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| 1 | Cellular and molecular mechanisms in the pathogenesis of liver fibrosis:An update显示文摘There have been considerable recent advances towards a better understanding of the complex cellular and molecular network underlying liver fibrogenesis.Recent data indicate that the termination of fibrogenic processes and the restoration of deficient fibrolytic pathways may allow the reversal of advanced fibrosis and even cirrhosis.Therefore,efforts have been made to better clarify the cellular and molecular mechanisms that are involved in liver fibrosis.Activation of hepatic stellate cells(HSCs)remains a central event in fibrosis,complemented by other sources of matrix-producing cells,including portal fibroblasts,fibrocytes and bone marrow-derived myofibroblasts.These cells converge in a complex interaction with neighboring cells to provoke scarring in response to persistent injury.Defining the interaction of different cell types,revealing the effects of cytokines on these cells and characterizing the regulatory mechanisms that control gene expression in activated HSCs will enable the discovery of new therapeutic targets.Moreover,the characterization of different pathways associated with different etiologies aid in the development of disease-specific therapies.This article outlines recent advances regarding the cellular and molecular mechanisms involved in liver fibrosis that may be translated into future therapies.The pathogenesis of liver fibrosis associated with alcoholic liver disease,non-alcoholic fatty liver disease and viral hepatitis are also discussed to emphasize the various mechanisms involved in liver fibrosis. | Gülsüm ?zlem Elpek | 2014 | World Journal of Gastroenterology2014，20，23： | 82 |
| 2 | Liver fibrosis and hepatic stellate cells: Etiology, pathological hallmarks and therapeutic targets显示文摘Liver fibrosis is a reversible wound-healing process aimed at maintaining organ integrity, and presents as the critical pre-stage of liver cirrhosis, which will eventually progress to hepatocellular carcinoma in the absence of liver transplantation. Fibrosis generally results from chronic hepatic injury caused by various factors, mainly viral infection, schistosomiasis, and alcoholism; however, the exact pathological mechanisms are still unknown. Although numerous drugs have been shown to have antifibrotic activity in vitro and in animal models, none of these drugs have been shown to be efficacious in the clinic. Importantly, hepatic stellate cells(HSCs) play a key role in the initiation, progression, and regression of liver fibrosis by secreting fibrogenic factors that encourage portal fibrocytes, fibroblasts, and bone marrow-derived myofibroblasts to produce collagen and thereby propagate fibrosis. These cells are subject to intricate cross-talk with adjacent cells, resulting in scarring and subsequent liver damage. Thus, an understanding of the molecular mechanisms of liver fibrosis and their relationships with HSCs is essential for the discovery of new therapeutic targets. This comprehensive review outlines the role of HSCs in liver fibrosis and details novel strategies to suppress HSC activity, thereby providing new insights into potential treatments for liver fibrosis. | Chong-Yang Zhang Wei-Gang Yuan Pei He Jia-Hui Lei Chun-Xu Wang | 2016 | World Journal of Gastroenterology2016，22，48： | 114 |
| 3 | Prevalence of minimal hepatic encephalopathy and quality of life evaluations in hospitalized cirrhotic patients in China显示文摘AIM:To investigate the prevalence of minimal hepatic encephalopathy(MHE)and to assess corresponding health-related quality of life(HRQoL)in hospitalized cirrhotic patients in China.METHODS:This multi-center cross-sectional study included 16 teaching hospitals,which were members of 'Hepatobiliary Cooperation Group,Society of Gastroenterology,Chinese Medical Association',from different areas of China carried out between June and October in 2011.All the eligible hospitalized cirrhotic patients(n = 538)were required to complete triplicate number connection tests combined with one digit symbol test for diagnosing MHE.Patients' clinical examination data were complemented by a modified questionnaire assessing HRQoL.Written informed consent was obtained from each patient.RESULTS:Male was predominant(68.6%)in 519 patients who met the criteria of the study,with a mean age of 49.17 ± 11.02 years.The most common cause of liver cirrhosis was chronic hepatitis B(55.9%).The prevalence of MHE was 39.9% and varied by ChildPugh-Classification score(CPC-A:24.8%,CPC-B:39.4% and CPC-C:56.1%,P < 0.01).MHE(P < 0.01)and higher CPC scores(P < 0.01)were associated with a high HRQoL scores(reflecting poorer quality of life).The prevalence of MHE was proportionate to CPC(P = 0.01)and high quality of life scores(P = 0.01).CONCLUSION:Hospitalized cirrhotic patients have a high prevalence of MHE that is proportionate to the degree of liver function and HRQoL impairment. | Ji-Yao Wang Ning-Ping Zhang Bao-Rong Chi Yu-Qing Mi Li-Na Meng Ying-Di Liu Jiang-Bin Wang Hai-Xing Jiang Jin-Hui Yang Yun Xu Xiao Li Jian-Ming Xu Guo Zhang Xin-Min Zhou Yu-Zheng Zhuge De-An Tian Jin Ye Yu-Lan Liu | 2013 | World Journal of Gastroenterology2013，19，30： | 64 |
| 4 | 原发性胆汁性肝硬化(又名原发性胆汁性胆管炎)诊断和治疗共识(2015)显示文摘一、概述原发性胆汁性肝硬化(primary biliary cirrhosis,PBC)是一种慢性肝内胆汁淤积性疾病。其发病机制尚不完全清楚,可能与遗传背景及环境等因相互作用所导致的异常自身免疫反应有关。PBC多见于中老年女性,最常见的临床表现为乏力和皮肤瘙痒;其病理特点为进行性、非化脓性、破坏性肝内小胆管炎,最终可发展至肝硬化。 | | 2015 | 肝脏2015，20，12： | 62 |
| 5 | Pathogenesis of liver cirrhosis显示文摘Liver cirrhosis is the final pathological result of various chronic liver diseases,and fibrosis is the precursor of cirrhosis.Many types of cells,cytokines and miRNAs are involved in the initiation and progression of liver fibrosis and cirrhosis.Activation of hepatic stellate cells(HSCs)is a pivotal event in fibrosis.Defenestration and capillarization of liver sinusoidal endothelial cells are major contributing factors to hepatic dysfunction in liver cirrhosis.Activated Kupffer cells destroy hepatocytes and stimulate the activation of HSCs.Repeated cycles of apoptosis and regeneration of hepatocytes contribute to pathogenesis of cirrhosis.At the molecular level,many cytokines are involved in mediation of signaling pathways that regulate activation of HSCs and fibrogenesis.Recently,miRNAs as a post-transcriptional regulator have been found to play a key role in fibrosis and cirrhosis.Robust animal models of liver fibrosis and cirrhosis,as well as the recently identified critical cellular and molecular factors involved in the development of liver fibrosis and cirrhosis will facilitate the development of more effective therapeutic approaches for these conditions. | Wen-Ce Zhou Quan-Bao Zhang Liang Qiao | 2014 | World Journal of Gastroenterology2014，20，23： | 67 |
| 6 | Study of liver cirrhosis over ten consecutive years in Southern China显示文摘AIM: To investigate the etiology and complications of liver cirrhosis(LC) in Southern China. METHODS: In this retrospective, cross-sectional study, we identified cases of liver cirrhosis admitted between January 2001 to December 2010 and reviewed the medical records. Patient demographics, etiologies and complications were collected, and etiological changes were illustrated by consecutive years and within twotime periods(2001-2005 and 2006-2010). All results were expressed as the mean ± SD or as a percentage. The χ2 test or Student's t-test was used to analyze the differences in age, gender, and etiological distribution, and one-way analysis of variance was applied to estimate the trends in etiological changes. We analyzed the relationship between the etiologies and complications using unconditioned logistic regression, and the risk of upper gastrointestinal bleeding(UGIB) and hepatocellular carcinoma(HCC) in the major etiological groups was evaluated as ORs. A P value less than 0.05 was considered significant. Statistical computation was performed using SPSS 17.0 software.RESULTS: In this study, we identified 6719(83.16%) male patients and 1361(16.84%) female patients. The average age of all of the patients was 50.5 years at the time of diagnosis. The distribution of etiological agents was as follows: viral hepatitis, 80.62% [hepatitis B virus(HBV) 77.22%, hepatitis C virus(HCV) 2.80%,(HBV + HCV) 0.58%]; alcohol, 5.68%; mixed etiology, 4.95%; cryptogenic, 2.93%; and autoimmune hepatitis, 2.03%; whereas the other included etiologies accounted for less than 4% of the total. Infantile hepatitis syndrome LC patients were the youngest(2.5 years of age), followed by the metabolic LC group(27.2 years of age). Viral hepatitis, alcohol, and mixed etiology were more prevalent in the male group, whereas autoimmune diseases, cryptogenic cirrhosis, and metabolic diseases were more prevalent in the female group. When comparing the etiological distribution in 2001-2005 with that in 2006-2010, the proportion of viral hepatitis decreased from 84.7% to 78.3%(P < 0.001), and the proportion of HBV-induced LC also decreased from 81.9% to 74.6%(P < 0.001). The incidence of mixed etiology, cryptogenic cirrhosis, and autoimmune diseases increased by 3.1%(P < 0.001), 0.5%(P = 0.158), and 1.3%(P < 0.001), respectively. Alcohol-induced LC remained relatively steady over the 10-year period. The ORs of the development of UGIB between HBV and other major etiologies were as follows: HCV, 1.07; alcohol, 1.89; autoimmune, 0.90; mixed etiology, 0.83; and cryptogenic, 1.76. The ORs of the occurrence of HCC between HBV and other major etiologies were as follows: HCV, 0.54; alcohol, 0.16; autoimmune, 0.05; mixed etiology, 0.58; and cryptogenic, 0.60.CONCLUSION: The major etiology of liver cirrhosis in Southern China is viral hepatitis. However, the proportions of viral hepatitis and HBV are gradually decreasing. Alcoholic LC patients exhibit a greater risk of experiencing UGIB, and HBV LC patients may have a greater risk of HCC. | Xing Wang Shang-Xiong Lin Jin Tao Xiu-Qing Wei Yuan-Ting Liu Yu-Ming Chen Bin Wu | 2014 | World Journal of Gastroenterology2014，20，37： | 72 |
| 7 | Acute esophageal variceal bleeding:Current strategies and new perspectives显示文摘Management of acute variceal bleeding has greatly improved over recent years. Available data indicates that general management of the bleeding cirrhotic patient by an experienced multidisciplinary team plays a major role in the f inal outcome of this complication. It is currently recommended to combine pharmacological and endoscopic therapies for the initial treatment of the acute bleeding. Vasoactive drugs (preferable somatostatin or terlipressin) should be started as soon as a variceal bleeding is suspected (ideally during transfer to hospital) and maintained afterwards for 2-5 d. After stabilizing the patient with cautious fluid and blood support, an emergency diagnostic endoscopy should be done and, as soon as a skilled endoscopist is available, an endoscopic variceal treatment (ligation as f irst choice, sclerotherapy if endoscopic variceal ligation not feasible) should be performed. Antibiotic prophylaxis must be regarded as an integral part of the treatment of acute variceal bleeding and should be started at admission and maintained for at least 7 d. In case of failure to control the acute bleeding, rescue therapies should be immediately started. Shunt therapies (especially tran sjugular intrahepatic portosystemic shunt) are very effective at controlling treatment failures after an acute variceal bleeding. Therapeutic developments and increasing knowledge in the prognosis of this complication may allow optimization of the management strategy by adapting the different treatments to the expected risk of complications for each patient in the near future. Theoretically, this approach would allow the initiation of early aggressive treatments in high-risk patients and spare low-risk individuals unnecessary proce dures. Current research efforts will hopefully clarify this hypothesis and help to further improve the outcomes of the severe complication of cirrhosis. | Salvador Augustin Antonio González Joan Genescà | 2010 | World Journal of Hepatology2010，2，7： | 44 |
| 8 | Diagnosis and management of bacterial infections in decompensated cirrhosis显示文摘Bacterial infections are one of the most frequent complications in cirrhosis and result in high mortality rates.Patients with cirrhosis have altered and impaired immunity,which favours bacterial translocation.Episodes of infections are more frequent in patients with decompensated cirrhosis than those with compensated liver disease.The most common and life-threatening infection in cirrhosis is spontaneous bacterial peritonitis followed by urinary tract infections,pneumonia,endocarditis and skin and soft-tissue infections.Patients with decompensated cirrhosis have increased risk of developing sepsis,multiple organ failure and death.Risk factors associated with the development of infections are severe liver failure,variceal bleeding,low ascitic protein level and prior episodes of spontaneous bacterial peritonitis (SBP).The prognosis of these patients is closely related to a prompt and accurate diagnosis.An appropriate treatment decreases the mortality rates.Preventive strategies are the mainstay of the management of these patients.Empirical antibiotics should be started immediately following the diagnosis of SBP and the first-line antibiotic treatment is third-generation cephalosporins.However,the efficacy of currently recommended empirical antibiotic therapy is very low in nosocomial infections including SBP,compared to community-acquired episodes.This may be associated with the emergence of infections caused by Enterococcus faecium and extended-spectrum β-lactamaseproducing Enterobacteriaceae,which are resistant to the first line antimicrobial agents used for treatment.The emergence of resistant bacteria,underlines the need to restrict the use of prophylactic antibiotics to patients with the greatest risk of infections.Nosocomial infections should be treated with wide spectrum antibiotics.Further studies of early diagnosis,prevention and treatment are needed to improve the outcomes in patients with decompensated cirrhosis. | Maria Pleguezuelo Jose Manuel Benitez Juan Jurado Jose Luis Montero Manuel De la Mata | 2013 | World Journal of Hepatology2013，5，1： | 44 |
| 9 | Portal vein thrombosis in cirrhosis: Controversies and latest developments显示文摘Portal vein thrombosis(PVT) is encountered in livercirrhosis, particularly in advanced disease. It has been a feared complication of cirrhosis, attributed to significant worsening of liver disease, poorer clinical outcomes and potential inoperability at liver transplantation; also catastrophic events such as acute intestinal ischaemia. Optimal management of PVT has not yet been addressed in any consensus publication.We review current literature on PVT in cirrhosis; its prevalence, pathophysiology, diagnosis, impact on the natural history of cirrhosis and liver transplantation,and management. Studies were identified by a search strategy using MEDLINE and Google Scholar. The incidence of PVT increases with increasing severity of liver disease: less than 1% in well-compensated cirrhosis, 7.4%-16% in advanced cirrhosis. Prevalence in patients undergoing liver transplantation is 5%-16%.PVT frequently regresses instead of uniform thrombus progression. PVT is not associated with increased risk of mortality. Optimal management has not been addressed in any consensus publication. We propose areas for future research to address unresolved clinical questions. | Damian J Harding M Thamara PR Perera Frederick Chen Simon Olliff Dhiraj Tripathi | 2015 | World Journal of Gastroenterology2015，21，22： | 42 |
| 10 | Long-term antiviral efficacy of entecavir and liver histology improvement in Chinese patients with hepatitis B virus-related cirrhosis显示文摘AIM: To evaluate the clinical outcomes of 240-wk treatment with entecavir(0.5 mg) in Chinese nucleosidenaive patients with cirrhosis.METHODS: A total of 204 nucleoside-naive patients with compensated(n = 96) or decompensated(n = 108) hepatitis B virus(HBV)-induced cirrhosis at the Department of Gastroenterology of the China-Japan Union Hospital(Jilin University, Changchun, China) who were treated with entecavir(0.5 mg) for 240 wk were enrolled in this study. Liver biopsy samples obtained from 38 patients prior to treatment(baseline) and at week 240 were evaluated by different independent histopathologists. Efficacy assessments included the proportions of patients who achieved an HBV DNA level < 500 copies/m L, the association of interleukin-28 B genetic variation with antivirus therapy, clinical outcomes, and histologic improvement. Changes in liver disease severity were analyzed, and liver histologic evaluation was performed in 38 patients with paired biopsies. Student t tests were used to compare the means of continuous variables between the groups, and the proportions of patients who achieved the endpoints were compared using the χ2 test.RESULTS: At week 240, 87.5% of the patients with compensated cirrhosis and 92.6% of the patients with decompensated cirrhosis achieved a HBV DNA level < 500 copies/m L. Three patients had genotypic entecavir resistance within the 240-wk period. No significant association was observed between virologic response and interleukin-28 genotype(CT, 88.2% vs CC, 90.6%). The proportion of patients with Child-Pughclass A disease was significantly increased at week 240(68%) from the baseline(47%; P < 0.01). The proportion of patients with Child-Pugh class B disease was significantly decreased at week 240(25%) from the baseline(39%; P = 0.02). In the patients with paired liver biopsies, the mean reduction in the Knodell necroinflammatory score from the baseline was 3.58 ± 1.03 points(7.11 ± 1.80 vs 3.53 ± 1.35, P < 0.01). The mean reduction in Ishak fibrosis score from the baseline was 1.26 ± 0.64 points(5.58 ± 0.50 vs 4.32 ± 0.81, P < 0.01).CONCLUSION: Entecavir is an effective treatment option for patients with HBV-related compensated or decompensated cirrhosis that can result in sustained virologic suppression and histologic improvement. | Yan Xu Yong-Gui Zhang Xu Wang Wen-Qian Qi Shao-You Qin Zhen-Hua Liu Jian Jiao Jiang-Bin Wang | 2015 | World Journal of Gastroenterology2015，21，25： | 50 |
| 11 | Hepatic inflammation and progressive liver fibrosis in chronic liver disease显示文摘Chronic liver inflammation drives hepatic fibrosis,and current immunosuppressive,anti-inflammatory,and anti-viral therapies can weaken this driver.Hepatic fibrosis is reversed,stabilized,or prevented in 57%-79%of patients by conventional treatment regimens,mainly by their anti-inflammatory actions.Responses,however,are commonly incomplete and inconsistently achieved.The fibrotic mechanisms associated with liver inflammation have been clarified,and anti-fibrotic agents promise to improve outcomes as adjunctive therapies.Hepatitis C virus and immune-mediated responses can activate hepatic stellate cells by increasing oxidative stress within hepatocytes.Angiotensin can be synthesized by activated hepatic stellate cells and promote the production of reactive oxygen species.Anti-oxidants(Nacetylcysteine,S-adenosyl-L-methionine,and vitamin E)and angiotensin inhibitors(losartin)have had antifibrotic actions in preliminary human studies,and they may emerge as supplemental therapies.Anti-fibrotic agents presage a new era of supplemental treatment for chronic liver disease. | Albert J Czaja | 2014 | World Journal of Gastroenterology2014，20，10： | 46 |
| 12 | Microbiota and the gut-liver axis:Bacterial translocation,inflammation and infection in cirrhosis显示文摘Liver disease is associated with qualitative and quantitative changes in the intestinal microbiota.In cirrhotic patients the alteration in gut microbiota is characterized by an overgrowth of potentially pathogenic bacteria(i.e.,gram negative species)and a decrease in autochthonous familiae.Here we summarize the available literature on the risk of gut dysbiosis in liver cirrhosis and its clinical consequences.We therefore described the features of the complex interaction between gut microbiota and cirrhotic host,the so called'gut-liver axis',with a particular attention to the acquired risk of bacterial translocation,systemic inflammation and the relationship with systemic infections in the cirrhotic patient.Such knowledge might help to develop novel and innovative strategies for the prevention and therapy of gut dysbiosis and its complication in liver cirrhosis. | Valerio Giannelli Vincenza Di Gregorio Valerio Iebba Michela Giusto Serena Schippa Manuela Merli Ulrich Thalheimer | 2014 | World Journal of Gastroenterology2014，20，45： | 43 |
| 13 | Gut microbiota and host metabolism in liver cirrhosis显示文摘The gut microbiota has the capacity to produce a diverse range of compounds that play a major role in regulatingthe activity of distal organs and the liver is strategically positioned downstream of the gut. Gut microbiota linked compounds such as short chain fatty acids, bile acids, choline metabolites, indole derivatives, vitamins, polyamines, lipids, neurotransmitters and neuroactive compounds, and hypothalamic-pituitary-adrenal axis hormones have many biological functions. This review focuses on the gut microbiota and host metabolism in liver cirrhosis. Dysbiosis in liver cirrhosis causes serious complications, such as bacteremia and hepatic encephalopathy, accompanied by small intestinal bacterial overgrowth and increased intestinal permeability. Gut dysbiosis in cirrhosis and intervention with probiotics and synbiotics in a clinical setting is reviewed and evaluated. Recent studies have revealed the relationship between gut microbiota and host metabolism in chronic metabolic liver disease, especially, non-alcoholic fatty liver disease, alcoholic liver disease, and with the gut microbiota metabolic interactions in dysbiosis related metabolic diseases such as diabetes and obesity. Recently, our understanding of the relationship between the gut and liver and how this regulates systemic metabolic changes in liver cirrhosis has increased. The serum lipid levels of phospholipids, free fatty acids, polyunsaturated fatty acids, especially, eicosapentaenoic acid, arachidonic acid, and docosahexaenoic acid have significant correlations with specific fecal flora in liver cirrhosis. Many clinical and experimental reports support the relationship between fatty acid metabolism and gut-microbiota. Various blood metabolome such as cytokines, amino acids, and vitamins are correlated with gut microbiota in probioticstreated liver cirrhosis patients. The future evaluation of the gut-microbiota-liver metabolic network and the intervention of these relationships using probiotics, synbiotics, and prebiotics, with sufficient nutrition could aid the development of treatments and prevention for liver cirrhosis patients. | Makoto Usami Makoto Miyoshi Hayato Yamashita | 2015 | World Journal of Gastroenterology2015，21，41： | 44 |
| 14 | Tumor necrosis factor-α and interleukin-6 in cirrhotic patients with spontaneous bacterial peritonitis显示文摘AIM:To evaluate the role of tumor necrosis factor-α(TNF-α) and interleukin-6(IL-6) in cirrhotic patients who have hepatic and renal impairment with spontaneous bacterial peritonitis(SBP).METHODS:We prospectively studied 120 cirrhotic patients with SBP and 80 cirrhotic patients with sterile ascitic fluid.They included 144 males and 56 females with ages ranging between 34 and 62 years.The diagnosis of cirrhosis was established by clinical and laboratory criteria that did not require histological confirmation.The severity of underlying liver disease was evaluated using Pugh's modification of Child's criteria(Child-Pugh scores).Ascitic fluid was sent to the laboratory for cell count,culture,sensitivity testing,and measurement of chemical elements(i.e.,albumin,glucose).Specimens were inoculated into aerobic and anaerobic blood culture bottles.Serum and ascitic fluid were also collected in sterile tubes at study entry(before the initiation of antibiotic treatment) and 48 h later.Assays for TNF-α and IL-6 in the serum and ascitic fluid were performed with an immunoenzymometric assay using manufacture's instructions.RESULTS:Cytokine levels in serum and ascitic fluid were significantly higher in the patients with SBP.(plasma TNF-α:135.35 ng/mL ± 11.21 ng/mL vs 92.86 ng/mL ± 17.56 ng/mL,P < 0.001;plasma IL-6:32.30 pg/mL ± 7.07 pg/mL vs 12.11 pg/mL ± 6.53 pg/mL,P < 0.001;ascitic fluid TNF-α:647.54 ± 107.11 ng/mL vs 238.43 ng/mL ± 65.42 ng/mL,P < 0.001);ascitic fluid IL-6:132.84 ng/mL ± 34.13 vs 40.41 ± 12.85 pg/mL,P < 0.001).About 48(40%) cirrhotic patients with SBP developed renal and hepatic impairment and showed significantly higher plasma and ascitic fluid cytokine levels at diagnosis of infection.[(plasma TNF-α:176.58 ± 17.84 vs 135.35 ± 11.21 ng/mL)(P < 0.001) and(IL-6:57.83 ± 7.85 vs 32.30 ± 7.07 pg/mL)(P < 0.001);ascitic fluid TNF-α:958.39 ± 135.72 vs 647.54 ± 107.11 ng/mL,(P < 0.001),ascitic fluid IL-6:654.74 ± 97.43 vs 132.84 ± 34.13 pg/mL,(P < 0.001)].Twenty nine patients(60.4%) with SBP and renal impairment died whereas,only four patients(5.55%) with SBP but without renal impairment died from gastrointestinal hemorrhage(P < 0.0005).CONCLUSION:It appears that TNF-α production may enhance liver cell injury and lead to renal impairment.This correlated well with the poor prognosis and significantly increased mortality associated with SBP in cirrhotic patients. | Muhammed AM Suliman Fawzy MH Khalil Salam SA Alkindi Anil V Pathare Ali AA Almadhani Neveen AAI Soliman | 2012 | World Journal of Gastrointestinal Pathophysiology2012，3，5： | 39 |
| 15 | Portal vein thrombosis in liver cirrhosis显示文摘Portal vein thrombosis(PVT) is considered to be a frequent complication of liver cirrhosis. However, unlike PVT in patients without cirrhosis, very few data are available on the natural history and management of PVT in cirrhosis, despite its association with potentially life-threatening conditions, such as gastroesophageal bleeding and acute intestinal ischemia. Moreover, no consensus regarding PVT in cirrhosis exists. Suggested causes of PVT in cirrhosis include reduced portal blood flow velocity, multiple congenital or acquired thrombophilic factors, inherited or acquired conditions, and derangement of liver architecture. However, the understanding of PVT in cirrhosis is incomplete. In addition, information on the management of PVT in cirrhosis is inadequate. The aims of this review are to:(1) assemble data on the physiopathological mechanism, clinical findings, diagnosis and management of PVT in cirrhosis;(2) describe the principal factors most frequently involved in PVT development; and(3) summarize the recent knowledge concerning diagnostic and therapeutic procedures. | Nao Kinjo Hirofumi Kawanaka Tomohiko Akahoshi Yoshi-hiro Matsumoto Masahiro Kamori Yoshihiro Nagao Naotaka Hashimoto Hideo Uehara Morimasa Tomikawa Ken Shirabe Yoshihiko Maehara | 2014 | World Journal of Hepatology2014，6，2： | 38 |
| 16 | Clinical implication of VEGF serum levels in cirrhotic patients with or without portal hypertension显示文摘INTRODUCTIONAngiogenesisorformationofnewbloodvesels,isatightlyregulatedprocesinwhichbloodveselssupplygrowingtisuewithnutrient... | Nimer Assy 1,4 , M Paizi 3,4 , D Gaitini 2, Y Baruch 1,4 and G Spira 3,4,5 | 1999 | World Journal of Gastroenterology1999，5，4： | 35 |
| 17 | De novo combined lamivudine and adefovir dipivoxil therapy vs entecavir monotherapy for hepatitis B virus-related decompensated cirrhosis显示文摘AIM:To compare efficacy of combined lamivudine(LAM)and adefovir dipivoxil(ADV)therapy with that of entecavir(ETV)monotherapy for hepatitis B virus(HBV)-related decompensated liver cirrhosis.METHODS:A total of 120 na ve patients with HBVrelated decompensated cirrhosis participated in this study.Sixty patients were treated with combined LAM and ADV therapy(LAM+ADV group),while the other60 were treated with ETV monotherapy(ETV group)for two years.Tests for liver and kidney function,alpha-fetoprotein,HBV serum markers,HBV DNA load,prothrombin time(PT),and ultrasonography or computed tomography scan of the liver were performed every1 to 3 mo.Repeated measure ANOVA and theχ2test were performed to compare the efficacy,side effects,and the cumulative survival rates at 48 and 96 wk.RESULTS:Forty-five patients in each group were observed for 96 wk.No significant differences in HBV DNA negative rates and alanine aminotransferase(ALT)normalization rates at weeks 48(χ2=2.12 and 2.88)and96(χ2=3.21 and 3.24)between the two groups were observed.Hepatitis B e antigen seroconversion rate in the LAM+ADV group at week 96 was significantly higher in the ETV group(43.5%vs 36.4%,χ2=4.09,P<0.05).Viral breakthrough occurred in 2 cases(4.4%)by week 48 and in 3 cases(6.7%)by week 96 in the LAM+ADV group,and no viral mutation was detected.In the ETV group,viral breakthrough occurred in 1 case(2.2%)at the end of week 96.An increase in albumin(F=18.9 and 17.3),decrease in total bilirubin and in ALT(F=16.5,17.1 and 23.7,24.8),reduced PT(F=22.7 and 24.5),and improved Child-Turcotte-Pugh and the model for end-stage liver disease scores(F=18.5,17.8,and 24.2,23.8)were observed in both groups.The cumulative rates of mortality and liver transplantation were 16.7%(10/60)and 18.3%(11/60)in the LAM+ADV and ETV groups,respectively.CONCLUSION:Both LAM+ADV combination therapy and ETV monotherapy can effectively inhibit HBV replication,improve liver function,and decrease mortality. | Jiang-Shan Lian Lin-Yan Zeng Jian-Yang Chen Hong-Yu Jia Yi-Min Zhang Dai-Rong Xiang Liang Yu Jian-Hua Hu Ying-Feng Lu Ling Zheng Lan-Juan Li Yi-Da Yang | 2013 | World Journal of Gastroenterology2013，19，37： | 36 |
| 18 | Portal hypertensive gastropathy:A systematic review of thepathophysiology,clinical presentation,natural history andtherapy显示文摘AIM: To describe the pathophysiology, clinical presentation, natural history, and therapy of portal hypertensive gastropathy(PHG) based on a systematic literature review.METHODS: Computerized search of the literature was performed via Pub Med using the following medical subject headings or keywords: 'portal' and 'gastropathy'; or 'portal' and 'hypertensive'; or 'congestive' and 'gastropathy'; or 'congestive' and 'gastroenteropathy'. The following criteria were applied for study inclusion: Publication in peer-reviewed journals, and publication since 1980. Articles were independently evaluated by each author and selected for inclusion by consensus after discussion based on the following criteria: Well-designed, prospective trials; recent studies; large study populations; and study emphasis on PHG. RESULTS: PHG is diagnosed by characteristic endoscopic findings of small polygonal areas of variable erythema surrounded by a pale, reticular border in a mosaic pattern in the gastric fundus/body in a patient with cirrhotic or non-cirrhotic portal hypertension. Histologic findings include capillary and venule dilatation, congestion, and tortuosity, without vascular fibrin thrombi or inflammatory cells in gastric submucosa. PHG is differentiated from gastric antral vascular ectasia by a different endoscopic appearance. The etiology of PHG is inadequately understood. Portal hypertension is necessary but insufficient to develop PHG because many patients have portal hypertension without PHG.PHG increases in frequency with more severe portal hypertension, advanced liver disease, longer liver disease duration, presence of esophageal varices, and endoscopic variceal obliteration. PHG pathogenesis is related to a hyperdynamic circulation, induced by portal hypertension, characterized by increased intrahepatic resistance to flow, increased splanchnic flow, increased total gastric flow, and most likely decreased gastric mucosal flow. Gastric mucosa in PHG shows increased susceptibility to gastrotoxic chemicals and poor wound healing. Nitrous oxide, free radicals, tumor necrosis factor-alpha, and glucagon may contribute to PHG development. Acute and chronic gastrointestinal bleeding are the only clinical complications. Bleeding is typically mild-to-moderate. Endoscopic therapy is rarely useful because the bleeding is typically diffuse. Acute bleeding is primarily treated with octreotide, often with concomitant proton pump inhibitor therapy, or secondarily treated with vasopressin or terlipressin. Nonselective β-adrenergic receptor antagonists, particularly propranolol, are used to prevent bleeding after an acute episode or for chronic bleeding. Iron deficiency anemia from chronic bleeding may require iron replacement therapy. Transjugular-intrahepaticportosystemic-shunt or liver transplantation is highly successful ultimate therapies because they reduce the underlying portal hypertension.CONCLUSION: PHG is important to recognize in patients with cirrhotic or non-cirrhotic portal hypertension because it can cause acute or chronic GI bleeding that often requires pharmacologic therapy. | Mihajlo Gjeorgjievski Mitchell S Cappell | 2016 | World Journal of Hepatology2016，8，4： | 38 |
| 19 | MR with Gd-EOB-DTPA in assessment of liver nodules in cirrhotic patients显示文摘To date the imaging diagnosis of liver lesions is based mainly on the identification of vascular features, which are typical of overt hepatocellular carcinoma(HCC), but the hepatocarcinogenesis is a complex and multistep event during which, a spectrum of nodules develop within the liver parenchyma, including benign small and large regenerative nodule(RN), low-grade dysplastic nodule(LGDN), high-grade dysplastic nodule(HGDN), early HCC, and well differentiated HCC. These nodules may be characterised not only on the basis of their respective different blood supplies, but also on their different hepatocyte function. Recently, in liver imaging the introduction of hepatobiliary magnetic resonance imaging contrast agent offered the clinicians the possibility to obtain, at once, information not only related to the vascular changes of liver nodules but also information on hepatocyte function. For this reasons this new approach becomes the most relevant diagnostic clue for differentiating low-risk nodules(LGDN-RN) from highrisk nodules(HGDN/early HCC or overt HCC) and consequently new diagnostic algorithms for HCC have been proposed. The use of hepatobiliary contrast agents is constantly increasing and gradually changing the standard of diagnosis of HCC. The main purpose of this review is to underline the added value of Gd-EOB-DTPA in early-stage diagnoses of HCC. We also analyse the guidelines for the diagnosis and management of HCC, the key concepts of HCC development, growth and spread and the imaging appearance of precursor nodules that eventually may transform into overt HCC. | Riccardo Inchingolo Riccardo Faletti Luigi Grazioli Eleonora Tricarico Marco Gatti Anna Pecorelli Davide Ippolito | 2018 | World Journal of Hepatology2018，10，7： | 37 |
| 20 | Spontaneous bacterial and fungal peritonitis in patients with liver cirrhosis: A literature review显示文摘Spontaneous bacterial(SBP) and spontaneous fungal peritonitis(SFP) can be a life-threatening infection in patients with liver cirrhosis(LC) and ascites. One of the possible mechanisms of developing SBP is bacterial translocation. Although the number of polymorphonuclear cells in the culture of ascitic fluid is diagnostic for SBP, secondary bacterial peritonitis is necessary to exclude. The severity of underlying liver dysfunction is predictive of developing SBP; moreover, renal impairment and infections caused by multidrug-resistant(MDR) organism are associated with a fatal prognosis of SBP. SBP is treated by antimicrobials, but initial empirical treatment may not succeed because of the presence of MDR organisms, particularly in nosocomial infections. Antibiotic prophylaxis is recommended for patients with LC at a high risk of developing SBP, gastrointestinal bleeding, or a previous episode of SBP, but the increase in the risk of developing an infection caused by MDR organisms is a serious concern globally. Less is known about SFP in patients with LC, but the severity of underlying liver dysfunction may increase the hospital mortality. SFP mortality has been reported to be higher than that of SBP partially because the difficulty of early differentiation between SFP and SBP induces delayed antifungal therapy for SFP. | Toru Shizuma | 2018 | World Journal of Hepatology2018，10，2： | 35 |
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