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Our study aims to examine the association between serum ferritin levels and NAFLD in Korean population. A total of 25,597 participants were selected from Korean National Health and Nutritional Examination Surveys 2007–2012. The NAFLD liver fat score (NLFS) was used to define NAFLD. Elevation of ALT levels was defined as ALT level > 40 IU\u002FL for male and ALT level > 31 IU\u002FL for female. Multiple logistic regression was used to examine the association of serum ferritin levels and NAFLD by sex. After adjusting for multiple covariates, the ORs (95% CI) of the elevated ALT levels were 1.56 (95% CI: 1.17–2.07), 1.84 (95% CI: 1.39–2.45), and 4.08 (95% CI: 3.08–5.40) for the second, third and fourth serum ferritin quartiles in male (p for trend \u003C 0.01), 1.67 (95% CI: 1.24–2.23), 2.23 (95% CI: 1.68–2.96), and 5.72 (95% CI: 4.32–7.60) for the second, third and fourth serum ferritin quartiles in female (p for trend \u003C 0.01). Serum ferritin levels were also significantly associated with NAFLD and liver fibrosis both in male and female. Elevation of serum ferritin level is significantly associated with NAFLD and blood ALT elevation in Korean general population.",{"EN":167,"VI":168},"Serum ferritin level is associated with liver steatosis and fibrosis in Korean general population","Nồng độ ferritin huyết thanh liên quan với tình trạng nhiễm mỡ và xơ hóa gan ở dân số chung Hàn Quốc",{"VOID":170},"Fan JG, Farrell GC. Epidemiology of non-alcoholic fatty liver disease in China. J Hepatol 2009;50:204–210\nAscha MS, Hanouneh IA, Lopez R, et al. The incidence and risk factors of hepatocellular carcinoma in patients with nonalcoholic steatohepatitis. Hepatology 2010;51:1972–1878\nOng JP, Pitts A, Younossi ZM. Increased overall mortality and liver-related mortality in non-alcoholic fatty liver disease. J Hepatol 2008;49:608–612\nYamada T, Fukatsu M, Suzuki S, et al. Fatty liver predicts impaired fasting glucose and type 2 diabetes mellitus in Japanese undergoing a health checkup. J Gastroenterol Hepatol 2010;25:352–356\nTargher G, Bertolini L, Padovani R, et al. Relations between carotid artery wall thickness and liver histology in subjects with nonalcoholic fatty liver disease. Diabetes Care 2006;29:1325–1330\nTargher G, Bertolini L, Padovani R, et al. Prevalence of nonalcoholic fatty liver disease and its association with cardiovascular disease among type 2 diabetic patients. Diabetes Care 2007;30:1212–1218\nLazo M, Hernaez R, Eberhardt MS, et al. Prevalence of nonalcoholic fatty liver disease in the United States: the Third National Health and Nutrition Examination Survey, 1988–1994. Am J Epidemiol 2013;178:38–45\nPark SH, Jeon WK, Kim SH, et al. Prevalence and risk factors of non-alcoholic fatty liver disease among Korean adults. J Gastroenterol Hepatol 2006;21:138–143\nLoomba R, Sanyal AJ. The global NAFLD epidemic. Nat Rev Gastroenterol Hepatol 2013;10:686–690\nYounossi ZM, Stepanova M, Afendy M, et al. Changes in the prevalence of the most common causes of chronic liver diseases in the United States from 1988 to 2008. Clin Gastroenterol Hepatol 2011;9:524–530\nValenti L, Dongiovanni P, Fracanzani AL, et al. Increased susceptibility to nonalcoholic fatty liver disease in heterozygotes for the mutation responsible for hereditary hemochromatosis. Dig Liver Dis 2003;35:172–178\nNelson JE, Bhattacharya R, Lindor KD, et al. HFE C282Y mutations are associated with advanced hepatic fibrosis in Caucasians with nonalcoholic steatohepatitis. Hepatology 2007;46:723–729\nKim CW, Chang Y, Sung E, et al. Serum ferritin levels predict incident non-alcoholic fatty liver disease in healthy Korean men. Metabolism 2012;61:1182–1188\nKowdley KV, Belt P, Wilson LA, et al. Serum ferritin is an independent predictor of histologic severity and advanced fibrosis in patients with nonalcoholic fatty liver disease. Hepatology 2012;55:77–85\nFracanzani AL, Valenti L, Bugianesi E, et al. Risk of nonalcoholic steatohepatitis and fibrosis in patients with nonalcoholic fatty liver disease and low visceral adiposity. J Hepatol 2011;54:1244–1249\nOh CM, Oh IH, Lee JK, et al. Blood cadmium levels are associated with a decline in lung function in males. Environ Res 2014;132:119–125\nRyu SY, Crespi CM, Maxwell AE. Drinking patterns among Korean adults: results of the 2009 Korean community health survey. J Prev Med Public Health 2013;46:183–191\nHaskell WL, Lee IM, Pate RR, et al. Physical activity and public health: updated recommendation for adults from the American College of Sports Medicine and the American Heart Association. Circulation 2007;116:1081–1093\nFleming RE, Ponka P. Iron overload in human disease. N Engl J Med 2012;366:348–359\nGrundy SM, Cleeman JI, Daniels SR, et al. Diagnosis and management of the metabolic syndrome: an American Heart Association\u002FNational Heart, Lung, and Blood Institute Scientific Statement. Circulation 2005;112:2735–2752\nOh SW. Obesity and metabolic syndrome in Korea. Diabetes Metab J 2011;35:561–566\nKotronen A, Peltonen M, Hakkarainen A, et al. Prediction of non-alcoholic fatty liver disease and liver fat using metabolic and genetic factors. Gastroenterology 2009;137:865–872\nLee JH, Kim D, Kim HJ, et al. Hepatic steatosis index: a simple screening tool reflecting nonalcoholic fatty liver disease. Dig Liver Dis 2010;42:503–508\nSterling RK, Lissen E, Clumeck N, et al. Development of a simple noninvasive index to predict significant fibrosis in patients with HIV\u002FHCV coinfection. Hepatology 2006;43:1317–1325\nEguchi Y, Hyogo H, Ono M, et al. Prevalence and associated metabolic factors of nonalcoholic fatty liver disease in the general population from 2009 to 2010 in Japan: a multicenter large retrospective study. J Gastroenterol 2012;47:586–595\nCleophas TJ, Zwinderman AH. Statistics applied to clinical studies. 5th ed. New York: Springer; 2012. p. 313–318\nPark SK, Ryoo JH, Kim MG, et al. Association of serum ferritin and the development of metabolic syndrome in middle-aged Korean men: a 5-year follow-up study. Diabetes Care 2012;35:2521–2526\nKim CH, Kim HK, Bae SJ, et al. Association of elevated serum ferritin concentration with insulin resistance and impaired glucose metabolism in Korean men and women. Metabolism 2011;60:414–420\nUtzschneider KM, Kahn SE. Review: the role of insulin resistance in nonalcoholic fatty liver disease. J Clin Endocrinol Metab 2006;91:4753–4761\nLing JC, Mohamed MN, Jalaludin MY, et al. Determinants of high fasting insulin and insulin resistance among overweight\u002Fobese adolescents. Sci Rep 2016;6:36270\nO’Malley G, Santoro N, Northrup V, et al. High normal fasting glucose level in obese youth: a marker for insulin resistance and beta cell dysregulation. Diabetologia 2010;53:1199–1209\nAlam F, Memon AS, Fatima SS. Increased body mass index may lead to hyperferritinemia irrespective of body iron stores. 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Safety and efficacy of elbasvir\u002Fgrazoprevir in patients with hepatitis C virus infection and compensated cirrhosis: an integrated analysis. Gastroenterology 2017;152(1372–82): e2",{"doi":1877},{"id":1873,"text":1904,"url":1875,"identifiers":1905},"Forns X, Lee SS, Valdes J, et al. Glecaprevir plus pibrentasvir for chronic hepatitis C virus genotype 1, 2, 4, 5, or 6 infections in adults with compensated cirrhosis (EXPEDITION-1): a single-arm, open-label, multicentre phase 3 trial. Lancet Infect Dis 2017;17:1062–1068",{"doi":1877},{"id":1873,"text":1907,"url":1875,"identifiers":1908},"Gane E, Poordad F, Zadeikis N, et al. Safety and pharmacokinetics of glecaprevir\u002Fpibrentasvir in adults with chronic genotype 1–6 hepatitis C virus infections and compensated liver disease. Clin Infect Dis 2019;69(10):1657–1664",{"doi":1877},{"id":1873,"text":1910,"url":1875,"identifiers":1911},"Maan R, van Tilborg M, Deterding K, et al. Safety and effectiveness of direct-acting antiviral agents for treatment of patients with chronic hepatitis C Virus infection and cirrhosis. Clin Gastroenterol Hepatol 2016;14(12):1821-1830.e6",{"doi":1877},{"id":20,"text":1913,"url":1914,"identifiers":1915},"Torgersen J, Newcomb CW, Carbonari DM, et al. Protease inhibitor-based direct-acting antivirals are associated with increased risk of aminotransferase elevations but not hepatic dysfunction or decompensation. J Hepatol 2021;75(6):1312–1322. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jhep.2021.07.021","https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jhep.2021.07.021",{"mag":1916,"pmc":1917,"openalex":1918,"pm":1919,"doi":1920},"3186867689","8604762","W3186867689","34333102","10.1016\u002Fj.jhep.2021.07.021",{"id":20,"text":1922,"url":1923,"identifiers":1924},"Berkan-Kawińska A, Piekarska A, Janczewska E, et al. Real-world effectiveness and safety of direct-acting antivirals in patients with cirrhosis and history of hepatic decompensation: Epi-Ter2 Study. Liver Int 2021;41(8):1789–1801. https:\u002F\u002Fdoi.org\u002F10.1111\u002Fliv.14858","https:\u002F\u002Fdoi.org\u002F10.1111\u002Fliv.14858",{"mag":1925,"openalex":1926,"pm":1927,"doi":1928},"3135822269","W3135822269","33655628","10.1111\u002Fliv.14858",{"id":20,"text":1930,"url":1931,"identifiers":1932},"Wong YJ, Nguyen MH. Is it safe to treat chronic hepatitis C patients with decompensated cirrhosis with protease inhibitor-based DAA? J Hepatol 2022;S0168–8278(22):00008–00013. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jhep.2021.12.037","http:\u002F\u002Fdx.doi.org\u002F10.1016\u002Fj.jhep.2021.12.037",{"doi":1933},"10.1016\u002Fj.jhep.2021.12.037",{"id":20,"text":1935,"url":1931,"identifiers":1936},"Wong YJ, Nguyen MH. Is it safe to treat chronic hepatitis C patients with decompensated cirrhosis with protease inhibitor-based DAA? Liver Int 2022. https:\u002F\u002Fdoi.org\u002F10.1111\u002Fliv.15214.10.1111\u002Fliv.15214",{"doi":1937},"10.1111\u002Fliv.15214.10.1111\u002Fliv.15214",{"id":20,"text":1939,"url":1940,"identifiers":1941},"Tanaka Y, Ogawa E, Huang CF, et al. HCC risk post-SVR with DAAs in East Asians: findings from the REAL-C cohort. Hepatol Int 2020;14(6):1023–1033. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs12072-020-10105-2","https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs12072-020-10105-2",{"mag":1942,"openalex":1943,"pm":1944,"doi":1945},"3109593593","W3109593593","33277685","10.1007\u002Fs12072-020-10105-2",{"id":1947,"text":1948,"url":1949,"identifiers":1950},"1ba212a2-9bf6-430c-b651-6d3396d67211","Verna EC, Morelli G, Terrault NA, et al. DAA therapy and long-term hepatic function in advanced\u002Fdecompensated cirrhosis: Real-world experience from HCV-TARGET cohort. J Hepatol 2020;73(3):540–548. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jhep.2020.03.031","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002FS0168827820301938",{"doi":1951},"10.1016\u002Fj.jhep.2020.03.031",{"id":20,"text":1953,"url":1954,"identifiers":1955},"Chesnaye NC, Stel VS, Tripepi G, et al. An introduction to inverse probability of treatment weighting in observational research. Clin Kidney J 2021;15(1):14–20. https:\u002F\u002Fdoi.org\u002F10.1093\u002Fckj\u002Fsfab158","https:\u002F\u002Fdoi.org\u002F10.1093\u002Fckj\u002Fsfab158",{"mag":1956,"openalex":1957,"pm":1958,"doi":1959},"3205211596","W3205211596","35035932","10.1093\u002Fckj\u002Fsfab158",{"id":1873,"text":1961,"url":1875,"identifiers":1962},"Hosmer DW, Hosmer T, Le Cessie S, Lemeshow S. A comparison of goodness-of-ft. tests for the logistic regression model. Stat Med 1997;16:965–980",{"doi":1877},{"id":1873,"text":1964,"url":1875,"identifiers":1965},"D’Amico G, Morabito A, D’Amico M, Pasta L, Malizia G, Rebora P, et al. Clinical states of cirrhosis and competing risks. J Hepatol 2018;68(3):563–576",{"doi":1877},{"id":1873,"text":1967,"url":1875,"identifiers":1968},"Curry MP, Oleary JG, Bzowej N, Muir AJ, Korenblat KM, Fenkel JM, et al. Sofosbuvir and velpatasvir for HCV in patients with decompensated cirrhosis. N Engl J Med 2015;373(27):2618–2628",{"doi":1877},{"id":1873,"text":1970,"url":1875,"identifiers":1971},"Welzel TM, Petersen J, Herzer K, Ferenci P, Gschwantler M, Wedemeyer H, et al. Daclatasvir plus sofosbuvir, with or without ribavirin, achieved high sustained virological response rates in patients with HCV infection and advanced liver disease in a real-world cohort. Gut 2016;65(11):1861–1870",{"doi":1877},{"id":1973,"createTime":1974,"updateTime":1975,"relativeEntities":1976,"slug":1977,"properties":1978,"entityType":173,"verifyStatus":174,"verifyTime":1987,"verifyNote":176,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":1988,"fullTextUrl":20,"authors":1989,"publicationType":360,"publisherRelationship":2292,"citationCount":21,"citationInfo":2339,"publishDate":2341,"publishYear":1865,"citationAnalyzeStatus":1868,"lastCitationAnalyze":1975,"indexDatabases":2342,"openAccess":20,"references":2343,"isForceReanalyzing":412},"313658b3-06a5-440c-802a-5d0b88c7ec62","2024-01-19T23:56:09.218+00:00","2026-08-17T04:12:04.435+00:00",[],"3D-automatic-liver-and-spleen-assessment-in-predicting-overt-hepatic-encephalopathy-before-TIPS-a-multi-center-study",{"abstract":1979,"title":1981,"gsPaper":1983,"doi":1985},{"EN":1980},"Overt hepatic encephalopathy (HE) should be predicted preoperatively to identify suitable candidates for transjugular intrahepatic portosystemic shunt (TIPS) instead of first-line treatment. This study aimed to construct a 3D assessment-based model to predict post-TIPS overt HE. In this multi-center cohort study, 487 patients who underwent TIPS were subdivided into a training dataset (390 cases from three hospitals) and an external validation dataset (97 cases from another two hospitals). Candidate factors included clinical, vascular, and 2D and 3D data. Combining the least absolute shrinkage and operator method, support vector machine, and probability calibration by isotonic regression, we constructed four predictive models: clinical, 2D, 3D, and combined models. Their discrimination and calibration were compared to identify the optimal model, with subgroup analysis performed. The 3D model showed better discrimination than did the 2D model (training: 0.719 vs. 0.691; validation: 0.730 vs. 0.622). 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Comput Biol Med. 2016;78:49–57","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002FS0010482516302372",{"doi":2454},"10.1016\u002Fj.compbiomed.2016.09.011",{"id":2456,"createTime":2457,"updateTime":2458,"relativeEntities":2459,"slug":2460,"properties":2461,"entityType":173,"verifyStatus":174,"verifyTime":2472,"verifyNote":176,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":2473,"fullTextUrl":20,"authors":2474,"publicationType":360,"publisherRelationship":2516,"citationCount":21,"citationInfo":2564,"publishDate":2567,"publishYear":2565,"citationAnalyzeStatus":2568,"lastCitationAnalyze":2569,"indexDatabases":2570,"openAccess":20,"references":20,"isForceReanalyzing":412},"ec6429e2-4cea-4d04-8166-c42bcb1240ac","2024-01-26T19:50:16.283+00:00","2026-07-28T16:51:46.564+00:00",[],"Twist-in-hepatocellular-carcinoma-pathophysiology-and-therapeutics",{"abstract":2462,"title":2464,"gsPaper":2466,"references":2468,"doi":2470},{"EN":2463},"Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related disease worldwide. Although HCC is mainly associated with viral hepatitis and alcoholic cirrhosis, numerous physiological and biochemical events are associated with HCC progression. The transcription factor Twist, which plays a key role in epithelial to mesenchymal transition, is reported to be associated with HCC. Overexpression of Twist causes various biochemical changes, such as increase of cell proliferation, reduction of apoptosis, cell cycle deregulation, generation of hepatic cancer stem cells, and in some cases, drug resistance. These changes result in various physiological changes, such as angiogenesis, cellular migration and invasion, and vasculogenic mimicry, which ultimately causes hepatocellular metastasis. Interestingly, targeting Twist via different strategies, especially small RNA technology, has shown promising therapeutic potential for future HCC treatment.",{"EN":2465},"Twist in hepatocellular carcinoma: pathophysiology and therapeutics",{"VOID":2467},"[\"10570094221334417973\"]",{"VOID":2469},"Jemal A, Bray F, Center MM, Ferlay J, Ward E, Forman D. CA Cancer J Clin. 2011;61(2):69–90\nMaluccio M, Covey A. Recent progress in understanding, diagnosing, and treating hepatocellular carcinoma. CA Cancer J Clin. 2012;62(6):394–399\nRobins SL, Cotran RS. Neoplasia. In: Kumar V, Abbas AK, Fausto N, editors. Pathologic Basis of Disease. 7th ed. India: Thomson; 2009. 292–306\nChen CJ, Yang HI, Su J, Jen CL, You SL, Lu SN, et al. Risk of hepatocellular carcinoma across a biological gradient of serum hepatitis B virus DNA level. JAMA. 2006;295(1):65–73\nTania M, Khan MA, Fu J. Epithelial to mesenchymal transition inducing transcription factors and metastatic cancer. 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Ann Surg Oncol. 2013;20(Suppl 3):S625–S635",{"VOID":2471},"10.1007\u002Fs12072-015-9634-0","2024-09-13T09:03:23.019+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs12072-015-9634-0",[2475,2490,2503],{"id":2476,"sortIndex":21,"researcher":20,"roles":2477,"affiliations":2478,"properties":2487,"displayName":2489,"givenName":20,"familyName":20},"3b7029f6-3d34-400b-808e-2b276ac911e5",[184],[2479],{"id":2480,"sortIndex":21,"affiliation":2481,"properties":20},"06f3d822-bb80-429c-9b8d-2ddfb7c4916f",{"id":2480,"createTime":20,"updateTime":20,"relativeEntities":2482,"slug":20,"properties":2483,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2486,"statistic":20},[],{"title":2484},{"VI":2485},"Medical College Affiliated to Hunan Normal University, Changsha, China",[],{"title":2488},{"VI":2489},"Hui 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safety of nucleos(t)ide analogue (NA) treatment cessation remains one of the most controversial topics in the management of chronic hepatitis B (CHB) patients. This study investigated the efficiency of 48-week pegylated-interferon (peg-IFN) alfa-2a consolidation therapy on viral relapse after discontinued NA treatment in CHB patients who achieved hepatitis B e antigen (HBeAg) seroconversion for > 1 year. NA-treated HBeAg-positive patients who achieved the standard of discontinued NA treatment (i.e. time of HBeAg seroconversion > 1 year) were randomly assigned to receive peg-IFN consolidation (n = 24) treatment or continue original NA therapy (n = 24) for 48 weeks. The treatments were then discontinued, and the patients were observed up to 144 weeks. The primary endpoint was the proportion of patients with viral relapse at week 144 among those who received at least one dose of study drug or had at least one study visit [modified intention-to-treat population (mITT)]. Of the 24 patients who received peg-IFN treatment, 6 (25%) experienced viral relapse and 8 (36.3%) showed HBsAg loss during 96 weeks of treatment-free follow-up. Of the patients who underwent NA consolidation treatment, only 1 (4.3%) of 23 patients showed HBsAg loss and 14 (58.3%) of 24 patients experienced viral relapse during follow-up. HBsAg level decline \u003C 0.25 log10 IU\u002FmL at week 96 was significantly associated with viral relapse. A 48-week peg-IFN alfa-2a consolidation therapy increased the rate of HBsAg loss and sustained viral replication suppression in HBeAg-positive patients who achieved HBeAg seroconversion for > 1 year after NA treatment discontinuation.",{"EN":2581},"Pegylated-interferon consolidation treatment versus nucleos(t)ide analogue consolidation treatment in non-cirrhotic hepatitis B patients with hepatitis B e antigen seroconversion: an open-label pilot trial",{"VOID":2583},"[]",{"VOID":2585},"European Association for the Study of the Liver. EASL clinical practice guidelines: management of hepatitis B virus infection. J Hepatol. 2017;67:370–98.\nLiaw YF, Kao JH, Piratvisuth T, Chan HL, Chien RN, Liu CJ, et al. Asian-Pacificconsensus statement on the management of chronic hepatitis B: a 2012 update. Hepatol Int. 2012;6:531–61.\nLok A, McMahon B. Chronic hepatitis B. Hepatology. 2007;45:507–39.\nYuen MF, Wong DK, Fung J, Ip P, But D, Hung I, et al. HBsAg seroclearance in chronic hepatitis B in Asian patients: replicative level and risk of hepatocellular carcinoma. Gastroenterology. 2008;135:1192–9.\nHan Meifang, Jiang Jiaji, Hou Jinlin, Tan Deming, Sun Yongtao, Zhao Mianzhi, et al. Sustained immune control in HbeAg positive patients who switched from entecavir therapy to pegylated interferon-2a:1 year follow-up of the OSST study. Antiviral Therapy. 2016;21:337–44.\nTerrault NA, Bzowej NH, Chang KM, Hwang JP, Jonas MM, Murad MH. AASLD guidelines for treatment of chronic hepatitis B. Hepatology. 2016;63:261.\nSarin SK, Kumar M, Lau GK, Abbas Z, Chan HL, Chen CJ, et al. Asian-Pacific clinical practice guidelines on the management of hepatitis B: a 2015 update. Hepatol Int. 2016;10:1–98.\nYeh CT, Hsu CW, Chen YC, Liaw YF. Withdrawal of lamivudine in HBeAg-positive chronic hepatitis B patients after achieving effective maintained virological suppression. J Clin Virol. 2009;45:114–8.\nChaung KT, Ha NB, Trinh HN, Garcia RT, Nguyen HA, Nguyen KK, et al. High frequency of recurrent viremia after hepatitis B e antigen seroconversion and consolidation therapy. J Clin Gastroenterol. 2012;46:865–70.\nRidruejo E, Silva MO. Safety of long-term nucleos(t)ide treatment in chronic hepatitis B. Expert Opin Drug Saf. 2012;11:357–60.\nPetersen J, Dandri M. Optimal therapy for chronic hepatitis B: hepatitis B virus combination therapy? Liver Int. 2015;35(Suppl. 1):114–20.\nThimme R, Dandri M. Dissecting the divergent effects of interferon-alpha on immune cells: time to rethink combination therapy in chronic hepatitis B? J Hepatol. 2013;58:205–9.\nNing Q, Han M, Sun Y, et al. Switching from entecavir to PegIFN alfa-2a in patients with HBeAg-positive chronic hepatitis B: a randomised open-label trial (OSST trial). J Hepatol. 2014;61:777–84. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jhep.2014.05.044.\nBrouwer WP, Xie Q, Sonneveld MJ, Zhang N, Zhang Q, Tabak F, et al. Adding pegylated interferon to entecavir for hepatitis B e antigen-positive chronic hepatitis B: a multicenter randomized trial (ARES study). Hepatology. 2015;61:1512–22. https:\u002F\u002Fdoi.org\u002F10.1002\u002Fhep.27586.\nLim SG, Yang WL, Ngu J, Tan J, Ahmed TT, Dan YY, et al. Switch or add-on peginterferon for chronic hepatitis B patients already on nucleos(t)ide analogue therapy (SWAP study): provisional analysis—add-on therapy superior. J Hepatol. 2017;66:S60. https:\u002F\u002Fdoi.org\u002F10.1016\u002FS0168-8278(17)30382-3.\nMicco Lorenzo, Peppa Dimitra, Loggi Elisabetta, Schurich Anna, Jefferson Lucy, et al. Differential boosting of innate and adaptive antiviral responses during pegylated-interferon-alpha therapy of chronic hepatitis B. J Hepatol. 2013;58:225–33. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jhep.2012.11.007.\nPeng Hu, Shang Jia, Zhang Wenhong, Gong Guozhong, Li Yongguo, Chen Xinyue, et al. HBsAg loss with Peg-interferon Alfa-2a in Hepatitis B patients with partial response to nucleos(t)ide analog: new switch study. J Clin Transl Hepatol. 2018;6:1–10. https:\u002F\u002Fdoi.org\u002F10.14218\u002FJCTH.2017.00072.\nBoni C, Laccabue D, Lampertico P, Giuberti T, Vigano M, Schivazappa S, et al. Restored function of HBV-specific T cells after long-term effective therapy with nucleos(t)ide analogues. Gastroenterology. 2012;143:963–73.\nBuster EH, Flink HJ, Cakaloglu Y, Simon K, Trojan J, Tabak F, et al. Sustained HBeAg and HBsAg loss after long-term follow-up of HBeAg-positive patients treated with peginterferon alpha-2 b. Gastroenterology. 2008;135:459–67.\nJanssen HLA, van Zonneveld M, Senturk H, et al. Pegylated interferonalfa-2b alone or in combination with lamivudine for HBeAg-positive chronic hepatitis B: a randomised trial. Lancet. 2005;365:123–9.\nVigan M, Invernizzi F, Grossi G, Lampertico P. Review article: the potential of interferon and nucleos(t)ide analogue combination therapy in chronic hepatitis B infection. Aliment Pharmacol Ther. 2016;44:653–61.\nMarcellin P, Ahn SH, Ma X, et al. Combination of tenofovir disoproxil fumarate and peginterferon α-2a increases loss of hepatitis B surface antigen in patients with chronic hepatitis B. Gastroenterology. 2016;150:134–44.\nTakkenberg RB, Jansen L, de Niet A, et al. Baseline hepatitis B surface antigen (HBsAg) as predictor of sustained HBsAg loss in chronic hepatitis B patients treated with peginterferon alfa-2a and adefovir. Antivir Ther. 2013;18:895–904.\nPiratvisuth T, Marcellin P, Pepescu M, Kapprell HP, Rothe V, Lu ZM. Hepatitis B surface antigen: association with sustained response to peginterferon alfa-2a in hepatitis B e-antigen-positive patients. Hepatol Int. 2013;7:429–36.\nChen CH, Lu SN, Hung CH, Wang JH, Hu TH, Chang Chien CS, et al. The role of hepatitis B surface antigen quantification in predicting HBsAg loss and HBV relapse after discontinuation of lamivudine treatment. J Hepatol. 2014;61:515–22.",{"VOID":2587},"10.1007\u002Fs12072-019-09957-0","2024-06-25T07:56:51.278+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs12072-019-09957-0",[2591,2606,2619,2634,2647,2662],{"id":2592,"sortIndex":21,"researcher":20,"roles":2593,"affiliations":2594,"properties":2603,"displayName":2605,"givenName":20,"familyName":20},"54b44068-151a-48a7-9506-081ec188917b",[184],[2595],{"id":2596,"sortIndex":21,"affiliation":2597,"properties":20},"02569968-6208-4eb2-8a44-02824dd1debd",{"id":2596,"createTime":20,"updateTime":20,"relativeEntities":2598,"slug":20,"properties":2599,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2602,"statistic":20},[],{"title":2600},{"VI":2601},"Department of Infectious Diseases, Zhejiang Provincial People’s Hospital, People’s Hospital Hang Zhou Medical College, Zhejiang, China",[],{"title":2604},{"VI":2605},"Ying Zhou",{"id":2607,"sortIndex":84,"researcher":20,"roles":2608,"affiliations":2609,"properties":2616,"displayName":2618,"givenName":20,"familyName":20},"1cedad8b-fa71-4776-b1b4-bc5438c60327",[184],[2610],{"id":2596,"sortIndex":21,"affiliation":2611,"properties":20},{"id":2596,"createTime":20,"updateTime":20,"relativeEntities":2612,"slug":20,"properties":2613,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2615,"statistic":20},[],{"title":2614},{"VI":2601},[],{"title":2617},{"VI":2618},"Rong 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is universally recommended in Budd–Chiari syndrome [BCS]. Vitamin K epoxide reductase complex 1 (VKORC1) and CYP2C9 are involved in the metabolism of warfarin. The present study was done to assess whether these mutations are associated with the risk of bleeding in patients with BCS receiving warfarin. Patients diagnosed with BCS underwent genotyping for three single nucleotide polymorphisms [SNPs]—two for the CYP2C9 and one for the VKORC1 haplotype. The patients were followed up for at least 12 months and all bleeding episodes were recorded. Patients with and without mutations were compared for bleeding complications and a crude odds ratio [crude OR] was derived for the association between bleeding and presence or absence of mutant alleles. Eighty patients [mean (SD) age 27.47 (8.93) years, 35 male] with BCS underwent genetic testing. 37\u002F80 (46.2%) patients had mutation of CYP2C9 and\u002For VKORC1; 22\u002F80 (27.5%) had either of the mutant alleles of CYP2C9 and, similarly, 22\u002F80 (27.5%) had the VKORC mutation. Over a median follow-up of 20 (range 12–96) months, 21\u002F80 (26.3%) patients had bleeding complications. Patients with mutant SNPs had a higher risk of bleeding than those without [14\u002F37 vs. 7\u002F43, p = 0.04, crude OR (95% CI) 3.13 (1.1–8.9)]. The presence of mutations in VKORC1 or CYP2C9 is associated with increased risk of bleeding in patients with BCS on warfarin. Such patients with SNPs of CY2C9 or VKORC1 haplotype should be monitored intensively while receiving warfarin.",{"EN":2737},"Mutations in CYP2C9 and\u002For VKORC1 haplotype are associated with higher bleeding complications in patients with Budd–Chiari syndrome on warfarin",{"VOID":2583},{"VOID":2740},"Horton JD, San Miguel FL, Membreno F, et al. Budd–Chiari syndrome: illustrated review of current management. Liver Int. 2008;28:455–66.\nZhang C, Gu V, Zhu G, Luo T, Yan C, Wang Z. Hybrid treatment for Budd–Chiari syndrome—a case report by 11-year follow up. Ann Vasc Surg. 2017;38(e1–319):e6.\nValla DC. Primary Budd–Chiari syndrome. J Hepatol. 2009;50:195–203.\nBogin V, Marcos A, Shaw-Stiffel T. Budd–Chiari syndrome: in evolution. Eur J Gastroenterol Hepatol. 2005;17:33–5.\nLimdi NA, McGwin G, Goldstein JA, et al. Influence of CYP2C9 and VKORC1 1173C\u002FT genotype on the risk of hemorrhagic complications in African-American and European-American patients on warfarin. Clin Pharmacol Ther. 2008;83:312–21.\nJorgensen AL, FitzGerald RJ, Oyee J, Pirmohamed M, Williamson PR. Influence of CYP2C9 and VKORC1 on patient response to warfarin: a systematic review and meta-analysis. PLoS One. 2012;7:e44064.\nFinkelman BS, Gage BF, Johnson JA, Brensinger CM, Kimmel SE. Genetic warfarin dosing: tables versus algorithms. J Am Coll Cardiol. 2011;57:612–8.\nGage BF, Eby C, Johnson JA, Deych E, et al. Use of pharmacogenetic and clinical factors to predict the therapeutic dose of warfarin. Clin Pharmacol Ther. 2008;84:326–31.\nInternational Warfarin Pharmacogenetics Consortium, Klein TE, Altman RB, Eriksson N, et al. Estimation of the warfarin dose with clinical and pharmacogenetic data. N Engl J Med. 2009;360:753–64.\nPlessier A, Valla DC. Budd–Chiari syndrome. Semin Liver Dis. 2008;28:259–69.\nMontano-Loza AJ, Tandon P, Kneteman N, Baily R, Bain VG. Rotterdam score predicts early mortality in Budd–Chiari syndrome, and surgical shunting prolongs transplant free survival. Aliment Pharmacol Ther. 2009;30:1060–9.\nMalinchoc M, Kamath PS, Gordon FD, Peine CJ, Rank J, ter Borg PC. A model to predict poor survival in patients undergoing transjugular intrahepatic portosystemic shunts. Hepatology. 2000;31:864–71.\nFlockhart DA, O’Kane D, Williams MS, ACMG Working Group on Pharmacogenetic Testing of CYP2C9, VKORC1 Alleles for Warfarin Use, et al. Pharmacogenetic testing of CYP2C9 and VKORC1 alleles for warfarin. Genet Med. 2008;10:139–50.\nCOUMADIN-Warfarin Sodium Tablet) [package insert]. Princeton: Bristol-Myers Squibb Pharma Company; 2015. Available from: http:\u002F\u002Fdailymed.nlm.nih.gov\u002Fdailymed\u002FdrugInfo.cfm?setid=d91934a0-902e-c26c-23ca-d5accc4151b6. Accessed 20 Apr 2018.\nSridharan K, Modi T, Bendkhale S, Kulkarni D, Gogtay NJ, Thatte UM. Association of genetic polymorphisms of CYP2C9 and VKORC1 with bleeding following warfarin: a case-control study. Curr Clin Pharmacol. 2016;11(1):62–8.\nDe Franchis R, Baveno VI faculty. Expanding consensus in portal hypertension: report of the Baveno VI Consensus Workshop: stratifying risk and individualizing care for portal hypertension. J Hepatol. 2015;63(3):743–52.\nSchulman S, Kearon C. Definition of major bleeding in clinical investigations of antihemostatic medicinal products in non-surgical patients. J Thromb Haemost. 2005;3:692–4.\nSandén P, Renlund H, Svensson PJ, Själander A. Bleeding complications in venous thrombosis patients on well-managed warfarin. J Thromb Thrombolysis. 2016;41(2):351–8.\ndo Delga MG, Seijo S, Yepes I, et al. Efficacy and safety of anticoagulation on patients with cirrhosis and portal vein thrombosis1. Clin Gastroenterol Hepatol. 2012;10:776–83.\nDarwish MS, Plessier A, Hernandez-Guerra M, et al. Etiology, management, and outcome of the Budd–Chiari syndrome. Ann Intern Med. 2009;151:167–75.\nSeijo S, Plessier A, Hoekstra J, et al. Good long term outcome of Budd–Chiari syndrome with a step-wise management. Hepatology. 2013;57:1962–8.\nShukla A, Bhatia SJ. Outcome of patients with primary hepatic venous obstruction treated with anticoagulants alone. Indian J Gastroenterol. 2010;29(1):8–11.\nPasmant E, de Beauvoir C, Plessier A, Labreuche J, Bezeaud A. VKORC1 and CYP2C9 genetic polymorphisms in hepatic or portal vein thrombosis. Thromb Res. 2010;126(2):e134–6.\nBenusiglio PR, Desmeules J, de Moerloose P, Dayer P. Oral anticoagulation and pharmacogenetics: importance in the clinical setting. Rev Med Suisse. 2007;3(124):2030 (2033-4, 2036).\nAdithan C, Gerard N, Vasu S, Balakrishnan R, Shashindran CH, Krishnamoorthy R. Allele and genotype frequency of CYP2C9 in Tamilnadu population. Eur J Clin Pharmacol. 2003;59:707–9.\nShalia K, Doshi SM, Parikh S, et al. Prevalence of VKORC1 and CYP2C9 gene polymorphisms in Indian population and its effect on warfarin response. JAPI. 2012;60:34–8.\nPirmohamed M, Burnside G, Eriksson N, EU-PACT Group, et al. A randomized trial of genotype-guided dosing of warfarin. N Engl J Med. 2013;369(24):2294–303.\nKimmel SE, French B, Kasner SE, COAG Investigators, et al. A pharmacogenetic versus a clinical algorithm for warfarin dosing. N Engl J Med. 2013;369(24):2283–93.\nJohnson JA, Caudle KE, Gong L, et al. Clinical pharmacogenetics implementation consortium (CPIC) guideline for pharmacogenetics-guided warfarin dosing: 2017 update. Clin Pharmacol Ther. 2017;102(3):397–404.\nTripodi A, Mannucci PM. The coagulopathy of chronic liver disease. N Engl J Med. 2011;365(2):147–56.\nMekaj YH, Mekaj AY, Duci SB, Miftari EI. New oral anticoagulants: their advantages and disadvantages compared with vitamin K antagonists in the prevention and treatment of patients with thromboembolic events. Ther Clin Risk Manag. 2015;11:967–77.",{"VOID":2742},"10.1007\u002Fs12072-018-9922-6","2024-06-25T12:40:34.619+00:00","http:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs12072-018-9922-6",[2746,2761,2774,2787,2802,2815,2828],{"id":2747,"sortIndex":21,"researcher":20,"roles":2748,"affiliations":2749,"properties":2758,"displayName":2760,"givenName":20,"familyName":20},"d2743d40-0859-486d-b3bc-387d926a6507",[184],[2750],{"id":2751,"sortIndex":21,"affiliation":2752,"properties":20},"55a032ca-1207-44f5-8ab4-a21f62da2a50",{"id":2751,"createTime":20,"updateTime":20,"relativeEntities":2753,"slug":20,"properties":2754,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2757,"statistic":20},[],{"title":2755},{"VI":2756},"Department of Gastroenterology, Seth GS Medical College and KEM Hospital, Mumbai, India",[],{"title":2759},{"VI":2760},"Akash Shukla",{"id":2762,"sortIndex":84,"researcher":20,"roles":2763,"affiliations":2764,"properties":2771,"displayName":2773,"givenName":20,"familyName":20},"2e726893-7e8e-4c96-b254-566fdd1e20c4",[184],[2765],{"id":2751,"sortIndex":21,"affiliation":2766,"properties":20},{"id":2751,"createTime":20,"updateTime":20,"relativeEntities":2767,"slug":20,"properties":2768,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2770,"statistic":20},[],{"title":2769},{"VI":2756},[],{"title":2772},{"VI":2773},"Abhinav 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Bhatia",{"url":2744,"publisher":2842,"properties":2884},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":2843,"slug":10,"properties":2844,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":2848,"manageAffiliations":2853,"indexDatabases":2864,"url":80,"thumbnailPath":20,"statistic":2879,"gsStatistic":20,"type":152,"analyzePriority":20},[],{"issn":2845,"title":2846,"eissn":2847},{"VOID":13},{"EN":15},{"VOID":17},[2849],{"id":24,"createTime":20,"updateTime":20,"relativeEntities":2850,"label":2851,"description":2852,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":27},{},[2854,2859],{"id":31,"createTime":20,"updateTime":20,"relativeEntities":2855,"slug":20,"properties":2856,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2858,"statistic":20},[],{"title":2857},{"EN":35},[],{"id":38,"createTime":20,"updateTime":20,"relativeEntities":2860,"slug":20,"properties":2861,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2863,"statistic":20},[],{"title":2862},{"EN":42},[44],[2865,2872],{"id":47,"indexDatabase":2866,"url":58,"indexYears":59,"academicFieldIds":2871,"indexDatabaseRanking":62},{"id":49,"createTime":20,"updateTime":20,"relativeEntities":2867,"label":2868,"description":2869,"key":55,"publicationTags":2870,"standard":20},[],{"EN":52,"VI":52},{"EN":52,"VI":54},[57],[61],{"id":64,"indexDatabase":2873,"url":77,"indexYears":20,"academicFieldIds":2878,"indexDatabaseRanking":20},{"id":66,"createTime":20,"updateTime":20,"relativeEntities":2874,"label":2875,"description":2876,"key":73,"publicationTags":2877,"standard":20},[],{"EN":69,"VI":69},{"EN":71,"VI":72},[75,76],[79],{"impactFactor":21,"impactFactorByYear":2880,"i10Index":95,"i10IndexLast5Year":96,"totalPublication":97,"totalPublicationByYear":2881,"totalCitation":113,"totalCitationByYear":2882,"totalCitationPerPublication":132,"totalCitationPerPublicationByYear":2883,"hindexLast5Year":117,"hindex":117},{"2012":83,"2013":84,"2014":85,"2015":86,"2016":87,"2017":88,"2018":89,"2019":90,"2020":91,"2021":92,"2022":93,"2023":94},{"2007":99,"2008":100,"2009":101,"2010":102,"2011":103,"2012":100,"2013":104,"2014":105,"2015":106,"2016":107,"2017":96,"2018":100,"2019":104,"2020":108,"2021":109,"2022":110,"2023":111,"2024":112},{"2007":115,"2008":116,"2009":117,"2010":118,"2011":119,"2012":120,"2013":121,"2014":122,"2015":123,"2016":124,"2017":125,"2018":126,"2019":127,"2020":128,"2021":129,"2022":130,"2023":131,"2024":84},{"2007":134,"2008":135,"2009":136,"2010":137,"2011":138,"2012":139,"2013":140,"2014":141,"2015":142,"2016":143,"2017":144,"2018":145,"2019":146,"2020":147,"2021":148,"2022":149,"2023":150,"2024":151},{"pages":2885,"volume":2887},{"VOID":2886},"214-221",{"VOID":408},"2019-01-08",[57,75],{"id":2891,"createTime":2892,"updateTime":2893,"relativeEntities":2894,"slug":2895,"properties":2896,"entityType":173,"verifyStatus":174,"verifyTime":2907,"verifyNote":176,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":2908,"fullTextUrl":20,"authors":2909,"publicationType":360,"publisherRelationship":2951,"citationCount":21,"citationInfo":2999,"publishDate":3002,"publishYear":3000,"citationAnalyzeStatus":19,"lastCitationAnalyze":3003,"indexDatabases":3004,"openAccess":20,"references":20,"isForceReanalyzing":412},"4b1f5f91-d095-4cbc-80f3-119ce81ccd8f","2024-01-19T01:09:38.056+00:00","2026-07-17T14:56:45.855+00:00",[],"Virus-induced-hepatocellular-carcinoma-with-special-emphasis-on-HBV",{"abstract":2897,"title":2899,"gsPaper":2901,"references":2903,"doi":2905},{"EN":2898},"Hepatocellular carcinoma (HCC) is a common malignant tumor with high lethality, and the hepatitis B virus (HBV) is a chief cause. HBV can accelerate HCC via multiple mechanisms. First, HBV induces immune reactions that lead to repeated hepatic inflammation, fibrosis and a deficient immune microenvironment. Subsequently, HBV can modify host genes near the insertion point through DNA integration to cause host cell genome instability and to generate carcinogenic fusion proteins. Additionally, HBV expresses diverse active proteins, especially HBx and HBs, which have a range of transactivation functions such as regulation of apoptosis, interference with intracellular signaling pathways, and alteration of epigenetics. Currently, primary prevention measures for HBV-induced HCC focus on vaccination and antiviral treatment. Here, we report the epidemiology, the molecular mechanism and the progress in therapeutic strategies for controlling HBV-induced HCC.",{"EN":2900},"Virus-induced hepatocellular carcinoma with special emphasis on HBV",{"VOID":2902},"[\"996017247526706685\"]",{"VOID":2904},"Croaqh CM, Lubel JS. 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Hepatology. 2015;62(4):1190–1200",{"VOID":2906},"10.1007\u002Fs12072-016-9779-5","2024-05-15T17:01:46.196+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs12072-016-9779-5",[2910,2925,2938],{"id":2911,"sortIndex":21,"researcher":20,"roles":2912,"affiliations":2913,"properties":2922,"displayName":2924,"givenName":20,"familyName":20},"a8d445cb-5da5-4bca-ad06-258198e7adc0",[184],[2914],{"id":2915,"sortIndex":21,"affiliation":2916,"properties":20},"c1abf888-8d0f-469c-a36b-23a993847a89",{"id":2915,"createTime":20,"updateTime":20,"relativeEntities":2917,"slug":20,"properties":2918,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2921,"statistic":20},[],{"title":2919},{"EN":2920},"Department of Infectious Disease, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China",[],{"title":2923},{"VI":2924},"Ming 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Taiwan, the national hepatitis B virus vaccination program and national viral hepatitis therapy program were implemented to control the infections of hepatitis viruses and their progressive illnesses. Studies have evaluated the impacts of two national health programs on many liver-related diseases, but not on acute and chronic viral hepatitis. The purpose of this study was to evaluate the impact on the mortality of acute and chronic viral hepatitis. Poisson regression models were used to estimate the adjusted rate ratios of the different period groups and corresponding 95% confidence intervals for childhood, adulthood and elderhood, and to estimate the adjusted rate ratios of vaccinated cohorts and corresponding 95% confidence intervals. Compared with period of 2000–2003, the adjusted rate ratios for period groups of 2008–2011 and 2012–2015 reported a significantly increasing risk of acute and chronic viral hepatitis mortality, except for the childhood and female adulthood. For population without vaccination, the adjusted rate ratios of acute and chronic viral hepatitis B mortality were 0.99 (95% CIs 0.88–1.12), 1.30 (95% CIs 1.17–1.45) and 1.42 (95% CIs 1.28–1.55) for periods of 2004–2007, 2008–2011 and 2012–2015, respectively, comparing with unimplemented period of national viral hepatitis therapy program. Compared with 1967–1983 cohorts, the adjusted rate ratio of 1984–2000 cohorts was 0.46 (95% CIs 0.28–0.75), and the adjusted rate ratios were 0.49 (95% CIs 0.28–0.87) and 0.35 (95% CIs 0.11–1.05) for male and female, respectively. This study revealed the significantly higher mortality rates of acute and chronic viral hepatitis during the implemented period of national viral hepatitis therapy program, comparing the unimplemented period. Such ineffectiveness may be attributable to the low coverage rate. The national vaccination program was currently an effective strategy for controlling the mortality of viral hepatitis.",{"EN":3015},"The impact of national viral hepatitis therapy program and hepatitis B vaccination program on mortality from acute and chronic viral hepatitis in Taiwan",{"VOID":3017},"[\"1461706787791885157\"]",{"VOID":3019},"Polaris Observatory C. Global prevalence, treatment, and prevention of hepatitis B virus infection in 2016: a modelling study. Lancet Gastroenterol Hepatol 2018;3(6):383–403. https:\u002F\u002Fdoi.org\u002F10.1016\u002FS2468-1253(18)30056-6\nPolaris Observatory HCVC. Global prevalence and genotype distribution of hepatitis C virus infection in 2015: a modelling study. Lancet Gastroenterol Hepatol 2017;2(3):161–176. https:\u002F\u002Fdoi.org\u002F10.1016\u002FS2468-1253(16)30181-9\nStanaway JD, Flaxman AD, Naghavi M, Fitzmaurice C, Vos T, Abubakar I, et al. 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Aristolochic acids and their derivatives are widely implicated in liver cancers in Taiwan and throughout Asia. Sci Transl Med 2017;9(412):eaan6446. https:\u002F\u002Fdoi.org\u002F10.1126\u002Fscitranslmed.aan6446\nSu WJ, Liu CC, Liu DP, Chen SF, Huang JJ, Chan TC, et al. Effect of age on the incidence of acute hepatitis B after 25 years of a universal newborn hepatitis B immunization program in Taiwan. J Infect Dis 2012;205(5):757–762. https:\u002F\u002Fdoi.org\u002F10.1093\u002Finfdis\u002Fjir852\nWait S, Chen DS. Towards the eradication of hepatitis B in Taiwan. Kaohsiung J Med Sci 2012;28(1):1–9. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.kjms.2011.10.027\nSu S-Y, Chiang C-J, Yang Y-W, Lee W-C. Secular trends in liver cancer incidence from 1997 to 2014 in Taiwan and projection to 2035: an age-period-cohort analysis. J Formosan Med Assoc 2019;118:444–449. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jfma.2018.07.001\nWorld Health Organization. Global health sector strategy on viral hepatitis 2016–2021. http:\u002F\u002Fwww.who.int\u002Fhepatitis\u002Fstrategy2016-2021\u002Fghss-hep\u002Fen\u002F. Accessed June 2016\nLin YY, Huang CS. Aging in Taiwan: building a society for active aging and aging in place. Gerontologist 2016;56(2):176–183. https:\u002F\u002Fdoi.org\u002F10.1093\u002Fgeront\u002Fgnv107\nWang HH, Tsay SF. Elderly and long-term care trends and policy in Taiwan: challenges and opportunities for health care professionals. Kaohsiung J Med Sci 2012;28(9):465–469. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.kjms.2012.04.002\nExecutive Yuan, Taiwan, ROC. Long-term care 2.0 plan for greater peace of mind. https:\u002F\u002Fenglish.ey.gov.tw\u002FNews_Hot_Topic.aspx?n=FE8C5966F81D8273&sms=BBB420E471DAF6C0. 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