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( Dae Hoe Gu ),( Min Seon Park ),( Tae Jung Yun ),( Seok Bae Yoon ),( Sun Young Yim ),( Jin Yong Jung ),( Jin Dong Kim ),( Yeon Seok Seo ),( Hyung Joon Yim ),( Soon Ho Um ),( Ho Sang Ryu ),( Yun Ji Pa 대한간학회 2013 춘·추계 학술대회 (KASL) Vol.2013 No.1
Background: The use of antiviral agent has changed the prognosis of patients with hepatitis B virus (HBV)-related end stage liver disease. In these patients, therefore, a more efficient prognostic model for determining early mortality is necessary to properly select those who require liver transplantation. In this study, we aimed to develop a new prognostic model. Methods: We retrospectively analyzed a total of consecutive 194 patients with decompensated HBV-related liver cirrhosis (≥CTP score 7, ascites, or jaundice) who had initially started antiviral treatment in Korea university Anam hospital. Univariate and multivariate cox-regression modeling was used to develop a model for predicting 6-month mortality Results: The study population was predominantly male (128/194) and median age was 51 years. Antiviral agents were administered for a median of 41 months (lamivudine in 157 patients, entecavir in 37). At baseline 147 and 12 patients had ascites and encephalopathy, respectively, with a mean CTP score of 9. Twenty-one (10.8%) patients died within the first 6 months of treatment. Univariate analysis revealed that baseline variables such as age, the presence of ascites or encephalopathy, serum bilirubin, prothrombin time, albumin, Na, BUN, alkaline phosphatase, and HBV DNA levels were associated with the deaths within 6-months (all P<0.05). Among them serum bilirubin, prothrombin time, HBV DNA levels and age were found to be independent risk factors in multivariate analysis. Using these four risk factors, we developed new scoring system to predict 6-months mortality. This new prediction model showed AUROC of 0.941, higher than those of CTP score and MELD score which were 0.893 and 0.862, respectively. Conclusions: This newly developed prediction model for early mortality will be useful in selecting the candidates of urgent liver transplantation in patients with decompensated HBV-related liver cirrhosis.
( Min Seon Park ),( Dae Hoe Gu ),( Tae Jung Yun ),( Seok Bae Yoon ),( Sun Young Yim ),( Jin Yong Jung ),( Jin Dong Kim ),( Yeon Seok Seo ),( Hyung Joon Yim ),( Soon Ho Um ),( Ho Sang Ryu ),( Yun Ji Pa 대한간학회 2013 춘·추계 학술대회 (KASL) Vol.2013 No.1
Background: The roadmap concept is the treatment strategy in chronic hepatitis B for switching the antiviral drug based on early virologic response. We applied this concept to telbivudine therapy. The aim of this study was to evaluate the efficacy of telbivudine based response guided treatment compared with entecavir monotherapy in chronic hepatitis B hepatitis patients. Methods: We included 261 consecutive patients with previously untreated chronic hepatitis B in two treatment groups : entecavir monotherapy group (n=159) and telbivudine based response guided treatment group (n=102). The telbivudine group was then divided into two subgroups depending on whether to switch entecavir based on the serum hepatitis B virus (HBV) DNA level(>20 IU/mL or not) after 6 months of treatment. Serial HBV DNA level ware checked at baseline and every 3month. Results: A total of 261 patients were enrolled in this study: 159 men and 102 women, with mean age of 47.2 years. The baseline demographics and characteristics associated underlying liver disease in the 2 treatment groups were well balanced. Among 102 patients on telbivudine, 65 had undetectable HBV DNA after 6 months and continued telbivudine monotherapy. 37 had incomplete virological response and they switched to entecavir monotherapty at 6 months. Cumulative virological response rates (75.0% vs. 73.2% at 12 months, P=0.507) and cumulative biochemical response rate (77.3% vs. 87.4%, P=0.066) were not significantly different between telbivudine based response guided treatment group and entecavir monotherapy group. However, cumulative viral breakthrough developed only in telbivudine based response-guided treatment group (12% vs. 0% at 24 months, P=0.000). Conclusions: This study showed that telbivudine based response- guided antiviral treatment in patients with chronic hepatitis B did not suppress virologic breakthrough compared to entecavir monotherapy from the beginning of treatment.
Park, Jun-Gyu,Kim, Hyun-Jeong,Matthijnssens, Jelle,Alfajaro, Mia Madel,Kim, Deok-Song,Son, Kyu-Yeol,Kwon, Hyoung-Jun,Hosmillo, Myra,Ryu, Eun-Hye,Kim, Ji-Yun,Cena, Rohani B,Lee, Ju-Hwan,Kang, Mun-Il,Pa BioMed Central 2013 Veterinary research Vol.44 No.-
<P>Direct interspecies transmissions of group A rotaviruses (RVA) have been reported under natural conditions. However, the pathogenicity of RVA has never been directly compared in homologous and heterologous hosts. The bovine RVA/Cow-tc/KOR/K5/2004/G5P[7] strain, which was shown to possess a typical porcine-like genotype constellation similar to that of the G5P[7] prototype RVA/Pig-tc/USA/OSU/1977/G5P9[7] strain, was examined for its pathogenicity and compared with the porcine G5P[7] RVA/Pig-tc/KOR/K71/2006/G5P[7] strain possessing the same genotype constellation. The bovine K5 strain induced diarrhea and histopathological changes in the small intestine of piglets and calves, whereas the porcine K71 strain caused diarrhea and histopathological changes in the small intestine of piglets, but not in calves. Furthermore, the bovine K5 strain showed extra-intestinal tropisms in both piglets and calves, whereas the porcine K71 strain had extra-intestinal tropisms in piglets, but not in calves. Therefore, we performed comparative genomic analysis of the K71 and K5 RVA strains to determine whether specific mutations could be associated with these distinct clinical and pathological phenotypes. Full-length sequencing analyses for the 11 genomic segments for K71 and K5 revealed that these strains were genetically nearly identical to each other. Two nucleotide mutations were found in the 5′ untranslated region (UTR) of NSP5 and the 3′ UTR of NSP3, and eight amino acid mutations in VP1-VP4 and NSP2. Some of these mutations may be critical molecular determinants for RVA virulence and/or pathogenicity.</P>