIIa) or activated prothrombin complex concentrate treatment procedures exhibited transient and partial success only. The patient exhibited thereafter several muscle and joint bleedings with two targets joints (left ankle and right knee), but he had never life-threatening haemorrhage. Both patients complained increasing right iliopelvic pain for 24–36 h with slight lameness, after a long step. None of them exhibited fever. At diagnosis P1 was 11-year old and inhibitor appeared 3 months ago was very low or undetectable (<0.6 or 1 BU with FVIII ≤ 1%). P2 was 13-year old and received daily infusions of plasmatic FVIII (100 UI kg−1) associated with on-demand rFVIIa treatment. The inhibitor rate was 15.1 BU, whereas it was only 2.

After the diagnosis of an internus obturator muscle haematoma in Patient 2 (P2) in November 2011, we performed an exhaustive research of such a case in our patient database including severe and moderate inherited haemophilia A (n = 260; about 20% with actual or past medical history of inhibitor) and B (n = 63; about 2% with actual or past medical history of inhibitor). A second patient (P1), displaying the same diagnosis than P2, was identified in November 1987; both patients exhibited an inhibitor to FVIII at the time of the bleeding event. Ultrasonography (US),

Computed Tomography (CT) and Magnetic Resonance Imaging (MRI) were performed, respectively, at first or secondly according to their availability and their results. The radiologic BTK inhibitor ic50 criteria of haematoma of the obturator internus muscle corresponded to the definition proposed by Ali et al. as an ‘asymmetry in size or focal blood attenuation in the substance of the muscle’ [4], notably in the CT pictures. The two patients (P1 and P2) had no other medical history than an inherited haemophilia A. P1 has

been lately diagnosed with a sporadic moderate haemophilia (FVIII, 2–3%) at 7 years of age because of a traumatic right thigh haematoma that had required local treatment only. At 11-year old, he was firstly infused with plasmatic FVIII concentrate (16 days exposure) to cover a surgery for appendicular peritonitis. click here Within the following

2 months spontaneous muscular and joint bleedings (left iliopsosas, right knee, left FK506 calf, left forearm) occurred concomitantly to a low level inhibitor of FVIII (FVIII < 1%; inhibitor, 1–2 Bethesda Unit (BU)). P2 has been diagnosed with a sporadic severe haemophilia (FVIII < 1%; non-sens Ser568X mutation) at 8 months of age because of multiple ecchymoses and muscle haematomas. A persisting high-titre inhibitor occurred rapidly at 12 months old under on-demand treatment with recombinant FVIII therapy (6 days exposure; history peak titre, 53 BU). Successive immune tolerance and recombinant activated FVII (rFVIIa) or activated prothrombin complex concentrate treatment procedures exhibited transient and partial success only. The patient exhibited thereafter several muscle and joint bleedings with two targets joints (left ankle and right knee), but he had never life-threatening haemorrhage. Both patients complained increasing right iliopelvic pain for 24–36 h with slight lameness, after a long step. None of them exhibited fever. At diagnosis P1 was 11-year old and inhibitor appeared 3 months ago was very low or undetectable (<0.6 or 1 BU with FVIII ≤ 1%). P2 was 13-year old and received daily infusions of plasmatic FVIII (100 UI kg−1) associated with on-demand rFVIIa treatment. The inhibitor rate was 15.1 BU, whereas it was only 2.

001) in the number of hyperplastic nodules between HBx/shp53 and HBx, between HBx/shp53 and empty/shp53, between HBx and NRAS/shp53, and between empty/shp53 and NRAS/shp53. Significant differences (P < 0.01) were seen between NRAS/shp53 and HBx/NRAS and between NRAS/shp53 and

Gfp. Marginal significance (P < 0.05) was seen between HBx/shp53 and HBx/NRAS, between HBx/shp53 and Gfp, between HBx and HBx/NRAS/shp53, and between empty/shp53 and HBx/NRAS/shp53 (Fig. 3A). A statistical analysis using the two-tailed Mann-Whitney test indicated highly significant differences (P < 0.001) in the weight percentage between HBx/shp53 and empty/shp53 and between HBx and empty/shp53. Significant differences (P < 0.01) were seen between http://www.selleckchem.com/screening/anti-infection-compound-library.html HBx/shp53 and Gfp, between HBx and Gfp, between empty/shp53 and HBx/NRAS/shp53, and between HBx/NRAS/shp53 and Gfp. Marginal significance (P < 0.05) was seen between HBx/shp53 and HBx/NRAS, Tamoxifen research buy between HBx and HBx/NRAS, between empty/shp53 and NRAS/shp53, between NRAS/shp53 and Gfp, and between HBx/shp53 and Gfp (Fig. 3B). Mice injected with NRAS alone generally had weak expression levels of Ctnnb1 detectable by IHC (Fig. 4). Hyperplastic nodules induced by NRAS coinjected with shp53 generally had higher Ctnnb1 expression levels but not the levels

seen in HBx or HBx/shp53 mice (Fig. 4). As expected, HBx/NRAS mice had heterogeneous staining patterns for selleck kinase inhibitor Ctnnb1 (Fig. 4). In contrast, hyperplastic nodules from NRAS or NRAS/shp53 mice were highly positive for pAkt by IHC (Fig. 5). Using the SB transposon system and hydrodynamically introducing transgenes specifically into the

livers of Fah-null/SB transposase–expressing recipient mice, we could dissect the contributions of various gene components of HBV by inducing liver hyperplasia in these animals. Our results demonstrate the oncogenic effect of the HBx transgene when it is hydrodynamically delivered into hepatocytes repopulating a liver. The low penetrance or delayed tumorigenic latency of HBx in injected mice may reflect the long latency of HBV-induced cirrhosis and tumorigenesis in infected humans. The fact that we observed an effect of HBx alone may indicate that its expression can cooperate with the process of hepatocyte regrowth to induce liver hyperplasia. Mice injected with HBx alone seem to have higher liver to whole mass percentages, and this indicates that HBx may have a hyperproliferative effect during HBV-induced liver tumorigenesis (Fig. 3B). Tumor latency was reduced and the oncogenic effect was augmented when HBx was coinjected with shp53. This is especially important because approximately 50% of human patients with HCC have mutations in the TP53 gene. HBx has been shown to bind TP53 and inactivate its activity,9, 11 but our data indicate that this mechanism must not impair TP53 function sufficiently for tumor formation.

Thus, VWF levels are reduced in individuals who have a blood group O, and this reduction is secondary to a reduced half-life with a corresponding increase in VWFpp/VWF:Ag ratio [32,33]. Accelerated

clearance of VWF is Ulixertinib in vivo also seen in individuals with an autoimmune antibody to VWF [6]. This results in a rapid clearance of VWF but not VWFpp. Thus, the VWFpp/VWF:Ag ratio is markedly increased. Clinical syndromes with accelerated clearance of VWF are therefore suggested by (i) an elevated VWF/VWF:Ag ratio, (ii) normal platelet VWF:Ag with reduced plasma VWF, (iii) an excessive desmopressin response between steady-state plasma VWF and the 30 min or 1 h assay of plasma VWF or (iv) a reduced mTOR inhibitor VWF survival after desmopressin. Interestingly, when VWF has increased clearance, FVIII also appears to have accelerated clearance. The converse is

not usually seen. If there is an antibody to FVIII (acquired haemophilia), VWF is not usually reduced. With the exception of an acquired antibody to VWF, other causes of reduced VWF are the result of an abnormal host VWF. Treatment with exogenous VWF would be expected to be normal. In contrast, acquired autoimmune VWD will result in accelerated clearance of exogenous VWF. Although infused r-FVIII has a reduced survival in the absence of VWF, that survival is not affected by an antibody to VWF. Thus, continuous FVIII has been clinically effective in some cases of acquired

autoimmune VWD. Few studies have established the biological predictive markers of surgical bleeding in VWD [34,35]. Ziv reported [36] that postoperative bleeding could have been avoided in 83% of the cases if a preoperative family or bleeding history had been obtained. However, until recently, no quantitative description of bleeding symptoms in VWD has been available to fully appreciate their diagnostic relevance to discriminate between a significant bleeding history and trivial symptoms in VWD. A further question for the clinician is whether patients with a history of severe bleeding may be at higher risk of bleeding during invasive procedures (e.g., tooth extraction, surgery). This is clinically relevant, because the laboratory evaluation of mild bleeding disorders selleck chemical has no practical value as a guideline for the optimal antihaemorrhagic prophylaxis, as abnormal laboratory tests do not predict clinical bleeding. In the MCMDM-1VWD study, by using a standardized bleeding questionnaire to establish a bleeding score (BS), the association between spontaneous, mucocutaneous bleeding symptoms (epistaxis, cutaneous bleeding and menorrhagia) and bleeding after surgery or tooth extraction in patients with type 1 VWD was evaluated [37]. Interestingly, the BS showed a predictive value similar to VWF level for bleeding after tooth extraction, but was superior to VWF measurement for the prediction of bleeding after surgery.

Conclusion: As the childhood onset of those disorders, at first the differential diagnosis was EHPVO, but then we concluded the diagnosis is NCPF based on portal venous system patency. The etiology is still idiopathic. Key Word(s): 1. Banti’s syndrome; 2. non-cirrhotic portal fibrosis; 3. childhood onset Presenting Author: JIN TAO Additional

Authors: XIUQING WEI, ZHIE WU, BIN WU Corresponding Author: JIN TAO Affiliations: 3rd Affiliated Hospital of Sun Yat-Sen University, 3rd Affiliated Hospital of Sun Yat-Sen University, 3rd Affiliated Hospital of Sun Yat-Sen University Objective: To analyze the clinical characters of cavernous transformation of portal vein (CTPV) and its potential causes. Methods: Clinical data of patients diagnosed as CTPV and treated in our hospital from June of 2006 to May BGB324 clinical trial of 2010 were collected. The clinical characters and related diseases of CTPV were analyzed retrospectively. selleck kinase inhibitor Results: 83 patients were enrolled in this research. The main symptoms of these patients were abdominal pain, up digestive tract hemorrhage and the clinical manifestation caused by portal hypertension and the corresponding original diseases. The diagnosis

of CTPV was confirmed according to more than once examination of color doppler sonography and CT/MRI. Among these 83 patients, complications including: cirrhosis (60 cases), hepatocarcinoma (48 cases), history of abdominal surgery (24 cases), hepatic artery-portal vein fistula (HA-PVF, 15 cases), diabetes (8 cases), Budd-Chiari syndrome and pancreatic carcinoma (2 cases for each). Conclusion: Portal hypertension complicated with up digestive tract haemorrhage is the main clinical character of CTPV; Cirrhosis and hepatocarcinoma are main causes of CTPV, while HA-PVF and diabetes may be its potential causes. Key Word(s): 1. cavernous transformation of portal vein; 2. cirrhosis; 3. hepatocarcinoma; 4. hepatic artery-portal vein fistula; 5. diabetes Presenting Author: XIUQING WEI Additional find more Authors: JIN TAO,

HONG TIAN, BIN WU Corresponding Author: XIUQING WEI Affiliations: The Third Affiliated Hospital of Sun Yat-Sen University; Third Affiliated Hospital, Sun Yat-Sen University; The Third Affiliated Hospital of Sun Yat-Sen University Objective: To introduce a rare cause of portal vein thrombosis and ascites. Methods: The medical course of a rare patient with portal vein thrombosis and ascites caused by idiopathic hypereosinophilic syndrome was presented in brief. Results: A 25-year old man had suffered from abdominal distention and ascites for one month. On physical examination, ascites was found. Hypereosinophilia was found by routine blood test without an identifiable underlying cause. An almost completed portal vein thrombosis was showed by ultrasound B examination and CT scan. The patient was prescribed high-dose corticosteroids and warfarin.