Older adults who undertake very limited activity, either because

Older adults who undertake very limited activity, either because of their type of work or the effect of musculoskeletal problems, may need only a very low dose or infrequent regimen. It is our practise to tailor

prophylaxis based on all available information and to regularly suggest that patient tries a new regimen. If a regimen buy PXD101 is changed, it is very important that a review takes place after 6–8 weeks, to establish whether any undesired events have occurred and also to give the patient confidence that the regimen can be adjusted again if problems have occurred. This review can often be carried out by a haemophilia specialist nurse by telephone or email supported by electronic web-based bleed reporting systems [25,26]. There is much current interest in FVIII/FIX concentrates with prolonged half-lives. These products have an obvious potential for allowing more convenient prophylaxis. It is important to recognize, however, that by prolonging the half-life the patient will spend longer with low factor levels and these will occur during the day and the night. It is possible that higher troughs may need to be maintained.

Alternatively, improved adherence may be an advantage of longer half-life products (Fig. 4). Clinical trials are underway to establish the effects of different products and regimens and the results are keenly awaited. Prophylaxis is the treatment of choice for people with severe haemophilia and the use of personalized

regimens is a logical extension to weight-based dosing. Introducing BGJ398 in vivo cost-effective low dose frequent regimens will help to make optimal therapy available to more people. PC has acted as a paid consultant for and received research support from Bayer, Baxter, Novo Nordisk and CSL Behring. “
“Joint destruction in early adulthood brings the patients to the orthopaedic clinics. If a haemophilic patient becomes disabled, it shows a number of factors such as timely diagnosis, availability of appropriate treatment depending on the country, access and affordability to treatments and equally importantly the responsibility of the patient in managing self care by remaining compliant by prescribed treatment regimen. We assessed the functional level by functional independence score in haemophilia (FISH). Overall, 104 patients with haemophilia A and 29 with haemophilia B MCE公司 were evaluated. We assessed the function of the patients by FISH. We divided the sum scores into weak (FISH score 8–16), moderate (17–24), and good (25–32). For evaluating the level of functional deficit in a 2 × 2 table, we categorized the weak and moderate levels into Disordered Group and the good level into Not-Disordered Group. The average age was 26.9 ± 14.24. Each 1 year increase in age can increase 1.07 fold the possibility of being placed in Disordered Function Group. Severe haemophilia can increase 7.34 fold, presence of inhibitor can increase 9.75 fold and home self-care increases 3.

Animals were allowed food and water ad

Animals were allowed food and water ad GSK2118436 datasheet libitum. All animals received humane care according to the criteria outlined in the Guide for the Care and Use of Laboratory Animals prepared by the National Academy of Sciences. Hepatocytes were isolated by adaptation of the calcium two-step collagenase perfusion technique as described.15, 17 Hepatocytes were plated on collagen-coated six-well plates

(BD Biosciences, San Jose, CA) at 250,000 cells/well. After the initial 2-hour attachment period, plating media was changed to either HGM complete with growth factors (+GF) HGF (supplemented at 40 ng/mL) and EGF (supplemented at 20 ng/mL) or without growth factors (−GF) and every 48 hours thereafter. Cells were harvested Birinapant clinical trial on day 0 (2-hour plated), 2, 4, 6, 8, and 10 for RNA and protein. Total RNA was extracted from plated cells using the RNABee

reagent (Invitrogen, Carlsbad, CA) according to the manufacturer’s protocol. The isolated RNA was treated with Turbo DNA-free (Ambion, Austin, TX) according to the manufacturer’s instructions. RNA was quantified by spectrophotometry at 260 nm and purity was assessed by optical density 260/280 ratio. The RNA was stored at −80°C. The experiment was repeated in three rats and their messenger RNA (mRNA) was pooled for further processing in primary hepatocytes as well as 70% partial hepatectomy (PHx) experiments. Four micrograms RNA per sample was reverse-transcribed using random hexamer to complementary DNA (cDNA) by using SuperScriptIII reverse transcriptase (Invitrogen, La Jolla, CA) according to the manufacturer’s protocol. A no reverse transcriptase (RT) control was also

included. The gene-specific primers used for rat were as follows. REST, cMyc, Klf4, Nanog (SuperArray Bioscience, Cat. no. PPR45101A, PPR45580A, PPR43919A, and PPR59663A, respectively). Oct4 forward: 5′-GGC GTT CTC TTT GCA AAG GTG TTC-3′; Oct4 reverse: 5′-CTC GAA CCA CAT CCT TCT CT-3′. Expression levels of REST, Oct4, cMyc, and Klf4 were determined by qRT-PCR using SYBR green and levels were normalized relative to expression of MCE cyclophilin in each sample. Fold change in gene expression was calculated by using the 2(−ΔΔCt) method.18 Reverse-transcribed samples were amplified in parallel on an ABI prism 7000 SDS instrument (Applied Biosystems, Foster City, CA). qRT-PCR for each sample was performed in triplicate in a 20-μL reaction with 50 ng of cDNA, 5 picomoles of each primer, and 1× SYBR green PCR mix (Applied Biosystems). The standard conditions for real-time PCR were as follows: 2 minutes at 50°C, 10 minutes at 95°C followed by 40 cycles of 15 seconds denaturation at 95°C, and elongation at 60°C for 45 seconds. A dissociation curve analysis was performed at the end of every run. A no RT and a no template control were also included in every run.

Animals were allowed food and water ad

Animals were allowed food and water ad AZD6738 research buy libitum. All animals received humane care according to the criteria outlined in the Guide for the Care and Use of Laboratory Animals prepared by the National Academy of Sciences. Hepatocytes were isolated by adaptation of the calcium two-step collagenase perfusion technique as described.15, 17 Hepatocytes were plated on collagen-coated six-well plates

(BD Biosciences, San Jose, CA) at 250,000 cells/well. After the initial 2-hour attachment period, plating media was changed to either HGM complete with growth factors (+GF) HGF (supplemented at 40 ng/mL) and EGF (supplemented at 20 ng/mL) or without growth factors (−GF) and every 48 hours thereafter. Cells were harvested NVP-BGJ398 on day 0 (2-hour plated), 2, 4, 6, 8, and 10 for RNA and protein. Total RNA was extracted from plated cells using the RNABee

reagent (Invitrogen, Carlsbad, CA) according to the manufacturer’s protocol. The isolated RNA was treated with Turbo DNA-free (Ambion, Austin, TX) according to the manufacturer’s instructions. RNA was quantified by spectrophotometry at 260 nm and purity was assessed by optical density 260/280 ratio. The RNA was stored at −80°C. The experiment was repeated in three rats and their messenger RNA (mRNA) was pooled for further processing in primary hepatocytes as well as 70% partial hepatectomy (PHx) experiments. Four micrograms RNA per sample was reverse-transcribed using random hexamer to complementary DNA (cDNA) by using SuperScriptIII reverse transcriptase (Invitrogen, La Jolla, CA) according to the manufacturer’s protocol. A no reverse transcriptase (RT) control was also

included. The gene-specific primers used for rat were as follows. REST, cMyc, Klf4, Nanog (SuperArray Bioscience, Cat. no. PPR45101A, PPR45580A, PPR43919A, and PPR59663A, respectively). Oct4 forward: 5′-GGC GTT CTC TTT GCA AAG GTG TTC-3′; Oct4 reverse: 5′-CTC GAA CCA CAT CCT TCT CT-3′. Expression levels of REST, Oct4, cMyc, and Klf4 were determined by qRT-PCR using SYBR green and levels were normalized relative to expression of MCE cyclophilin in each sample. Fold change in gene expression was calculated by using the 2(−ΔΔCt) method.18 Reverse-transcribed samples were amplified in parallel on an ABI prism 7000 SDS instrument (Applied Biosystems, Foster City, CA). qRT-PCR for each sample was performed in triplicate in a 20-μL reaction with 50 ng of cDNA, 5 picomoles of each primer, and 1× SYBR green PCR mix (Applied Biosystems). The standard conditions for real-time PCR were as follows: 2 minutes at 50°C, 10 minutes at 95°C followed by 40 cycles of 15 seconds denaturation at 95°C, and elongation at 60°C for 45 seconds. A dissociation curve analysis was performed at the end of every run. A no RT and a no template control were also included in every run.

The present study unveils

The present study unveils Luminespib solubility dmso the entire framework of the Fas-mediated signaling pathway in hepatocytes, placing the mitochondrial pathway of apoptosis as a potent loop for amplifying activation of the caspase cascade to execute complete and rapid cell death in hepatocytes. We thank Xiao-Ming Yin (Department of Pathology and Laboratory Medicine, Indiana University School of Medicine) for providing the anti-mouse Bid antibody. Additional Supporting Information may be found in the online version of this article. “
“Aim:  Previous studies evaluating the possibilities

of interspousal sexual transmission of hepatitis C virus (HCV) have yielded many conflicting results. The aim of this study was to clarify the source of HCV infection in acute hepatitis C patients using phylogenetic

analyses of nucleotide sequences of HCV E1 region. Methods:  Four acute hepatitis C patients were hospitalized in 2002–2007. The diagnosis was based on medical records, laboratory tests including HCV markers, and ultrasonographic examination of the liver. In each spouse of four patients, serum HCV antibody was assayed. In the subjects whose serum HCV antibody was positive, additional tests on HCV viral load and genotype were carried out. Then phylogenetic analyses of nucleotide sequences of partial HCV E1 region (440 nucleotides) of the patients and their spouses were performed. Results:  Hepatitis C virus antibody changed from negative to positive in the Venetoclax research buy course of hospitalization and HCV RNA could be detected in every patient. Therefore they were diagnosed as acute hepatitis caused by HCV infection. In every spouse of four patients, HCV antibody and HCV RNA were positive. Three of four couples had the identical genotype and homogeneity of nucleotide sequences of HCV E1

region in three couples ranged from 97.9% to 100%. The results of phylogenic analyses suggested that interspousal HCV infection occurred 上海皓元 in the three couples. Conclusion:  In conclusion, interspousal infection might be one of the important sources of acute HCV infection in Japan. The usefulness of phylogenetic analysis of nucleotide sequences of HCV E1 region for clarifying interspousal HCV infection was validated. “
“Now this is not the end. It is not even the beginning of the end. But it is, perhaps, the end of the beginning —Winston Churchill These are extraordinary times in the history of hepatitis C virus (HCV) drug development. We waited 13 years between the approval of ribavirin (RBV) in 1998 and the approval of telaprevir and boceprevir in 2011. The trajectory of drug discovery and clinical trials has gone from exponential to warp speed since the European Association for the Study of the Liver (EASL) meeting in April 2011, and two articles are perfect examples of what has changed the world of hepatitis C: interferon (IFN)-free combination therapy and, in one of the trials, eradication of the virus.

(Hepatology 2013; 58:1964–1976) Hepatocyte nuclear factor-4α (HNF

(Hepatology 2013; 58:1964–1976) Hepatocyte nuclear factor-4α (HNF4α), a member check details of the nuclear hormone receptor superfamily, is essential for the differentiation of the hepatic lineage and for maintaining the function of mature hepatocytes.[1-3] Loss of HNF4α expression is a critical event in the progression of hepatocellular carcinoma (HCC) and is inversely associated with HCC differentiation

status.[4, 5] A previous study from this laboratory demonstrated that up-regulating HNF4α could reverse the malignant phenotypes of HCC by inducing redifferentiation of HCC cells to hepatocytes.[6] We also demonstrated that HNF4α administration could attenuate liver fibrosis and block hepatocarcinogenesis in rats.[7, 8] Interestingly, a recent study by others reported that transient inhibition of HNF4α could initiate hepatocellular oncogenesis through a microRNA (miRNA)-inflammatory feedback circuit.[9] The imprinted delta-like 1 homolog R788 order (DLK1)-iodothyronine deiodinase 3 (DIO3) region on human chromosome 14q32 contains more than 60 miRNAs that are transcribed from only the maternal chromosome.[10] These miRNAs are organized into two clusters: one is between Meg3

and Meg8; the other (miR-379-656 cluster) is between Meg8 and miRNA containing gene (Mirg).[11, 12] A loss of the imprinted DLK1-DIO3 region results in developmental abnormalities and fetal lethality.[13] The degree of activation of this region is positively correlated with the pluripotency level of stem cells.[14, 15] The DLK1-DIO3 region is also a cancer susceptibility locus and dysregulation of the miRNAs in this region has been found in some human tumors.[16-18] Down-regulation of these miRNAs is regarded as a common molecular event in

carcinogenesis, especially in many kinds of epithelial malignancy.[19-22] However, several studies have reported increased expression of these miRNAs in acute promyelocytic leukemia (APL), endometrial carcinosarcomas, and invasive cervical cancer.[23-25] A report by Luk et al.[26] indicated that the DLK1-DIO3 miRNA cluster is up-regulated in a cohort of HCC patients with poor survival due to a change in imprinting status of the locus. In the present report, we demonstrate that HNF4α can induce transcription medchemexpress of the miR-379-656 cluster and that several miRNAs of this cluster exhibit inhibitory effects on HCC cells in vitro. We also show that miR-134, an miRNA in the miR-379-656 cluster, contributes to HNF4α-induced malignancy reversion by targeting KRAS. The recombinant AdHNF4α adenoviruses, expressing HNF4α or the AdGFP control, were constructed in our laboratory as described.[6] The human miR-134 gene was polymerase chain reaction (PCR)-amplified from Hep3B genomic DNA and cloned into the transfer plasmid, Adtrack-CMV. Homologous recombination with the AdEasy vector system and production of adenovirus AdmiR-134 were performed as described.

(Hepatology 2013; 58:1964–1976) Hepatocyte nuclear factor-4α (HNF

(Hepatology 2013; 58:1964–1976) Hepatocyte nuclear factor-4α (HNF4α), a member DMXAA datasheet of the nuclear hormone receptor superfamily, is essential for the differentiation of the hepatic lineage and for maintaining the function of mature hepatocytes.[1-3] Loss of HNF4α expression is a critical event in the progression of hepatocellular carcinoma (HCC) and is inversely associated with HCC differentiation

status.[4, 5] A previous study from this laboratory demonstrated that up-regulating HNF4α could reverse the malignant phenotypes of HCC by inducing redifferentiation of HCC cells to hepatocytes.[6] We also demonstrated that HNF4α administration could attenuate liver fibrosis and block hepatocarcinogenesis in rats.[7, 8] Interestingly, a recent study by others reported that transient inhibition of HNF4α could initiate hepatocellular oncogenesis through a microRNA (miRNA)-inflammatory feedback circuit.[9] The imprinted delta-like 1 homolog BIBW2992 molecular weight (DLK1)-iodothyronine deiodinase 3 (DIO3) region on human chromosome 14q32 contains more than 60 miRNAs that are transcribed from only the maternal chromosome.[10] These miRNAs are organized into two clusters: one is between Meg3

and Meg8; the other (miR-379-656 cluster) is between Meg8 and miRNA containing gene (Mirg).[11, 12] A loss of the imprinted DLK1-DIO3 region results in developmental abnormalities and fetal lethality.[13] The degree of activation of this region is positively correlated with the pluripotency level of stem cells.[14, 15] The DLK1-DIO3 region is also a cancer susceptibility locus and dysregulation of the miRNAs in this region has been found in some human tumors.[16-18] Down-regulation of these miRNAs is regarded as a common molecular event in

carcinogenesis, especially in many kinds of epithelial malignancy.[19-22] However, several studies have reported increased expression of these miRNAs in acute promyelocytic leukemia (APL), endometrial carcinosarcomas, and invasive cervical cancer.[23-25] A report by Luk et al.[26] indicated that the DLK1-DIO3 miRNA cluster is up-regulated in a cohort of HCC patients with poor survival due to a change in imprinting status of the locus. In the present report, we demonstrate that HNF4α can induce transcription medchemexpress of the miR-379-656 cluster and that several miRNAs of this cluster exhibit inhibitory effects on HCC cells in vitro. We also show that miR-134, an miRNA in the miR-379-656 cluster, contributes to HNF4α-induced malignancy reversion by targeting KRAS. The recombinant AdHNF4α adenoviruses, expressing HNF4α or the AdGFP control, were constructed in our laboratory as described.[6] The human miR-134 gene was polymerase chain reaction (PCR)-amplified from Hep3B genomic DNA and cloned into the transfer plasmid, Adtrack-CMV. Homologous recombination with the AdEasy vector system and production of adenovirus AdmiR-134 were performed as described.

She was therefore treated with oral prednisolone and later,

She was therefore treated with oral prednisolone and later,

azathioprine, for potential autoimmune enteropathy, and responded well clinically. Incidentally, during the gastroscopy, it was noted that the esophagus looked “off-color”, with multiple flat pigmented areas (Figure 1). Targeted biopsies showed melanin deposits in the dendritic cells of the basal portion of squamous epithelium and within the lamina propria (Figure 2—Masson-Fontana stain). Esophageal melanocytosis is a rare but benign condition, first described by De La Pava et al. in 1963. Its natural history is unknown, and some have suggested it may be a precursor of esophageal melanoma, although such transformation has never been reported. The esophagus does not normally contain melanocytes, but abberant migration from the neural crest may occur.

Ipatasertib Histologically, the condition is characterized by the presence learn more of increased numbers of melanocytes in the basal layer of esophageal squamous epithelium, and an increased quantity of melanin; immunohistochemistry shows staining for S100, melanin A, and HMB-45. In a recent review, only 34 cases were found in the literature, 21 of whom were Indians. However, melanocytes were identified in the esophagus in 4 to 7.7% of autopsies, suggesting only the extreme cases were detected endoscopically, seen in 0.07–0.15% of gastroscopies. The male to female ratio is approximately 2:1. Pigmentation tends to affect the mid- and lower-esophagus,

and usually appears black, but may be gray, brown, or blue. The esophagus is affected in a patchy manner, typically appearing as flat, oval or linear, irregularly delineated lesions. The etiology of the condition is poorly understood, but has been suggested to relate to chronic inflammation, such as chronic reflux esophagitis. It has been reported in association with a number of conditions, including Addision’s disease, Laugier-Hunziger syndrome, oral melanoma, and esophageal squamous cell carcinoma, as well as being present in up to 30% of patients with esophageal melanoma. Differential diagnoses include malignant melanoma, benign nevus (very rare, one case report only), anthracosis, exogenous dye ingestion, hemosiderosis, lipofuscin deposition, and necrosis. medchemexpress Due to the condition’s presumed benign course, neither treatment nor surveillance is currently indicated. Contributed by “
“We read with great interest the study by Falleti et al. in which the authors report that the rs7041 G>T and rs4588 C>A single nucleotide polymorphisms (SNPs) of the vitamin D-binding protein gene are predictors of the treatment outcome of patients with chronic hepatitis C.[1] The authors found that patients with any combination of three or more rs7041 G and rs4588 C alleles (wild type [WT+]) achieve a sustained virologic response (SVR) at a greater rate than patients with other genotypes (WT−).

Results: Of ninety (90) patients enrolled, 66 were male (733%) a

Results: Of ninety (90) patients enrolled, 66 were male (73.3%) and 24 were female (26.7%); majority with chronic hepatitis B. Sixty (66.7%) of the 90 patients were found to have large EV. The distribution of large EV according to CTP classification was as follows: A, 63.16%; B, 62.8% and C, 75%. Large EV was independently associated with total bilirubin higher than 1.9 mg/dL (p = 0.010), INR higher than 1.65 (p = 0.018), Decitabine in vivo and platelet count lower than 105,500/mm3 (p = 0.02). Platelet count lower

than 105,500/mm3 had the highest discriminative value for presence of large EV (sensitivity = 73.33%; specificity = 73.33%; area under receiver operating characteristics = 0.783). Conclusions: Large EV were found in 66.7% of patients with liver cirrhosis who underwent hospitalization. In patients with liver cirrhosis, the existence of thrombocytopenia may predict large EV which warrant prophylactic therapy. Key Word(s): 1. large esophageal varices; 2. liver cirrhosis; 3. platelets Presenting Author: R428 purchase LU CHIN HUANG Additional Authors: MING CHE LEE, YUNG HSIANG HSU Corresponding Author: LU CHIN HUANG Affiliations: Buddhist Tzu Chi General Hospital, Buddhist Tzu Chi General Hospital Objective: The patients who had simultaneous hepatocellular carcinoma and cholangiocarcinoma was not frequent. In order to investigate the

manifestations of patients with hepatocholangiocarcinoma, we performed this retrospective study. Methods: From August 1986 to April 2014, the 上海皓元医药股份有限公司 patients with diagnosis of hepatocholangiocarcinoma were included. The age,

gender, alpha fetoprorein (AFP), carbohydrate antigen 19-9 (CA 19-9), HBsAg and anti-HCV was recorded. The size, location of tumor, treatment, follow up duration and survival status was recorded. Results: A total of 10 patients (M 8, F2) were included. The average age was 58.1 years (49–71). The AFP was 38414 ng/mL (5.3–382000 ng/mL, normal <8.1), CA 19-9 was 378 IU/mL (25–1632 IU/mL, normal <37). Hepatitis B, hepatitis C infection rate was 50%, 30%. The size of tumor was 6.7 cm (2–13 cm). The location of tumor was right lobe 50%, left lobe 30%, and both lobes 20%. The treatments included surgery (2), surgery plus chemotherapy (2), surgery plus radiotherapy (2), transarterial chemoembolization (1), chemotherapy (1), and supportive care (2). The follow up duration was 10.6 months (1 month-2.6 years). The 3 months, 6 months, and 1 year survival rate was 90%, 70%, and 55.6%. Conclusion: 1. Hepatocholangiocarcinoma was not a frequent disease. We collected 10 patients in the past 27 years. 2. The average age was 58.1 years. 3. The average AFP was 38414 ng/mL. 4. Hepatitis B, hepatitis C infection rate was 50%, 30%. 5. The 6 months, and 1 year survival rate was 70% and 55.6%, respectively. Key Word(s): 1. hepatocholangiocarcinoma; 2.

Results: Of ninety (90) patients enrolled, 66 were male (733%) a

Results: Of ninety (90) patients enrolled, 66 were male (73.3%) and 24 were female (26.7%); majority with chronic hepatitis B. Sixty (66.7%) of the 90 patients were found to have large EV. The distribution of large EV according to CTP classification was as follows: A, 63.16%; B, 62.8% and C, 75%. Large EV was independently associated with total bilirubin higher than 1.9 mg/dL (p = 0.010), INR higher than 1.65 (p = 0.018), Wnt mutation and platelet count lower than 105,500/mm3 (p = 0.02). Platelet count lower

than 105,500/mm3 had the highest discriminative value for presence of large EV (sensitivity = 73.33%; specificity = 73.33%; area under receiver operating characteristics = 0.783). Conclusions: Large EV were found in 66.7% of patients with liver cirrhosis who underwent hospitalization. In patients with liver cirrhosis, the existence of thrombocytopenia may predict large EV which warrant prophylactic therapy. Key Word(s): 1. large esophageal varices; 2. liver cirrhosis; 3. platelets Presenting Author: www.selleckchem.com/products/Everolimus(RAD001).html LU CHIN HUANG Additional Authors: MING CHE LEE, YUNG HSIANG HSU Corresponding Author: LU CHIN HUANG Affiliations: Buddhist Tzu Chi General Hospital, Buddhist Tzu Chi General Hospital Objective: The patients who had simultaneous hepatocellular carcinoma and cholangiocarcinoma was not frequent. In order to investigate the

manifestations of patients with hepatocholangiocarcinoma, we performed this retrospective study. Methods: From August 1986 to April 2014, the MCE公司 patients with diagnosis of hepatocholangiocarcinoma were included. The age,

gender, alpha fetoprorein (AFP), carbohydrate antigen 19-9 (CA 19-9), HBsAg and anti-HCV was recorded. The size, location of tumor, treatment, follow up duration and survival status was recorded. Results: A total of 10 patients (M 8, F2) were included. The average age was 58.1 years (49–71). The AFP was 38414 ng/mL (5.3–382000 ng/mL, normal <8.1), CA 19-9 was 378 IU/mL (25–1632 IU/mL, normal <37). Hepatitis B, hepatitis C infection rate was 50%, 30%. The size of tumor was 6.7 cm (2–13 cm). The location of tumor was right lobe 50%, left lobe 30%, and both lobes 20%. The treatments included surgery (2), surgery plus chemotherapy (2), surgery plus radiotherapy (2), transarterial chemoembolization (1), chemotherapy (1), and supportive care (2). The follow up duration was 10.6 months (1 month-2.6 years). The 3 months, 6 months, and 1 year survival rate was 90%, 70%, and 55.6%. Conclusion: 1. Hepatocholangiocarcinoma was not a frequent disease. We collected 10 patients in the past 27 years. 2. The average age was 58.1 years. 3. The average AFP was 38414 ng/mL. 4. Hepatitis B, hepatitis C infection rate was 50%, 30%. 5. The 6 months, and 1 year survival rate was 70% and 55.6%, respectively. Key Word(s): 1. hepatocholangiocarcinoma; 2.

Results: Of ninety (90) patients enrolled, 66 were male (733%) a

Results: Of ninety (90) patients enrolled, 66 were male (73.3%) and 24 were female (26.7%); majority with chronic hepatitis B. Sixty (66.7%) of the 90 patients were found to have large EV. The distribution of large EV according to CTP classification was as follows: A, 63.16%; B, 62.8% and C, 75%. Large EV was independently associated with total bilirubin higher than 1.9 mg/dL (p = 0.010), INR higher than 1.65 (p = 0.018), Everolimus clinical trial and platelet count lower than 105,500/mm3 (p = 0.02). Platelet count lower

than 105,500/mm3 had the highest discriminative value for presence of large EV (sensitivity = 73.33%; specificity = 73.33%; area under receiver operating characteristics = 0.783). Conclusions: Large EV were found in 66.7% of patients with liver cirrhosis who underwent hospitalization. In patients with liver cirrhosis, the existence of thrombocytopenia may predict large EV which warrant prophylactic therapy. Key Word(s): 1. large esophageal varices; 2. liver cirrhosis; 3. platelets Presenting Author: GSK1120212 concentration LU CHIN HUANG Additional Authors: MING CHE LEE, YUNG HSIANG HSU Corresponding Author: LU CHIN HUANG Affiliations: Buddhist Tzu Chi General Hospital, Buddhist Tzu Chi General Hospital Objective: The patients who had simultaneous hepatocellular carcinoma and cholangiocarcinoma was not frequent. In order to investigate the

manifestations of patients with hepatocholangiocarcinoma, we performed this retrospective study. Methods: From August 1986 to April 2014, the 上海皓元医药股份有限公司 patients with diagnosis of hepatocholangiocarcinoma were included. The age,

gender, alpha fetoprorein (AFP), carbohydrate antigen 19-9 (CA 19-9), HBsAg and anti-HCV was recorded. The size, location of tumor, treatment, follow up duration and survival status was recorded. Results: A total of 10 patients (M 8, F2) were included. The average age was 58.1 years (49–71). The AFP was 38414 ng/mL (5.3–382000 ng/mL, normal <8.1), CA 19-9 was 378 IU/mL (25–1632 IU/mL, normal <37). Hepatitis B, hepatitis C infection rate was 50%, 30%. The size of tumor was 6.7 cm (2–13 cm). The location of tumor was right lobe 50%, left lobe 30%, and both lobes 20%. The treatments included surgery (2), surgery plus chemotherapy (2), surgery plus radiotherapy (2), transarterial chemoembolization (1), chemotherapy (1), and supportive care (2). The follow up duration was 10.6 months (1 month-2.6 years). The 3 months, 6 months, and 1 year survival rate was 90%, 70%, and 55.6%. Conclusion: 1. Hepatocholangiocarcinoma was not a frequent disease. We collected 10 patients in the past 27 years. 2. The average age was 58.1 years. 3. The average AFP was 38414 ng/mL. 4. Hepatitis B, hepatitis C infection rate was 50%, 30%. 5. The 6 months, and 1 year survival rate was 70% and 55.6%, respectively. Key Word(s): 1. hepatocholangiocarcinoma; 2.