Objective:Hepatocellular carcinoma(HCC)is the most common primary liver cancer,the fifth most common cancer and the third most common global cause of cancer related deaths.Chronic alcohol consumption is a well-known r...Objective:Hepatocellular carcinoma(HCC)is the most common primary liver cancer,the fifth most common cancer and the third most common global cause of cancer related deaths.Chronic alcohol consumption is a well-known risk factor for HCC.Acetaldehyde,a main metabolite of ethanol oxidation.展开更多
Of dietary monosaccharides,fructose is primarily metabolized by aldolase B(ALDOB)in the liver,whereas glucose is metabolized elsewhere in the body.It has been documented that overconsumption of dietary fructose,especi...Of dietary monosaccharides,fructose is primarily metabolized by aldolase B(ALDOB)in the liver,whereas glucose is metabolized elsewhere in the body.It has been documented that overconsumption of dietary fructose,especially industrial fructose,associates significantly with advanced inflammation in chronic hepatitis C(CHC)patients.However,little is known about whether impaired fructolysis might attribute to CHC hepatopathogenesis.Herein we found that the level of ALDOB protein was significantly reduced in CHC patients and mice that were persistently infected by hepatitis C virus(HCV).In vitro,HCV infection activated caspase-1,and caspase-3 to a lesser extent,which proteolyzed ALDOB and blocked fructose metabolism in hepatocytes.Downregulation of ALDOB attenuated HCV replication,indicating an intrinsic anti-HCV role for homeostatic fructolysis.On the other hand,reduced ALDOB caused intracellular fructose 1-phosphate accumulation that provoked severe cellular toxicity through intracellular ATP depletion and heightened glycation,which was aggravated by HCV infection.Taken together,these results have unveiled that inflammatory activation of caspase-1 impairs homeostatic fructolysis and exacerbates liver damage.展开更多
Aims:Although useful for distinguishing drug-induced liver injury(DILI)from autoimmune hepatitis(AIH),liver biopsy is an invasive examination,and the presence of antinuclear antibody(ANA)positivity in patients with DI...Aims:Although useful for distinguishing drug-induced liver injury(DILI)from autoimmune hepatitis(AIH),liver biopsy is an invasive examination,and the presence of antinuclear antibody(ANA)positivity in patients with DILI could lead to excessive use of biopsy.Hence,we aimed to identify screening markers for histological features of AIH in patients with ANA-positive DILI and verify their clinical outcomes after 1 year.Methods:This retrospective study included patients with ANA-positive DILI,who underwent liver biopsy between January 2017 and April 2022.Two pathologists identified histological features of AIH.We detected the independent indicators associated with histological features of AIH using logistic regression.We evaluated their diagnostic ability for histological features of AIH using the receiver operating characteristic curve.The followup period to determine clinical outcomes was 1 year after DILI onset.Theχ2 test or Fisher's exact test was used to compare categorical data and the Wilcoxon rank-sum test was used to compare continuous variables.Twosided p<0.05 was considered to indicate significance.Results:The final analysis included 125 patients with ANA-positive DILI,of whom 18 had AIH-like histology.Factors independently associated with AIH-like histology included globulin levels(odds ratio[OR]=1.154,95%confidence interval[CI]=1.046-1.288;p=0.006)and ANA titer≥1:1000(OR=3.531,95%CI=1.136-11.303;p=0.029).The optimal globulin cutoff indicating AIH-like histology was 31.8 g/L.This globulin level in combination with ANA titer≥1:1000(area under the curve=0.785,95%CI=0.738-0.832)provided a sensitivity of 100%and a specificity of 57%for indicating histological features of AIH in patients with ANA-positive DILI.During follow-up,more patients developed AIH in the group with AIH-like histology than in the group without AIH-like histology(35.3%vs.0,p<0.001).Conclusions:For patients with ANA-positive DILI and ANA titer≥1:1000 or globulin≥31.8 g/L,liver biopsy is recommended to determine the presence of histological features of AIH and guide further monitoring.展开更多
Alcohol-associated liver disease(ALD)is caused by longterm heavy alcohol consumption.The disease is still a significant contributor to the morbidity burden of liver diseases in America and some European countries.A tr...Alcohol-associated liver disease(ALD)is caused by longterm heavy alcohol consumption.The disease is still a significant contributor to the morbidity burden of liver diseases in America and some European countries.A trend of increasing incidence of ALD has also been observed in Asia over the past two decades.[1]Alcohol excise taxes are taxes imposed on alcoholic beverages and these taxes are typically included in the product price.Increasing the alcohol excise taxes is among the most efficient and cost-effective interventions for reducing excessive consumption of alcohol in the population.Increasing alcohol excise taxes indirectly increases the price of alcohol,which may exceed some consumers’intention or purchase ability,thereby reducing alcohol use and misuse.A study showed that doubling of spirits excise taxes would reduce per capita consumption of spirits by 8–10%,while the number of cases requiring liver transplantation for ALD would decrease by 6–7%.展开更多
TRIM22, a tripartite-motif （TRIM） protein, is upregulated upon interferon alpha （IFNa） administration to hepatitis C virus （HCV）-infected patients. However, the physiological role of TRIM22 upregulation remains ...TRIM22, a tripartite-motif （TRIM） protein, is upregulated upon interferon alpha （IFNa） administration to hepatitis C virus （HCV）-infected patients. However, the physiological role of TRIM22 upregulation remains unclear. Here, we describe a potential antiviral function of TRI M22＇s targeting of the HCV NSSA protein. NS5A is important for HCV replication and for resistance to I FNa therapy. During the first 24 h following the initiation of I FNa treatment, upregulation of TRIM22 in the peripheral blood mononuclear cells （PBMCs） of HCV patients correlated with a decrease in viral titer. This phenomenon was confirmed in the hepatocyte-derived cell line Huh-7, which is highly permissive for HCV infection. TRIM22 over-expression inhibited HCV replication, and Small interfering RNA （siRNA）-mediated knockdown of TRIM22 diminished IFNα-induced anti-HCV function. Furthermore, we determined that TRIM22 ubiquitinates NS5A in a concentration-dependent manner. In summary, our results suggest that TRIM22 upregulation is associated with HCV decline during IFNα treatment and Dlavs an important role in controlling HCV replication in vitro.展开更多
Copper plays an important role in many metabolic activities in the human body.Copper level in the human body is in a state of dynamic equilibrium.Recent research on copper metabolism has revealed that copper dyshomeos...Copper plays an important role in many metabolic activities in the human body.Copper level in the human body is in a state of dynamic equilibrium.Recent research on copper metabolism has revealed that copper dyshomeostasis can cause cell damage and induce or aggravate some diseases by affecting oxidative stress,proteasome,cuprotosis,and angiogenesis.The liver plays a central role in copper metabolism in the human body.Research conducted in recent years has unraveled the relationship between copper homeostasis and liver diseases.In this paper,we review the available evidence of the mechanism by which copper dyshomeostasis promotes cell damage and the development of liver diseases,and identify the future research priorities.展开更多
Background and Aims:Approximately 10%of patients with acute decompensated(AD)cirrhosis develop acute-on-chronic liver failure(ACLF)within 28 days.Such cases have high mortality and are difficult to predict.Therefore,w...Background and Aims:Approximately 10%of patients with acute decompensated(AD)cirrhosis develop acute-on-chronic liver failure(ACLF)within 28 days.Such cases have high mortality and are difficult to predict.Therefore,we aimed to establish and validate an algorithm to identify these patients on hospitalization.Methods:Hospitalized patients with AD who developed ACLF within 28 days were considered pre-ACLF.Organ dysfunction was defined accord-ing to the chronic liver failure-sequential organ failure as-sessment(CLIF-SOFA)criteria,and proven bacterial infec-tion was taken to indicate immune system dysfunction.A retrospective multicenter cohort and prospective one were used to derive and to validate the potential algorithm,re-spectively.A miss rate of<5%was acceptable for the calcu-lating algorithm to rule out pre-ACLF.Results:In the deri-vation cohort(n=673),46 patients developed ACLF within 28 days.Serum total bilirubin,creatinine,international normalized ratio,and present proven bacterial infection at admission were associated with the development of ACLF.AD patients with≥2 organ dysfunctions had a higher risk for pre-ACLF patients[odds ratio=16.58195%confidence interval:(4.271-64.363),p<0.001].In the derivation co-hort,67.5%of patients(454/673)had≤1 organ dysfunction and two patients(0.4%)were pre-ACLF,with a miss rate of 4.3%(missed/total,2/46).In the validation cohort,65.9%of patients(914/1388)had≤1 organ dysfunction,and four(0.3%)of them were pre-ACLF,with a miss rate of 3.4%(missed/total,4/117).Conclusions:AD patients with≤1 organ dysfunction had a significantly lower risk of developing ACLF within 28 days of admission and could be safely ruled out with a pre-ACLF miss rate of<5%.展开更多
Dear Editor,Human enteroviruses(HEVs)comprise polioviruses,coxsackieviruses,echoviruses,rhinoviruses,and the enterovirus subgroups and belong to the genus Enterovirus in the family Picornaviridae(Baggen et al.2018).Th...Dear Editor,Human enteroviruses(HEVs)comprise polioviruses,coxsackieviruses,echoviruses,rhinoviruses,and the enterovirus subgroups and belong to the genus Enterovirus in the family Picornaviridae(Baggen et al.2018).The HEV genome was thought to contain a single open reading frame(ORF)encoding one polyprotein,which was post-translationally processed into structural capsid proteins(VP1-4)and non-structural accessory proteins(2A,2B,2C,3A,3B,3C,3D)(Baggen et al.2018).Recently,we and others,have identified an additional upstream ORF(Guo et al.2019a;Lulla et al.2019)(ORF2/uORF).展开更多
Aim:The study aimed to investigate the short-term outcomes of hospitalized patients with chronic liver disease(CLDs)and assess the prognostic impact of predisposition and precipitants,which currently remains unclear.M...Aim:The study aimed to investigate the short-term outcomes of hospitalized patients with chronic liver disease(CLDs)and assess the prognostic impact of predisposition and precipitants,which currently remains unclear.Methods:The study included 3970 hospitalized patients with CLDs from two prospective longitudinal multicenter studies(NCT02457637 and NCT03641872)conducted in highly endemic hepatitis B virus(HBV)areas.Competing risk analysis was used to evaluate the effect of predispositions,including the etiology and severity of CLDs and precipitants;on sequential 28,90,and 365-day liver transplantation(LT)-free mortality.Results:Among all enrolled patients,76.8%of adverse outcomes(including death and LT)within one year occurred within 90 days.Compared with alcoholic etiology,the association of HBV etiology with poorer outcomes was remarkably on the 28th day(hazard ratio[HR],1.81;95%confidence interval[CI],1.07-3.06;p=0.026);however,and dimin-ished or became insignificant at 90 days and 365 days.Cirrhosis increased the adjusted risk for 365-day(HR,1.50;CI,1.13-1.99;p=0.004)LT-free mortality when compared with noncirrhosis.In patients with cirrhosis,prior decompensation(PD)independently increased the adjusted risk of 365-day LT-free mortality by 1.25-fold(p=0.021);however,it did not increase the risk for 90-day mortality.Neither the category nor the number of precipitants influenced the adjusted risk of 28 or 90-day LT-free mortality.Conclusions:The 90-day outcome should be considered a significant endpoint for evaluating the short-term prognosis of hospitalized patients with CLD.Predisposing factors,other than etiology,mainly affected the delayed(365-day)outcome.Timely effective therapy for CLD etiology,especially antiviral treatments for HBV,and post-discharge long-term surveillance monitoring in cirrhotic patients undergoing PD are suggested to enhance disease management and reduce mortality.展开更多
文摘Objective:Hepatocellular carcinoma(HCC)is the most common primary liver cancer,the fifth most common cancer and the third most common global cause of cancer related deaths.Chronic alcohol consumption is a well-known risk factor for HCC.Acetaldehyde,a main metabolite of ethanol oxidation.
基金the National Natural Science Foundation of China(81530067,31621061,31300716)the Ministry of Science and Technology(2015CB554304)+2 种基金the Hubei Provincial Natural Science Foundation(2013CFB487)Shandong Laboratory Microecological Biomedicine(JNL-2023002B)the Fundamental Research Funds for the Central Universities(2022ZFJH003).
文摘Of dietary monosaccharides,fructose is primarily metabolized by aldolase B(ALDOB)in the liver,whereas glucose is metabolized elsewhere in the body.It has been documented that overconsumption of dietary fructose,especially industrial fructose,associates significantly with advanced inflammation in chronic hepatitis C(CHC)patients.However,little is known about whether impaired fructolysis might attribute to CHC hepatopathogenesis.Herein we found that the level of ALDOB protein was significantly reduced in CHC patients and mice that were persistently infected by hepatitis C virus(HCV).In vitro,HCV infection activated caspase-1,and caspase-3 to a lesser extent,which proteolyzed ALDOB and blocked fructose metabolism in hepatocytes.Downregulation of ALDOB attenuated HCV replication,indicating an intrinsic anti-HCV role for homeostatic fructolysis.On the other hand,reduced ALDOB caused intracellular fructose 1-phosphate accumulation that provoked severe cellular toxicity through intracellular ATP depletion and heightened glycation,which was aggravated by HCV infection.Taken together,these results have unveiled that inflammatory activation of caspase-1 impairs homeostatic fructolysis and exacerbates liver damage.
基金National Natural Science Foundation of China,Grant/Award Number:81972265 and 82170602National Natural Science Foundation of Jilin Province,Grant/Award Number:20200201324JC+1 种基金Project for Middle-aged and Young Excellent Technological Innovation Talents of Jilin Province,Grant/Award Number:20220508079RCProject for Health Talents of Jilin Province,Grant/Award Number:JLSWSRCZX 2021-079。
文摘Aims:Although useful for distinguishing drug-induced liver injury(DILI)from autoimmune hepatitis(AIH),liver biopsy is an invasive examination,and the presence of antinuclear antibody(ANA)positivity in patients with DILI could lead to excessive use of biopsy.Hence,we aimed to identify screening markers for histological features of AIH in patients with ANA-positive DILI and verify their clinical outcomes after 1 year.Methods:This retrospective study included patients with ANA-positive DILI,who underwent liver biopsy between January 2017 and April 2022.Two pathologists identified histological features of AIH.We detected the independent indicators associated with histological features of AIH using logistic regression.We evaluated their diagnostic ability for histological features of AIH using the receiver operating characteristic curve.The followup period to determine clinical outcomes was 1 year after DILI onset.Theχ2 test or Fisher's exact test was used to compare categorical data and the Wilcoxon rank-sum test was used to compare continuous variables.Twosided p<0.05 was considered to indicate significance.Results:The final analysis included 125 patients with ANA-positive DILI,of whom 18 had AIH-like histology.Factors independently associated with AIH-like histology included globulin levels(odds ratio[OR]=1.154,95%confidence interval[CI]=1.046-1.288;p=0.006)and ANA titer≥1:1000(OR=3.531,95%CI=1.136-11.303;p=0.029).The optimal globulin cutoff indicating AIH-like histology was 31.8 g/L.This globulin level in combination with ANA titer≥1:1000(area under the curve=0.785,95%CI=0.738-0.832)provided a sensitivity of 100%and a specificity of 57%for indicating histological features of AIH in patients with ANA-positive DILI.During follow-up,more patients developed AIH in the group with AIH-like histology than in the group without AIH-like histology(35.3%vs.0,p<0.001).Conclusions:For patients with ANA-positive DILI and ANA titer≥1:1000 or globulin≥31.8 g/L,liver biopsy is recommended to determine the presence of histological features of AIH and guide further monitoring.
基金sponsored by the National Natural Science Foundation of China(Nos.81972265 and 82170602)the National Natural Science Foundation of Jilin Province(No.20200201324JC)+1 种基金the Project for Middle-aged and Young Excellent Technological Innovation Talents of Jilin Province(No.20220508079RC)the Project for Health Talents of Jilin Province(No.JLSWSRCZX 2021-079).
文摘Alcohol-associated liver disease(ALD)is caused by longterm heavy alcohol consumption.The disease is still a significant contributor to the morbidity burden of liver diseases in America and some European countries.A trend of increasing incidence of ALD has also been observed in Asia over the past two decades.[1]Alcohol excise taxes are taxes imposed on alcoholic beverages and these taxes are typically included in the product price.Increasing the alcohol excise taxes is among the most efficient and cost-effective interventions for reducing excessive consumption of alcohol in the population.Increasing alcohol excise taxes indirectly increases the price of alcohol,which may exceed some consumers’intention or purchase ability,thereby reducing alcohol use and misuse.A study showed that doubling of spirits excise taxes would reduce per capita consumption of spirits by 8–10%,while the number of cases requiring liver transplantation for ALD would decrease by 6–7%.
文摘TRIM22, a tripartite-motif （TRIM） protein, is upregulated upon interferon alpha （IFNa） administration to hepatitis C virus （HCV）-infected patients. However, the physiological role of TRIM22 upregulation remains unclear. Here, we describe a potential antiviral function of TRI M22＇s targeting of the HCV NSSA protein. NS5A is important for HCV replication and for resistance to I FNa therapy. During the first 24 h following the initiation of I FNa treatment, upregulation of TRIM22 in the peripheral blood mononuclear cells （PBMCs） of HCV patients correlated with a decrease in viral titer. This phenomenon was confirmed in the hepatocyte-derived cell line Huh-7, which is highly permissive for HCV infection. TRIM22 over-expression inhibited HCV replication, and Small interfering RNA （siRNA）-mediated knockdown of TRIM22 diminished IFNα-induced anti-HCV function. Furthermore, we determined that TRIM22 ubiquitinates NS5A in a concentration-dependent manner. In summary, our results suggest that TRIM22 upregulation is associated with HCV decline during IFNα treatment and Dlavs an important role in controlling HCV replication in vitro.
基金sponsored by the National Natural Science Foundation of China(Nos.81972265,82170602)the National Natural Science Foundation of Jilin Province(No.20200201324JC)+1 种基金the Project for Middle-aged and Young Excellent Technological Innovation Talents of Jilin Province(No.20220508079RC)the Project for Health Talents of Jilin Province(No.JLSWSRCZX 2021-079).
文摘Copper plays an important role in many metabolic activities in the human body.Copper level in the human body is in a state of dynamic equilibrium.Recent research on copper metabolism has revealed that copper dyshomeostasis can cause cell damage and induce or aggravate some diseases by affecting oxidative stress,proteasome,cuprotosis,and angiogenesis.The liver plays a central role in copper metabolism in the human body.Research conducted in recent years has unraveled the relationship between copper homeostasis and liver diseases.In this paper,we review the available evidence of the mechanism by which copper dyshomeostasis promotes cell damage and the development of liver diseases,and identify the future research priorities.
基金the National Science and Technology Major Project(2018ZX10723203,2018ZX10302206)National Natural Science Foundation of China(82070650,81270533,81470038)+7 种基金National Key Research and Development Program of China(2017YFC0908100)Local Innova-tive and Research Teams Project of Guangdong Pearl River Talents Program(2017BT01S131)Key Scientific and Technological Program of Guangzhou City(201508020262)Department of Science and Technology of Guangdong Province(2014B020228003,2015B020226004)Clinical Research Program of Nanfang Hospital,Southern Medical University(2018CR037,2020CR026)Key-Area Research and Development Program of Guangdong Province(2019B020227004)Clinical Research Startup Program of Southern Medical University by High-level University Construction Funding of Guangdong Provincial Department of Education(LC2019ZD006,LC2016PY005)President Foundation of Nanfang Hospital,Southern Medical University(2019Z003).
文摘Background and Aims:Approximately 10%of patients with acute decompensated(AD)cirrhosis develop acute-on-chronic liver failure(ACLF)within 28 days.Such cases have high mortality and are difficult to predict.Therefore,we aimed to establish and validate an algorithm to identify these patients on hospitalization.Methods:Hospitalized patients with AD who developed ACLF within 28 days were considered pre-ACLF.Organ dysfunction was defined accord-ing to the chronic liver failure-sequential organ failure as-sessment(CLIF-SOFA)criteria,and proven bacterial infec-tion was taken to indicate immune system dysfunction.A retrospective multicenter cohort and prospective one were used to derive and to validate the potential algorithm,re-spectively.A miss rate of<5%was acceptable for the calcu-lating algorithm to rule out pre-ACLF.Results:In the deri-vation cohort(n=673),46 patients developed ACLF within 28 days.Serum total bilirubin,creatinine,international normalized ratio,and present proven bacterial infection at admission were associated with the development of ACLF.AD patients with≥2 organ dysfunctions had a higher risk for pre-ACLF patients[odds ratio=16.58195%confidence interval:(4.271-64.363),p<0.001].In the derivation co-hort,67.5%of patients(454/673)had≤1 organ dysfunction and two patients(0.4%)were pre-ACLF,with a miss rate of 4.3%(missed/total,2/46).In the validation cohort,65.9%of patients(914/1388)had≤1 organ dysfunction,and four(0.3%)of them were pre-ACLF,with a miss rate of 3.4%(missed/total,4/117).Conclusions:AD patients with≤1 organ dysfunction had a significantly lower risk of developing ACLF within 28 days of admission and could be safely ruled out with a pre-ACLF miss rate of<5%.
基金This work was supported in part by funding from the National Natural Science Foundation of China(81772183 and 31800150)the Department of Science and Technology of Jilin Province(No.20190304033YY and 20180101127JC)+2 种基金the open project of Key Laboratory of Organ Regeneration and Transplantation,Ministry of Educationthe Program for JLU Science and Technology Innovative Research Team(2017TD-08)Fundamental Research Funds for the Central Universities。
文摘Dear Editor,Human enteroviruses(HEVs)comprise polioviruses,coxsackieviruses,echoviruses,rhinoviruses,and the enterovirus subgroups and belong to the genus Enterovirus in the family Picornaviridae(Baggen et al.2018).The HEV genome was thought to contain a single open reading frame(ORF)encoding one polyprotein,which was post-translationally processed into structural capsid proteins(VP1-4)and non-structural accessory proteins(2A,2B,2C,3A,3B,3C,3D)(Baggen et al.2018).Recently,we and others,have identified an additional upstream ORF(Guo et al.2019a;Lulla et al.2019)(ORF2/uORF).
基金Clinical Research Plan of SHDC,Grant/Award Number:SHDC2020CR1037BShanghai Municipal Key Clinic Specialty,Grant/Award Number:shslczdzk00602+16 种基金National Key R&D Program of China,Grant/Award Number:2017YFC0908100National Science and Technology Major Project,Grant/Award Numbers:2018ZX10302206,2018ZX10723203,2017ZX10202202Shanghai Municipal Education Commission–Guofeng Clinical Medicine Grant Support,Grant/Award Number:20152213National Natural Science Foundation of China,Grant/Award Numbers:82170629,81930061,81900579,81970550,82070613,82070650,81972265,81870425,81774234Shanghai Hospital Development Commission,Grant/Award Number:16CR1024BChongqing Natural Science Foundation,Grant/Award Number:CSTC2019jcyjzdxmX0004Beijing Municipal Science&Technology Commission,Grant/Award Number:Z191100006619033Local Innovative and Research Teams Project of Guangdong Pearl River Talents Program,Grant/Award Number:2017BT01S131Clinical Research Program of Nanfang Hospital,Southern Medical University,Grant/Award Numbers:2018CR037,2020CR026Clinical Research Startup Program of Southern Medical University by High-level University Construction Funding of Guangdong Provincial Department of Education,Grant/Award Number:LC2019ZD006President Foundation of Nanfang Hospital,Southern Medical University,Grant/Award Number:2019Z003Foundation for Innovative Research Groups of Hubei Provincial Natural Science Foundation,Grant/Award Number:2018CFA031Hubei Province's Outstanding Medical Academic Leader Program and Project of Hubei University of Medicine,Grant/Award Numbers:FDFR201902,2020XGFYZR05Fundamental Research Funds for the Central Universities,Grant/Award Number:2021FZZX001-41Guangdong Basic and Applied Basic Research Foundation,Grant/Award Number:2020A1515010052Natural Fund of Guangdong Province,Grant/Award Number:2016A030313237Guangzhou City Science and Technology Project,Grant/Award Number:201607010064。
文摘Aim:The study aimed to investigate the short-term outcomes of hospitalized patients with chronic liver disease(CLDs)and assess the prognostic impact of predisposition and precipitants,which currently remains unclear.Methods:The study included 3970 hospitalized patients with CLDs from two prospective longitudinal multicenter studies(NCT02457637 and NCT03641872)conducted in highly endemic hepatitis B virus(HBV)areas.Competing risk analysis was used to evaluate the effect of predispositions,including the etiology and severity of CLDs and precipitants;on sequential 28,90,and 365-day liver transplantation(LT)-free mortality.Results:Among all enrolled patients,76.8%of adverse outcomes(including death and LT)within one year occurred within 90 days.Compared with alcoholic etiology,the association of HBV etiology with poorer outcomes was remarkably on the 28th day(hazard ratio[HR],1.81;95%confidence interval[CI],1.07-3.06;p=0.026);however,and dimin-ished or became insignificant at 90 days and 365 days.Cirrhosis increased the adjusted risk for 365-day(HR,1.50;CI,1.13-1.99;p=0.004)LT-free mortality when compared with noncirrhosis.In patients with cirrhosis,prior decompensation(PD)independently increased the adjusted risk of 365-day LT-free mortality by 1.25-fold(p=0.021);however,it did not increase the risk for 90-day mortality.Neither the category nor the number of precipitants influenced the adjusted risk of 28 or 90-day LT-free mortality.Conclusions:The 90-day outcome should be considered a significant endpoint for evaluating the short-term prognosis of hospitalized patients with CLD.Predisposing factors,other than etiology,mainly affected the delayed(365-day)outcome.Timely effective therapy for CLD etiology,especially antiviral treatments for HBV,and post-discharge long-term surveillance monitoring in cirrhotic patients undergoing PD are suggested to enhance disease management and reduce mortality.
