Background:Sorafenib is the first-line treatment agent for advanced hepatocellular carcinoma (HCC), but it is effective in very few patients. Thus, this study was intended to identify gene signatures associated with sorafenib response in HCC and construct a prognostic risk model based on these gene signatures. Methods:The gene expression level data of HCC were downloaded from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. First, we evaluated the HCC sensitivity to sorafenib of the samples and investigated the correlation between HCC sensitivity to sorafenib and clinical prognosis. By Weighted Gene Co-Expression Network Analysis (WGCNA) algorithm, the sorafenib resistance associated genes were obtained. Combined with the sorafenib resistance related data set, genes significantly associated sorafenib responses were screened. Then prognostic signature genes were screened to construct a risk prognosis model. The correlation of risk grouping with immune cells was explored. Results:A total of 399 significantly genes associated with sorafenib response were obtained, which were involved in metabolic and complement pathways. Finally, 5 signature genes (DNASE1L3, ACSL6, ACAN, BRSK1 and CD68) were identified, and a risk prognostic risk prediction model was constructed. The receiver operating characteristic (ROC) curves suggested that the model presented high predictive precision. Additionally, a nomogram was constructed based on pathologic stage and risk model status, which also had good prediction performance in survival prognosis. Moreover, there was a significant correlation between risk groups and immunity. Conclusions:Our study established a sorafenib response-related prognostic risk prediction model in HCC based on five signature genes (DNASE1L3, ACSL6, ACAN, BRSK1 and CD68), which had high predictive precision on sorafenib response.

Although Ubc9-mediated SUMOylation are recognized to regulate the multiple aspects of hepatic biological processes, its impact on hepatic senescence and metabolic dysfunction-associated steatotic liver disease (MASLD), however, is yet to be fully addressed. Herein noted an age-dependent decrease of hepatic Ubc9 expression is first noted along with an escalated decrease of protein SUMOylation, which is coupled with enhanced senescent marker expressions both in humans and mice. Interestingly, Ubc9 is dispensable for liver development at the embryonic stage. However, Ubc9 deficiency in hepatocytes rendered mice with an exacerbated hepatic aging phenotype and more susceptible to fatty liver disease and steatohepatitis following the challenge of a methionine- and choline-deficient (MCD)-diet. Ii is further demonstrated that nuclear ribosomal protein L3 (RPL3) interacts with DExD/H-box (DDX/DHX) helicases (DHX9), which then recruits RNA polymerase II to the p16 promoter to transcribe its expression, thereby exacerbating the hepatocyte aging process. However, Ubc9-mediated SUMOylation prevents RPL3 nuclear translocation, by which it represses the expression of senescent markers such as p16 to attenuate the hepatic aging process. Together, the study highlights that Ubc9-mediated SUMOylation of RPL3 could be an unappreciated mechanism against hepatic aging in clinical settings.

Solid organ transplantation has significantly prolonged the survival of patients with end-stage diseases. However, long-term use of immunosuppressants will increase the risk of post-transplantation diabetes mellitus (PTDM) in the recipients, thereby elevating the risk of infection, cardiovascular disease and death. In recent years, with persistent improvement of diagnostic criteria of PTDM, clinicians have deepened the understanding of this disease. Compared with type 2 diabetes mellitus, PTDM significantly differs in pathophysiological characteristics and clinical progression. Hence, different treatment strategies should be adopted. Early identification of risk factors of organ transplant recipients, early diagnosis and intervention are of significance for improving the quality of life of recipients, prolonging the survival of grafts and reducing the fatality of recipients. Therefore, the diagnosis, incidence and risk factors of PTDM were reviewed in this article, aiming to provide reference for clinicians to deliver prompt diagnosis and intervention for PTDM.

Non-alcoholic fatty liver disease (NAFLD) is a complex disease characterized by a massive accumulation of lipids in the liver, with a continuous progression of simple steatosis, non-alcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma. Non-alcoholic fatty liver disease is associated with obesity, insulin resistance, and metabolic syndrome; it is a severe public health risk and is currently the most common liver disease of the world. In addition to the fatty infiltration of the liver in non-alcoholic fatty liver disease patients, the field of liver transplantation faces similar obstacles. NAFLD and NASH primarily involve lipotoxicity, inflammation, oxidative stress, and insulin resistance. However, the precise mechanisms and treatments remain unclear. Therapeutic approaches encompass exercise, weight control, as well as treatments targeting antioxidants and anti-inflammatory pathways. The role of animal models in research has become crucial as a key tool to explore the molecular mechanisms and potential treatments for non-alcoholic fatty liver disease and non-alcoholic steatohepatitis. Here, we summarized the current understanding of the pathogenesis of non-alcoholic fatty liver disease and non-alcoholic steatohepatitis and discussed animal models commonly used in recent years.

Background and Aims Reducing reactive oxygen species (ROS) production has proven an effective way for alleviating oxidative stress during ischemia-reperfusion injury (IRI). Moreover, inhibition of Rac1 could reduce ROS production and prevent oxidative stress injury. Previous studies have suggested a positive interactivation feedback loop between Rac1 and hypoxia-inducible factor (HIF)-1α, the latter being up-regulated early during ischemia. The positive inter-activation between Rac1 and HIF-1α would aggravate ROS production, thereby promoting IRI. This study was designed to verify the effects of Rac1 inhibition on hepatic IRI both at animal and cellular levels and to explore the interaction between Rac1 and HIF-1α during hepatic IRI. Methods C57B/6 mice and AML-12 cells were used for the construction of hepatic IRI animal and cell models. Rac1 inhibition was achieved by NSC23766 (a specific Rac1 inhibitor). Lentiviral vectors were used for Rac1 knockdown. At designated time points, serum and liver tissues were collected from the mice and treated cells were collected for further analysis. Results NSC23766 treatment significantly alleviated the hepatic IRI in mice, manifesting as lower vacuolation score and less apoptosis cells, lower ROS and serum/liver alanine aminotransferase/aspartate aminotransferase levels, and fewer activated inflammatory cells. IRI of AML-12 was also alleviated by 50 µM NSC23766 or Rac1-knockdown, manifesting as reduced cell apoptosis, less extensive interruption of mitochondrial membrane potential, down-regulation of apoptosis, and effects on DNA damage-related proteins. Interestingly, Rac1 knockdown also down-regulated the expression level of HIF-1α. Conclusions Our study supports a protective effect of Rac1 inhibition on hepatic IRI. Aside from the classic topics of reducing ROS production and oxidative stress, our study showed an interaction between Rac1 and HIF-1α signaling during hepatic IRI.

Hepatobiliary malignancies, such as hepatocellular carcinoma (HCC) and biliary tract cancers, namely, gallbladder carcinoma and cholangiocarcinoma, are linked to a high rate of morbidity and mortality, depending on the phase of the disease. The intricate hepatobiliary anatomy and the need for accurate peroperative management, especially in patients with advanced liver disease, make these tumors difficult to treat. Surgical resection is a notable therapy for hepatobiliary cancers. Unnecessary or excessive liver excision influences patient rehabilitation, normal liver function, and postoperative complications. Hepatobiliary operations must therefore include accurate liver removal. The present advancements in imaging technology are aimed at improving the diagnostic efficacy of liver injury even more. Three-dimensional visual reconstruction is becoming more important in the diagnosis as well as treatment of a variety of disorders. In this paper, we proposed a novel three-dimensional visual reconstruction technology using enhanced nonuniform rational basis spline (ENURBS) combined with virtual surgical planning of Computed Tomography Angiography (CTA) images for precise liver cancer resection. The purpose of this project is to rebuild 2D CTA scan images of liver cancer into a 3D reconstructed model for efficient visualization and diagnosis of liver cancer and to prepare an effective preoperative surgical plan for precise liver excision based on a 3D recreated liver model. This method’s performance is compared to that of 2D planning in terms of accuracy and time taken to complete the plan. It is concluded that our proposed technique outperforms the planning technique based on 2D images.

Type I interferons (IFN) and their downstream effector signaling pathways play critical roles in the innate antiviral response. The underlying mechanisms that regulate IFN production and their effector signaling, especially by microRNAs, are well understood. We found that the expression of miR-93 was significantly downregulated by RNA virus infection in innate cells. miR-93 expression was also downregulated in influenza virus-infected patients. Furthermore, we showed that JAK1 is targeted by miR-93 to inhibit type I IFN's antiviral activity. Functionally, antagomir of miR-93 markedly reduced influenza virus replication in mice in vivo and prevented their death. Therefore, hosts recognize the invading RNA virus infection and activate RIG-I/JNK pathways to decrease miR-93 expression. The reduction of miR-93 feedback enhances the antiviral innate immune response by activating the IFN-JAK-STAT effectors type I, indicating miR-93 as a possible therapeutic target for infection with RNA viruses.

BACKGROUND Acute kidney injury (AKI) after surgery appears to increase the risk of death in patients with liver cancer. In recent years, machine learning algorithms have been shown to offer higher discriminative efficiency than classical statistical analysis. AIM To develop prediction models for AKI after liver cancer resection using machine learning techniques. METHODS We screened a total of 2450 patients who had undergone primary hepatocellular carcinoma resection at Changzheng Hospital, Shanghai City, China, from January 1, 2015 to August 31, 2020. The AKI definition used was consistent with the Kidney Disease: Improving Global Outcomes. We included in our analysis preoperative data such as demographic characteristics, laboratory findings, comorbidities, and medication, as well as perioperative data such as duration of surgery. Computerized algorithms used for model development included logistic regression (LR), support vector machine (SVM), random forest (RF), extreme gradient boosting (XGboost), and decision tree (DT). Feature importance was also ranked according to its contribution to model development. RESULTS AKI events occurred in 296 patients (12.1%) within 7 d after surgery. Among the original models based on machine learning techniques, the RF algorithm had optimal discrimination with an area under the curve value of 0.92, compared to 0.87 for XGBoost, 0.90 for DT, 0.90 for SVM, and 0.85 for LR. The RF algorithm also had the highest concordance-index (0.86) and the lowest Brier score (0.076). The variable that contributed the most in the RF algorithm was age, followed by cholesterol, and surgery time. CONCLUSION Machine learning algorithms are highly effective in discriminating patients at high risk of developing AKI. The successful application of machine learning models may help guide clinical decisions and help improve the long-term prognosis of patients.

MicroRNAs (miRNAs) participate in tumorigenesis, progression, recurrence and drug resistance of hepatocellular carcinoma (HCC). However, few miRNAs have been identified and entered clinical practice. Herein, we report that miR-29a is downregulated in tumor-initiating cells (T-ICs) and has an important function in liver T-ICs. Functional studies revealed that miR-29a knockdown promotes liver T-ICs self-renewal and tumorigenesis. Conversely, a forced miR-29a expression inhibits liver T-ICs self-renewal and tumorigenesis. Mechanistically, we find that miR-29a downregulates Bcl-2 via binding its mRNA 3'UTR in liver T-ICs. The correlation between miR-29a and Bcl-2 is validated in human HCC tissues. Furthermore, the miR-29a expression determines the responses of hepatoma cells to sorafenib treatment. Analysis of patient-derived xenografts (PDXs) further demonstrated that the miR-29a high patients are more sensitive to sorafenib treatment. In conclusion, our findings revealed the crucial role of the miR-29a in liver T-ICs expansion and sorafenib response, rendering miR-29a as an optimal target for the prevention and intervention of HCC.

BACKGROUND Hepatic epithelioid angiomyolipoma (HEAML) is a rare liver disease and is easily misdiagnosed. Enhanced recognition of HEAML is beneficial to the differential diagnosis of rare liver diseases. CASE SUMMARY We presented two cases of HEAML in Changzheng Hospital, Naval Medical University, and then collected and analyzed all reports about HEAML recorded in PubMed, MEDLINE, China Science Periodical Database, and VIP database from January 2000 to March 2018. A total of 409 cases of HEAML in 97 reports were collected, with a ratio of men to women of 1:4.84 and an age range from 12 years to 80 years (median 44 years). Among the patients with clinical symptoms mentioned, 61.93% (205/331) were asymptomatic, 34.74% (115/331) showed upper or right upper quadrant abdomen discomfort, while a few of them showed abdominal mass, gastrointestinal symptoms, low fever, or weight loss. The misdiagnosis rate of HEAML was as high as 40.34% (165/409) due to its nonspecific imaging findings. Most of the tumors were solitary and round in morphology, with clear boundaries. Ultrasound scan indicated low echo with internal nonuniformity and rich blood supply in most cases. Computer tomography/magnetic resonance imaging enhanced scan showed varied characteristics. The ratio of fast wash-in and fast wash-out, fast wash-in and slow wash-out, and delayed enhancement was roughly 4:5:1. A definite diagnosis of HEAML depended on the pathological findings of the epithelioid cells in lesions and the expression of human melanoma black 45, smooth muscle actin, melanoma antigen, and actin by immunohistochemical staining. HEAML had a relatively low malignant rate of 3.91%. However, surgical resection was the main treatment for HEAML, due to the difficulty diagnosing before operation. CONCLUSION HEAML is a rare and easily misdiagnosed disease, and it should be diagnosed carefully, taking into account clinical course, imaging, pathological ,and immunohistochemical findings.

MicroRNAs (miRNAs), a subgroup of small noncoding RNAs, play critical roles in tumor growth and metastasis. Accumulating evidence shows that the dysregulation of miRNAs is associated with the progression of hepatocellular carcinoma (HCC). However, the molecular mechanism by which miR-942-3p contributes to HCC remains undocumented. The association between miR-942-3p expression and the clinicopathological characteristics in HCC patients was analyzed by The Cancer Genome Atlas data set. The targets of miR-942-3p were identified by bioinformatic analysis and dual luciferase report assay. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and Transwell assays were performed to assess the functional role of miR-942-3p in HCC cells. Consequently, we found that miR-942-3p expression level was elevated in HCC tissues and cell lines as compared with the normal tissues and was associated with the pathological stage and tumor node metastasis (TNM) stage, acting as an independent prognostic factor of poor survival in patients with HCC. Ectopic expression of miR-942-3p enhanced the proliferation and invasive potential of HCC cells, but inhibition of miR-942-3p expression had the opposite effects. Mannose-binding lectin 2 (MBL2) was further identified as a direct target of miR-942-3p and possessed a negative correlation with miR-942-3p expression and unfavorable survival in patients with HCC. Restoration of MBL2 inhibited the progression of HCC cells and attenuated the tumor-promoting effects induced by miR-942-3p. In conclusion, miR-942-3p may act as an oncogenic factor in HCC cells by targeting MBL2 and provide a potential marker for patients with HCC.

Objective To investigate the protective effect of salvianolate against bile duct injury after donation after cardiac death (DCD) liver transplantation and its clinical application prospect. Methods Sixty recipients of DCD liver transplantation were randomly divided into two groups with 30 cases in each group. Salvianolate (250mg/d) was given daily for 14 days after operation in treatment group, and the same amount of normal saline was given in control group. The therapeutic regimen of anti-rejection and anti-infection is the same between the two groups. The incidence of early graft dysfunction (EAD), and the serous levels of total bilirubin (TB), alkaline phosphatase (ALP), γ-glutamyltransferase (GGT), total bile acid (TBA) 1 month, 6 months and 12 months after liver transplantation were compared between the two groups. Also, the platelets (PLT), prothrombin time (PT), activated partial prothrombin time (APTT) and fibrinogen (FIB) were compared between the two groups at 2 weeks after operation. Results There was no significant difference in baseline parameters between the two groups (P>0.05). Compared with the control group, the incidence of EAD was decreased in treatment group, but there was no significant difference [10.0%(3/30) vs. 23.3%(7/30), P=0.166]. The serous levels of TB, ALP, GGT and TBA in treatment group were lower than those in control group 1 month, 6 months and 12 months after operation: [TB: 1 month, (28.5±17.0)μmol/L vs. (39.8±20.1)μmol/L, P=0.025; 6 months, (24.5±10.6)μmol/L vs. (33.3±16.4) μmol/L, P=0.018; 12 months, (19.8±9.5)μmol/L vs. (26.4±14.1)μmol/L, P=0.037, ALP: 1 month, (147.3±76.9)U/L vs. (187.6±70.9)U/L, P=0.039; 6 months, (163.0±61.4)U/L vs. (198.1±51.6)U/L, P=0.020; 12 months, (167.9±59.9)U/L vs. (200.2±56.2)U/L, P=0.036, GGT: 1 month, (83.9±49.5)U/L vs. (113.6±61.1)U/L, P=0.043; 6 months, (130.9±48.7)U/L vs. (169.7±77.0)U/L, P=0.023; 12 months, (154.7±45.1)U/L vs. (182.5±59.8)U/L, P=0.047, TBA: 1 month, (6.6±2.1)μmol/L vs. (8.0±2.4)μmol/L, P=0.016; 6 months, (9.5±2.2)μmol/L vs. (12.1±3.4)μmol/L, P=0.001; 12 months, (12.5±2.7)μmol/L vs. (5.6±3.8)μmol/L, P=0.001]. However, there was no significant difference in PLT, PT, APTT and FIB between two groups [PLT: (148.6±88.6)×109/L vs. (152.8±74.4)×109/L, P=0.843; PT: (12.9±1.1)s vs. (13.0±1.1)s, P=0.617; APTT: (34.6±3.7)s vs. (34.9±3.4)s, P=0.716; FIB: (3.4±0.6)g/L vs. (3.2±0.6)g/L, P=0.270, repectively]. Conclusions Salvianolate has a protective effect against bile duct injury after DCD liver transplantation, and does not increase the risk of postoperative bleeding. DOI: 10.11855/j.issn.0577-7402.2019.02.07

Objective To explore the safety of liver transplantation recipients with Rh blood group mismatchming .Methods From May 2005 to December 2018 ,1546 cases of liver transplantation in our hospital were retrospectively analyzed . Among these cases ,5 cases of Rh blood group mismatched were Rh(-) recipients receiving Rh(+ ) donor liver .For each Rh blood group mismatched liver transplantation ,5 patients received the same Rh blood group liver allograft were matched according to a certain principle and were defined as Rh-mismatch group and Rh-match group respectively .The serum alanine aminotransferase (ALT ) ,aspartate aminotransferase (AST ) and creatinine(SCr)were compared between two groups at Days 7 & 14 post-operation .Serum total bilirubin(TB) ,gamma-glutamyl transpeptidase(GGT)were compared between two groups at Month 1 , 6 & 12 post-operation .Hemoglobin (Hb)were compared between two groups Month 1 ,3 & 6 post-operation . The rates of infection ,vascular complications and acute rejection was also compared . Indirect antiglobulin test (IAT)was used for detecting the production of anti-RhD antibody in patients in Rh-mismatch group at Month 1 ,6 & 12 post-operation .Results At the mentioned time ,no significant inter-group difference existed in serum ALT ,AST ,SCr ,TB ,GGT and blood Hb levels (all P>0 .05);Also ,no significant difference existed in the incidence of infection ,vascular complications or acute rejection(all P> 0 .05) .In Rhmismatch group ,4 recipients received Rh (+ )RBC transfusion during perioperative period and no hemolytic anemia occurred after operation .Rh(D) antibody was negative at all timepoints .Conclusions Taking into account the rarity of Rh-negative blood group in Chinese ,it is safe and feasible to carry out Rh blood group mismatched liver transplantation when donor or recipient with the same Rh blood group is not available .

Liver ischemia/reperfusion (I/R) injury is a complex and common clinical disease with limited therapeutic options. The aim of our study was to discover the candidate target genes in liver I/R injury and to further elucidate the potential regulatory mechanisms, especially the ones involving transcription factors and miRNAs. The analysis of mouse data set GSE10657 from Gene Expression Omnibus database (GEO) revealed 203 differentially expressed genes (DEGs) including 19 transcription factors (TFs). Functional and pathway enrichment analyses were conducted to explore their biological functions. We further obtained the targets of TFs and miRNAs, to form our TF-mRNA/TF-miRNA-mRNA co-regulatory network. In our network, we found that the important subunits of activator protein 1 (AP-1) including JUN, FOS and ATF3, were hub genes in liver I/R injury. AP-1 target genes were activated in our mouse models. AP-1 could transcriptionally activate phosphatase and tensin homolog (PTEN) while AP-1-dependent miRNAs countered this effect. In conclusion, this study suggested that AP-1, together with AP-1-dependent miRNAs formed a co-regulatory network enabling AP-1 target genes to be tightly controlled, which will complete the mechanism of liver ischemia/reperfusion injury and provide direction for finding potential therapeutic targets.

Alsterpaullone (Alp) is a small-molecule inhibitor that targets cyclin-dependent kinases to inhibit tumor cell activity. However, to the best of our knowledge, the effect of Alp on hepatoblastoma has not been investigated. Therefore, the function of Alp in apoptotic induction of hepatoblastoma cells and a potential mechanism of action were investigated. Results indicated that low doses of Alp (1 µM) significantly induced apoptosis in the HepG2 hepatoblastoma cell line. In vivo experiments of tumor suppression further indicated that Alp (3 mg/kg) exerted an inhibitory effect on HepG2 ×enograft tumor growth. Following Alp treatment, the expression level of B-cell lymphoma 2 (Bcl-2)-associated X protein, and cleaved caspase-3 and -9 in HepG2 cells was significantly increased; however, the expression of Bcl-2 was significantly decreased. In addition, phosphorylation of p38 mitogen-activated protein kinase (MAPK) significantly decreased Alp-induced caspase-3 and -9 activation. These results suggested that Alp induces apoptosis and inhibited proliferation via the p38MAPK signaling pathway. Therefore, Alp may be a therapeutic agent for treating hepatoblastoma.

目的建立并验证基于up-to-seven（Up7）标准肝细胞癌（HCC）肝移植术后患者的长期生存Cox回归预测模型,以辅助制定临床决策。方法回顾性分析251例符合Up7标准的HCC肝移植术后患者的临床和随访资料。采用逐步回归向前法进行多因素Cox回归分析,获得HCC肝移植术后患者长期生存的独立预测因素,并建立长期生存Cox回归预测模型。使用R 3.4.3软件获得预测模型评分,采用生存决策树方式确定模型的截断值。绘制预测模型在其他肝移植标准[上海复旦标准、加利福尼亚大学旧金山分校（UCSF）标准、意大利米兰（Milan）标准]下HCC肝移植术后患者的Kaplan-Meier生存曲线,并采用log-rank检验分析组间差异。采用受试者工作特征（ROC）曲线检验预测模型的预测效能。结果多因素Cox回归分析显示,甲胎蛋白（AFP）、总胆红素（T-Bil）、微血管侵犯（MVI）、肿瘤最大径（Diameter）是HCC肝移植术后患者长期生存的独立预测因素,据此建立的长期生存Cox回归预测模型命名为ATMD（AFP,T-Bil,MVI,Diameter）模型:h（t,x）=h0（t）exp[0.284×肿瘤最大径（cm）+0.773×MVI（是=1;否=0）+0.404×lg AFP（ng/m L）+0.003×T-Bil（μmol/L）],根据判别生存树设定ATMD模型截断值为1.44,评分＞1.44为高危组,≤1.44为低危组。符合Up7标准的高危组和低危组患者分别为87例和164例,符合上海复旦标准的分别为33例和144例,符合UCSF标准的分别为29例和134例,符合Milan标准的分别为29例和131例。Kaplan-Meier生存曲线分析显示,在Up7标准、上海复旦标准、UCSF标准和Milan标准下ATMD模型高危组和低危组患者累积生存率差异均有统计学意义（P＜0.001,P=0.008,P＜0.001,P=0.001）,ATMD模型预测的HCC肝移植术后3年生存的ROC曲线下面积分别是76.63%、75.87%、73.32%和69.41%。结论 ATMD模型对于符合Up7标准、上海复旦标准、UCSF标准和Milan标准的HCC肝移植术后生存情况有良好的预测能力,对符合以上标准的HCC肝移植患者的术前决策和术后风险评估有重要意义。

Objective To study liver transplantation in the treatment of alcoholic liver disease (ALD).Methods A retrospective study was conducted on 40 patients with ALD who underwent liver transplantation in the Changzheng Hospital of the Second Military Medical University from April 2005 to June 2017.The data were expressed as mean ± standard deviation ((-x) ±s) in populations with a normal distribution,and as median (min～max) in populations with an abnormal distribution.The survival rate was analyzed by life tables,and the Cox regression analysis was used for multivariate analysis.Results All patients were followed up until August 31,2017.The follow-up time was 2 ～ 4518 days,with a median of 997 days.Among the 40 patients,8 had already died (3 died of multiple organ failure,2 of biliary complications,1 of liver failure,1 of sepsis and 1 of recurrence of hepatocellular carcinoma (HCC).The 1-year survival rate was 81.0％,and the 5-year survival rate was 77.0％.Four of 40 patients developed tumor recurrence.The initial recurrence time was 189 ～ 337 days (median 236.5).The recurrence sites included the liver,colon combined with lungs,lungs,and lumbar vertebrae.Six of 40 (15.0％) patients had relapse in alcoholism.Multivariate analysis showed that age was a prognostic factor (RR =1.109,P ＜0.05).Years of drinking,daily amount of alcohol intake,abstinence,a previous history of upper gastrointestinal bleeding,a previous history of splenectomy,co-existing hepatocellular carcinoma,preoperative MELD score,preoperative Child-Pugh score,total operation time,anhepatic period,cold ischemia time,amount of intraoperative bleeding,postoperative alcoholism relapse,tumor recurrence or new onset of tumor were not significantly correlated with the postoperative survival rate (P＞0.05).Conclusions ALD patients were mostly 40 ～ 60 years old.Age was an independent factor affecting survival.The younger the patient,the better the prognosis.Other factors were of no prognostic significance.

Objective To summarize our experience in the diagnosis and treatment of hepatic epithelioid angiomyolipoma (HEAML),with the aim to reduce the future misdiagnosis rate.Methods The PubMed,Medline,China Science Periodical Database (CSPD),and VIP Databases were searched from January 2000 to March 2018 on all reports on HEAML.Results There were 409 cases of HEAML in 97 reports.The ratio of men to women was 1∶4.84.The age ranged from 12 to 80 years and the median age was 44 years.61.9％ of patients (205/331) were asymptomatic,while 34.7％ (115/331) had upper or right upper quadrant abdominal discomfort.Some patients presented with abdominal mass,gastrointestinal reaction,low grade fever or weight loss.The clinical symptoms in 78 patients were not mentioned in the reports.The misdiagnostic rate of HEAML was as high as 40.3％ (165/409).The imaging findings of HEAML were nonspecific.Ultrasound,CT and MRI scan usually showed contrast enhancement in the arterial phase.Most lesions were accompanied by central vessels with early drainage veins.The enhanced scans showed varied characteristics.The ratios of fast wash-in and fast wash-out,to fast wash-in and slow wash-out,and to delayed enhancement were roughly 4∶ 5∶ 1.A definitive diagnosis of HEAML is based on the pathological findings of epithelioid cells in the lesions and the expressions of HMB45,SMA,Melan-A and Actin on immunohistochemical staining.HEAML had a relatively low malignant rate of 3.9％.Surgical resection was the main treatment for HEAML.Conclusion HEAML was a rare and easily misdiagnosed disease.,which could be diagnosed by taking into account the clinical course,imaging,pathological and immunohistochemical findings.HEAML.