中文English
ISSN 1001-5256 (Print)
ISSN 2097-3497 (Online)
CN 22-1108/R

2019 Vol. 35, No. 2

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Editorial
Current status and research interests of the diagnosis and treatment of cholestatic liver disease
Yu YueCheng, Chen ChengWei
2019, 35(2): 241-246. DOI: 10.3969/j.issn.1001-5256.2019.02.001
Abstract:

Cholestatic liver disease ( CSLD) is a group of liver diseases which can cause cholestasis and has a complex etiology. Its pathogenesis remains unclear, and there are still no effective treatment measures. In the recent decade, new achievements have been made on various aspects of CSLD, which provides more help to accurate diagnosis and treatment and reflects many pending issues which need further research. This article introduces the research advances and problems in CSLD from the following six aspects: the“ascending”pathophysiology of CSLD, mechanisms of cholestasis-induced liver fibrosis and related management measures, association of enterohepatic circulation and intestinal microbiota with CSLD, pathogenesis and diagnosis/treatment of drug-induced cholestasis, pathogenesis and management of liver failure-associated cholestasis, and research advances in treatment targets and drug research and development for CSLD.

Discussions by experts
Pathogenesis of cholestasis-induced liver fibrosis and thoughts for blockade
Chen RuiLing, Ma Xiong
2019, 35(2): 247-251. DOI: 10.3969/j.issn.1001-5256.2019.02.002
Abstract:

Cholestasis refers to a pathological state of disorders in the formation, secretion, and excretion of bile flow, and liver fibrosis is a process of tissue repair induced by liver injury. Cholestatic liver disease is a chronic liver disease caused by cholestasis, progressive bile duct injury, and persistent intrahepatic inflammation, and it may cause cholangiocyte and hepatocyte injury, which will gradually progress to liver fibrosis. With reference to the current research advances, this article reviews the pathogenesis of cholestasis-induced liver fibrosis and the strategies for blockade.

Current status of the pathogenesis, diagnosis, and treatment of drug-induced cholestasis
Liu Meng, Yang XuanZi, Yu LeCheng
2019, 35(2): 252-257. DOI: 10.3969/j.issn.1001-5256.2019.02.003
Abstract:

Drug-induced cholestasis ( DRIC) mainly includes cholestasis-type and mixed-type drug-induced liver injury ( DILI) . The Roussel Uclaf Causality Assessment Method scale should be used to determine the causality between drug and cholestasis and other etiologies should be excluded. Liver biopsy may help with differential diagnosis. Drugs should be stopped after the development of DRIC to avoid stimulation, and ursodeoxycholic acid should be administered for treatment. DRIC has a complex pathogenesis, which involves the direct toxicity of drugs and their metabolites on hepatocytes and the biliary tree, immune and inflammatory response, gene polymorphism and inhibition of key enzymes and transporters in the pathways of drug metabolism and efflux, and HLA gene polymorphisms. Clarification of these pathogeneses helps with the early warning, prevention, and optimized treatment of DRIC.

Pathogenesis and management strategies of liver failure-associated cholestasis
Mao Qing
2019, 35(2): 258-261. DOI: 10.3969/j.issn.1001-5256.2019.02.004
Abstract:

Liver failure is severe liver injury caused by a variety of factors. Liver failure-associated cholestasis is serious hepatocellular intrahepatic cholestasis with massive hepatocyte necrosis, which manifests as rapid increases in both conjugated and unconjugated bilirubin, and the level of bilirubin is directly proportional to the severity of liver failure. Structural changes of liver tissue aggravate intrahepatic cholestasis, and intestinal microbiota can affect bilirubin and bile acid metabolism. The management strategies for liver failure-associated cholestasis include eliminating causes, promoting hepatocyte regeneration, and facilitating liver function recovery.

New therapeutic targets and drugs for cholestatic liver disease
Guo MengMeng, Xie Wen
2019, 35(2): 262-265. DOI: 10.3969/j.issn.1001-5256.2019.02.005
Abstract:

Cholestatic liver disease is caused by the damage of bile duct cells and hepatocytes due to bile duct injury, accumulation of bile acids, and persistent inflammation. If it is not treated in time, cholestasis can lead to liver fibrosis, liver cirrhosis, and even end-stage liver disease. Primary biliary cholangitis ( PBC) and primary sclerosing cholangitis ( PSC) are the two most common cholestatic liver diseases in adults, with unknown causes. Although ursodeoxycholic acid ( UDCA) can improve the prognosis of PBC patients and prolong survival time after liver transplantation, some patients have no response to UDCA. In addition, there are still no effective pharmacotherapies for PSC.With the research advances in molecular mechanism of bile acid regulation and a deeper understanding of immune pathways in recent years, several new drugs have emerged. This article introduces the new therapeutic targets and drugs for PBC and PSC.

Rationality of medication based on the “ascending” pathophysiology of cholestatic liver disease
Gu TianYi, Lu LunGen
2019, 35(2): 266-269. DOI: 10.3969/j.issn.1001-5256.2019.02.006
Abstract:

In recent years, some scholars have put forward the“ascending”pathophysiology of cholestatic liver disease, especially in primary biliary cholangitis ( PBC) and primary sclerosing cholangitis ( PSC) . According to this theory, cholestatic liver disease develops from the bottom to the top of the anatomical structure over time. Primary or early lesions are usually located in the “downstream”bile duct, with a major cause of immune-mediated biliary necrotizing inflammatory injury. When cholestasis occurs, the toxic effect mediated by bile salt will lead to the injury in the“upstream”liver parenchyma. Therefore, bile toxicity is of great importance during disease progression. According to this theory of“ascending”pathophysiology, there are different locations and causes of the disease in different disease stages, and therefore, it is necessary to establish a staging system for cholestatic liver disease and use different drugs in different stages, in order to use the existing drugs in a more effective manner and give directions for new drug development. However, there are still no early biochemical markers for cholestatic liver disease, and current clinical work should focus on the search for biomarkers with strong specificity and high sensitivity.

The role of enterohepatic circulation of bile acids and intestinal microbiota in the pathogenesis and treatment of cholestatic liver disease
Jia HaoYu, Yang ZhangQing
2019, 35(2): 270-274. DOI: 10.3969/j.issn.1001-5256.2019.02.007
Abstract:

Cholestatic liver disease refers to a liver disorder caused by cholestasis, which arise from a series of etiologies such as viruses, bacteria, parasites, drugs, poisons, autoimmunity, alcohol, stones, tumors, genetics, and metabolism. This disease has the main manifestations of a change in bile flow and excessive accumulation of bile acid toxicity. In the pathogenesis of cholestatic liver disease, not only does the enterohepatic circulation of endogenous bile acids work, but also the intestinal microbiota plays an important role by regulating metabolism and causing immune responses. In addition, more attention has been paid to the close interaction between intestinal microbiota and the enterohepatic circulation of bile acids. Bile acids can alter the composition of intestinal microbiota, which in turn affects the bile acid pool.In recent years, there has been increasing research on the relationship of the enterohepatic circulation of bile acids and intestinal microbiota with cholestatic liver disease, which may provide new research directions for the pathogenesis and treatment of cholestatic liver disease.

Therapeutic guidelines
The Chinese clinical practice guideline on liver transplantation for hepatocellular carcinoma (2018)
Organ Transplantation Branch, Chinese Medical Doctor Association, Chinese Society of Organ Transplantation, Chinese Medical Association
2019, 35(2): 275-280. DOI: 10.3969/j.issn.1001-5256.2019.02.008
Abstract(764) PDF (261KB)(1597)
Abstract:
Diagnosis, management, and treatment of pancreatic adenocarcinoma (V2018)
National Health Commission of the People’s Republic of China
2019, 35(2): 281-293. DOI: 10.3969/j.issn.1001-5256.2019.02.009
Abstract(368) PDF (564KB)(1380)
Abstract:
Standards for the diagnosis and treatment of pancreatic exocrine insufficiency (2018, Guangzhou)
Special Committee on Chronic Pancreatitis, Pancreatic Disease Specialized Committee, Chinese Medical Doctor Association
2019, 35(2): 294-298. DOI: 10.3969/j.issn.1001-5256.2019.02.010
Abstract:
Expert consensus on image-guided irreversible electroporation ablation for pancreatic cancer (2018)
Chinese Society of Interventional and Minimally Invasive Therapy, China Medicine Education Association
2019, 35(2): 299-302. DOI: 10.3969/j.issn.1001-5256.2019.02.011
Abstract:

An excerpt of International Liver Transplantation Society Asian consensus on the management of hepatitis C virus infection in resource limited setting—From noncirrhotic to decompensated disease and following liver transplantation

Shang LanLan, Chen XiaoYing, Li JunFeng, Chen Hong
2019, 35(2): 303-308. DOI: 10.3969/j.issn.1001-5256.2019.02.012
Abstract:
Original articles_Viral hepatitis

Clinical effect and safety of pegylated interferon-α-2a versus pegylated interferon-α-2b in treatment of chronic hepatitis B

Ji WeiJia, Yan XueBing
2019, 35(2): 309-314. DOI: 10.3969/j.issn.1001-5256.2019.02.013
Abstract:

Objective To investigate the clinical effect and safety of pegylated interferon-α-2 a ( PEG-IFN-α-2 a) versus pegylated interferon-α-2 b ( PEG-IFN-α-2 b) in the treatment of chronic hepatitis B ( CHB) . Methods The CHB patients who were treated with PEG-IFN-α-2 a ( 180 μg/week) or PEG-IFN-α-2 b ( 180 μg/week) in Department of Infectious Diseases in our hospital from January 2017 to June 2018 were enrolled. The two groups were compared in terms of the levels of HBsAg, HBV DNA, HBeAg, and alanine aminotransferase ( ALT) at 4, 12, 24, and 48 weeks of treatment, and the indices for antiviral effect at 48 weeks were used as main outcome measures. The above indices were compared between response group and non-response group. The independent samples t-test was used for comparison of normally distributed continuous data between two groups, and the Mann-Whitney U test was used for comparison of non-normally distributed continuous data between two groups; the chi-square test or the Fisher's exact test was used for comparison of categorical data between two groups. Results There were no significant differences between the PEG-IFN-α-2 a group and the PEG-IFN-α-2 b group in serum HBV DNA clearance rate ( 67. 6% vs 59. 4%, P > 0. 05) and HBeAg seroconversion rate ( 27. 2% vs 34. 6%, P >0. 05) . In the PEG-IFN-α-2 a group, the HBV DNA response group had a significantly lower baseline ALT level than the HBV DNA non-response group ( Z = 2. 390, P = 0. 016) ; the HBeAg response group had a significantly lower baseline HBeAg level than the HBeAg non-response group ( Z = 2. 286, P = 0. 021) . In the PEG-IFN-α-2 b group, the HBV DNA response group had significantly lower baseline HBV DNA level and baseline HBeAg level than the HBV DNA non-response group ( Z = 2. 154 and 2. 057, P = 0. 030 and0. 041) ; the HBeAg response group had a significantly lower baseline HBV DNA level than the HBeAg non-response group ( Z = 2. 052, P = 0. 042) . There were no significant differences in the incidence rates of adverse reactions between the two groups ( P > 0. 05) ; in the PEG-IFN-α-2 b group, one patient experienced Purtscher's retinopathy and one experienced thrombocytopenia, while no similar adverse reactions were observed in the PEG-IFN-α-2 a group. Conclusion Both PEG-IFN-α-2 a and PEG-IFN-α-2 b have strong antiviral and immunomodulatory effects in the treatment of CHB, with similar clinical effect and safety.

Serum level of interferon-λ3 in patients with chronic hepatitis B and its clinical significance
Duan YuanLi, Guan ShiHe, Yang Kai, Chen LiWen, Zhang Hao, Wang Xiu, Pan ZhengLan, Hou ShuWen, Wang ZhaoFei
2019, 35(2): 315-318. DOI: 10.3969/j.issn.1001-5256.2019.02.014
Abstract:

Objective To investigate the serum level of interferon-λ3 ( IFN-λ3) and its clinical significance in patients with chronic hepatitis B ( CHB) , as well as its association with nucleos ( t) ide analogue ( NA) treatment. Methods A total of 119 CHB patients who were treated in The Second Affiliated Hospital of Anhui Medical University from January 2017 to May 2018 were enrolled, and 22 HBsAg-negative individuals who underwent physical examination were enrolled as healthy control group. ELISA was used to measure the serum level of IFN-λ3, which was compared between CHB patients and healthy individuals. The association between serum IFN-λ3 level and HBeAg in CHB patients was analyzed; serum IFN-λ3 level was compared between the patients treated with different NAs; the influence of NAs on the level of IFN-λ3 in the supernatant of peripheral blood mononuclear cells ( PBMCs) was analyzed. An analysis of variance was used for comparison of normally distributed continuous data with homogeneity of variance between multiple groups; the Wilcoxon rank-sum test was used for comparison of non-normally distributed continuous data or continuous data with heterogeneity of variance between two groups, the Kruskal-Wallis H test was used for comparison between multiple groups, and the Nemenyi test was used for further comparison between two groups. A Spearman correlation analysis was also performed. Results The CHB group had a significantly lower serum IFN-λ3 level than the healthy control group [14. 7 ( 5. 9-28. 5) pg/ml vs 76. 1 ( 39. 4-112. 0) pg/ml, Z =-10. 114, P < 0. 001]. In the CHB patients who did not receive antiviral therapy, serum IFN-λ3 level was negatively correlated with log HBV DNA ( r =-0. 621, P < 0. 001) . The HBeAg-negative CHB patients had a significantly higher serum IFN-λ3 level than the HBeAg-positive CHB patients [16. 4 ( 9. 0-31. 3) pg/ml vs 8. 7 ( 2. 9-23. 2) pg/ml, Z =-2. 205, P = 0. 02]. The patients who received antiviral therapy with adefovir dipivoxil had a significantly higher serum IFN-λ3 level than those who were treated with entecavir, tenofovir, telbivudine, or lamivudine ( P < 0. 05) . In vitro experiment showed that there was no significant increase in serum IFN-λ3 level in the supernatant of PBMCs treated with NAs. Conclusion CHB patients have a significantly lower serum IFN-λ3 level than healthy individuals, and the CHB patients receiving antiviral therapy with adefovir dipivoxil have a relatively high serum IFN-λ3 level.

Influencing factors for hemolytic anemia in patients with chronic hepatitis C treated by ribavirin combined with pegylated interferon-α
Xu JinFeng, Zhang XiaoHui, Liu YaLi, Zhang Jing
2019, 35(2): 319-322. DOI: 10.3969/j.issn.1001-5256.2019.02.015
Abstract:

Objective To investigate the influencing factors for ribavirin ( RBV) -induced hemolytic anemia during the treatment of chronic hepatitis C using RBV combined with pegylated interferon-α ( PEG-IFNα) , and to provide a reference for early prediction of RBV-related hemolytic anemia in clinical practice. Methods A total of 235 patients with chronic hepatitis C who were given antiviral therapy with PEG-IFNα combined with RBV in Beijing YouAn Hospital from March 2016 to March 2018 were enrolled. Parameters of routine blood test, liver function parameters, liver stiffness measurement, HCV RNA, HCV viral genotype, and inosine triphosphate pyrophosphatase ( ITPA) genotype were determined before the antiviral therapy, and routine blood tests were performed at weeks 2, 4, 8, and 12 of treatment. The t-test was used for comparison of normally distributed continuous data between groups, and the Mann-Whitney U test was used for non-normally distributed continuous data between groups; the chi-square test or the Fisher's exact test was used for comparison of categorical data between groups. Univariate analysis and multivariate logistic regression analyses were used to determine the influencing factors for RBV-related hemolytic anemia, and a predictive model was established accordingly; the receiver operating characteristic curve was used to analyze the predictive value of this model for RBV-related hemolytic anemia. Results At weeks 2, 4, 8, and 12 of treatment, the ITPA ( rs1127354) genotype CC group had a significantly greater reduction in hemoglobin ( Hb) than the ITPA ( rs1127354) genotype AA + AC group ( all P < 0. 05) . At week 4 of treatment, there was a significant difference between the AA + AC group and the CC group in the proportion of patients with a > 30 g/L reduction in Hb ( 2. 38% vs 39. 9%, X2= 23. 175, P < 0. 001) or an Hb level of < 100 g/L ( 0 vs10. 88%, P = 0. 018) . The degree of reduction in Hb at week 2 ( odds ratio ( OR) = 1. 073, P < 0. 001) , ITPA ( rs1127354) genotype ( OR = 18. 920, P = 0. 005) , and baseline Hb level ( OR = 1. 032, P = 0. 024) were independent risk factors for a > 30 g/L reduction in Hb at week 4. Conclusion Patients with ITPA ( rs1127354) genotype CC tend to develop RBV-related hemolytic anemia. ITPA ( rs1127354) genotype, baseline Hb level, and degree of reduction in Hb at week 2 can be used to predict the development of RBV-related hemolysis during anti-HCV treatment, in order to achieve early warning and guide early intervention.

The mRNA expression of TIPE2, Foxp3, and CTLA-4 in peripheral blood mononucleated cells in patients with chronic hepatitis C and their clinical significance
Kong Li, Jin Meng, Wang WeiZhen, Zhao SuXian, Wang ShanShan
2019, 35(2): 323-327. DOI: 10.3969/j.issn.1001-5256.2019.02.016
Abstract:

Objective To investigate the mRNA expression of tumor necrosis factor-alpha-induced protein 8-like 2 ( TIPE2) , Foxp3 ( a functional molecule for regulatory T cells) , and cytotoxic T-lymphocyte-associated antigen 4 ( CTLA-4) in peripheral blood mononuclear cells ( PBMCs) in patients with chronic hepatitis C ( CHC) and their clinical significance. Methods A total of 80 CHC patients who were hospitalized in The Third Hospital of Hebei Medical University from May 2012 to December 2016 and did not receive antiviral drugs or immunoregulatory drugs were enrolled as CHC group, and 45 healthy volunteers were enrolled as controls. Quantitative real-time PCR was used to measure the mRNA expression of TIPE2, Foxp3, and CTLA-4 in PBMCs; the correlation between liver biochemical parameters and HCV RNA was observed, as well as the influence of TIPE2 on Foxp3 and CTLA-4. The t-test was used for comparison of continuous data between two groups, the chi-square test was used for comparison of categorical data between two groups, and Pearson correlation was used for correlation analysis. Results Compared with the healthy control group, the CHC group had a significant reduction in the mRNA expression of TIPE2 ( 0. 564 ± 0. 232 vs 0. 704 ± 0. 165, t = 3. 569, P < 0. 001) and significant increases in the mRNA expression of Foxp3 ( 0. 701 ± 0. 405 vs 0. 527 ± 0. 184, t = 2. 725, P = 0. 007) and CTLA-4 ( 0. 638 ± 0. 211 vs 0. 448 ± 0. 134, t = 5. 449, P < 0. 001) . The mRNA expression of TIPE2 was negatively correlated with serum alanine aminotransferase ( r =-0. 368, P = 0. 001) , aspartate aminotransferase ( r =-0. 417, P < 0. 001) , total bilirubin ( r =-0. 416, P < 0. 001) , and HCV RNA load ( r =-0. 327, P = 0. 003) and was positively correlated with the mRNA expression of Foxp3 ( r = 0. 461, P < 0. 001) and CTLA-4 ( r = 0. 257, P = 0. 021) . The mRNA expression of Foxp3 was negatively correlated with total bilirubin ( r =-0. 284, P = 0. 011) . Conclusion CHC patients have abnormalities in the mRNA expression of TIPE2 and the mRNA expression and function of Foxp3 and CTLA-4, which is associated with the degree of hepatocellular injury and viral replication. The TIPE2 gene may be involved in the pathogenesis of CHC by positively regulating immune response mediated by regulatory T cells.

Original articles_Liver fibrosis and liver cirrhosis
Value of hepatitis B virus core-related antigen in predicting the natural course of chronic hepatitis B and liver fibrosis regression
Sun Chao, Chang XiuJuan, Li XiaoDong, Yang YongPing
2019, 35(2): 328-333. DOI: 10.3969/j.issn.1001-5256.2019.02.017
Abstract:

Objective To investigate the clinical value of hepatitis B virus core-related antigen ( HBcrAg) in predicting the natural course of chronic hepatitis B ( CHB) and liver fibrosis regression. Methods A total of 138 CHB patients who were admitted to 302 Hospital of PLA, The First Affiliated Hospital of Zhengzhou University, and Fuzhou Infectious Disease Hospital from January 2013 to December 2015 were enrolled and divided into HBeAg-positive group with 69 patients and HBeAg-negative group with 69 patients. Of all patients, 109 with an Ishak score of ≥3 were treated with entecavir for 72 weeks. Liver biopsy specimens and serum were collected at baseline and after 72 weeks of treatment to observe histopathology and HBcrAg level. The t-test was used for comparison of normally distributed continuous data between two groups, and the Wilcoxon rank-sum test was used for comparison of non-normally distributed continuous data between two group. The chi-square test was used for comparison of categorical data between groups. A Spearman correlation analysis was also performed. The area under the receiver operating characteristic curve ( AUC) was used to analyze the value of HBcrAg in the diagnosis of liver fibrosis. Results In HBeAg-positive CHB patients, serum HBcrAg level was negatively correlated with liver fibrosis stage ( r =-0. 342, P = 0. 004) ; in HBeAg-negative CHB patients, serum HBcrAg level was positively correlated with liver fibrosis stage and inflammation ( r = 0. 439 and 0. 437, both P < 0. 001) . In HBeAg-positive patients, serum HBcrAg level had an AUC of 0. 705 in predicting advanced liver fibrosis and 0. 701 in predicting liver cirrhosis ( both P < 0. 05) ; in HBeAg-negative CHB patients, serum HBcrAg level had AUCs of0. 815, 0. 815, 0. 726, and 0. 675 in predicting mild liver fibrosis, marked liver fibrosis, advanced liver fibrosis, and liver cirrhosis, respectively ( all P < 0. 05) . After antiviral therapy, the group with a high serum HBcrAg level was more likely to experience liver fibrosis regression than that with a low level ( 53. 7% vs 32. 7%, χ2= 4. 888, P = 0. 027) . The patients with liver fibrosis regression had a significantly greater reduction in serum HBcrAg level than those without regression[1. 5 ( 0. 4-3. 2) log IU/ml vs 0. 8 ( 0. 1-1. 8) log IU/ml, Z =-1. 724, P = 0. 042]. Conclusion Serum HBcrAg can be used as a new marker in predicting liver fibrosis stage and liver fibrosis regression in clinical practice.

Value of FibroScan combined with gamma-glutamyl transpeptidase-to-platelet ratio in predicting liver fibrosis in patients with chronic hepatitis B:A preliminary study
Huang ChunMing, Yang Zhan, Nie YuQiang, Hu ZhongWei, Zhou YongJian, Zhan YuanJing, Guo JiaWei, Yu WeiHua
2019, 35(2): 334-337. DOI: 10.3969/j.issn.1001-5256.2019.02.018
Abstract:

Objective To investigate the value of FibroScan combined with gamma-glutamyl transpeptidase-to-platelet ratio ( GPR) in predicting liver fibrosis stage in patients with chronic hepatitis B ( CHB) . Methods A total of 278 patients who were diagnosed with CHB by liver biopsy in Guangzhou Eighth People's Hospital from January 2012 to December 2016 were enrolled. The value of GPR and FibroScan used alone or in combination in predicting liver fibrosis stage ( F0-F4) was analyzed. The Kruskal-Wallis H test was used for comparison of non-normally distributed continuous data between multiple groups and the Mann-Whitney U test was used for further comparison between two groups. The Spearman's correlation coefficient was used for correlation analysis. The area under the receiver operating characteristic curve ( AUC) was used to evaluate liver fibrosis stage. Results With liver biopsy as the gold standard, of all patients, 50 had stage F1 fibrosis, 104 had stage F2 fibrosis, 92 had stage F3 fibrosis, and 32 had stage F4 fibrosis. Liver stiffness measurement by FibroScan gradually increased with the increase in liver fibrosis stage ( P < 0. 05) , and GPR also increased gradually in patients with stage F1, F2, and F3 liver fibrosis ( P < 0. 05) . GPR and FibroScan were positively correlated with liver fibrosis ( r = 0. 419 and 0. 481, both P < 0. 001) , and GPR was positively correlated with FibroScan ( r = 0. 436, P < 0. 001) . According to AUC, FibroScan combined with GPR had a better diagnostic efficiency than FibroScan ( 0. 793 vs 0. 739, Z = 3. 044, P = 0. 002) or GPR ( 0. 793 vs 0. 740, Z = 2. 389, P = 0. 037) alone in predicting progressive liver fibrosis ( ≥F3) ; FibroScan combined with GPR had a better diagnostic efficiency than GPR alone ( 0. 782 vs0. 714, Z = 2. 130, P = 0. 033) in predicting marked liver fibrosis ( ≥F2) . Conclusion FibroScan combined with GPR has a certain advantage in predicting progressive liver fibrosis ( ≥F3) in CHB patients and can improve diagnostic efficiency.

Influencing factors for FibroTouch measurements in chronic hepatitis B patients based on liver pathology
Li ZhengXin, Chen YangYi, Zhao ZhiMin, Lyu Jing, Chen GaoFeng, Liu ChengHai
2019, 35(2): 338-344. DOI: 10.3969/j.issn.1001-5256.2019.02.019
Abstract:

Objective To investigate the changes in positive staining of CD34, CK7, and CK19 and amount of fibrous collagen deposition in patients with chronic hepatitis B ( CHB) and the pathological basis affecting FibroTouch measurements. Methods A retrospective analysis was performed for the clinical data of 72 CHB patients who visited Department of Liver Cirrhosis in Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine from January 2015 to December 2017. The amount of positive immunohistochemical staining of CD34, CK7, and CK19 was calculated, as well as the amount of fibrous collagen deposition in Masson trichrome staining and liver stiffness measurement ( LSM) by FibroTouch. The t-test was used for comparison of normally distributed continuous data between two groups. The Wilcoxon rank-sum test was used for comparison of non-normally distributed continuous data or continuous data with heterogeneity of variance between two groups. The chi-square test was used for comparison of categorical data between groups, and the Kruskal-Wallis H test was used for comparison of ranked data between multiple groups. The receiver operating characteristic ( ROC) curve was used to analyze the value of LSM in the diagnosis of hepatitis B cirrhosis, and the logistic regression model was used for multivariate analysis. Results With the increase in inflammation degree, there was no significant change in the amount of positive staining of CD34 ( P > 0. 05) , while there were significant increases in the amount of positive staining of CK19 and the amount of fibrous collagen deposition ( H = 9. 02 and 14. 12, P =0. 011 and 0. 001) . With the progression of liver fibrosis, there were significant increases in the amount of positive staining of CD34 and CK7 and the amount of fibrous collagen deposition ( H = 10. 26, 16. 29, and 22. 97, P = 0. 016, 0. 001, and < 0. 001) . The logistic regression analysis showed that the amount of positive staining of CK7 ( Wald = 4. 756, P = 0. 029) and the amount of fibrous collagen deposition ( Wald = 4. 757, P = 0. 029) were independent influencing factors for FibroTouch measurements. Conclusion Increases in the amount of fibrous collagen deposition and the amount of positive staining of CK7 may lead to increased FibroTouch measurements.

Changes in procoagulant and anticoagulant factors in patients with hepatitis B cirrhosis
Deng YongDong, Peng XueBin, Yao LiQiong, Li Hai, Tan BangYun, Ma ChaoQun
2019, 35(2): 345-348. DOI: 10.3969/j.issn.1001-5256.2019.02.020
Abstract:
Objective To investigate the changes in procoagulant and anticoagulant factors and routine coagulation markers in patients with hepatitis B cirrhosis and their clinical significance. Methods A total of 105 patients with hepatitis B cirrhosis who were admitted to Department of Infectious Diseases in The First Hospital of Lanzhou University from January 2017 to October 2018 were enrolled, and according to the Child-Pugh class, these patients were divided into group A ( 42 patients with Child-Pugh class A cirrhosis) , group B ( 39 patients with Child-Pugh class B cirrhosis) , and group C ( 24 patients with Child-Pugh class C cirrhosis) . Routine coagulation markers including prothrombin time ( PT) and activated partial prothrombin time ( APTT) , blood coagulation factors ( Ⅱ, Ⅴ, Ⅶ, Ⅷ, and Ⅺ) , anti-thrombin ( AT) , protein C ( PC) , and free protein S ( FPS) were measured for all patients. A one-way analysis of variance was used for comparison of continuous data between multiple groups, and the least significant difference t-test was used for further comparison between two groups; a Spearman correlation analysis was also performed. Results There were significant differences in PT and APTT between the three groups ( F = 55. 11 and 12. 09, both P < 0. 001) ; group C had significantly higher PT and APTT than groups A and B, and group B had significantly higher PT and APTT than group A ( all P < 0. 05) . There were significant differences in the activities of blood coagulation factorsⅡ, Ⅴ, Ⅶ, and XI between the three groups ( F = 32. 52, 14. 77, 38. 88, and 9. 24, all P < 0. 001) ; group C had significantly lower activities of these coagulation factors than groups B and A, and group B had significantly lower activities than group A ( all P < 0. 05) . There was a significant difference in the activity of blood coagulation factor Ⅷ between the three groups ( F = 4. 44, P < 0. 05) ; group C had a significantly higher activity than groups A and B ( P < 0. 05) , while there was no significant difference between group A and group B ( P >0. 05) . There were significant differences in the activities of AT, PC, and FPS between the three groups ( F = 25. 90, 30. 46, and 15. 58, all P < 0. 001) ; group C had significantly lower activities than groups B and A, and group B had significantly lower activities than group A ( all P < 0. 05) . The correlation analysis showed that Child-Pugh class was negatively correlated with blood coagulation factors Ⅱ, Ⅴ, Ⅶ, and Ⅺ and anticoagulant factors PC, FPS, and AT ( r =-0. 687, -0. 460, -0. 706, -0. 426, -0. 723, -0. 646, and-0. 468, all P < 0. 001) , and Child-Pugh class had the strongest correlation with blood coagulation factors Ⅱ and Ⅶ and the anticoagulant factor PC.Blood coagulation factors II and Ⅶ were positively correlated with the anticoagulant factor PC ( r = 0. 851 and 0. 745, both P < 0. 001) .Conclusion Patients with hepatitis B cirrhosis have reductions in both procoagulant and anticoagulant factors, and there is a significant correlation between them. An unstable balance may form in the body, which is not considered a conventional hypocoagulable state.
Efficacy of transjugular intrahepatic portosystemic shunt versus endoscopic cyanoacrylate injection in treatment of gastric variceal bleeding: A meta-analysis
Li Jing, Jiang Yong, Zhang Xu
2019, 35(2): 349-353. DOI: 10.3969/j.issn.1001-5256.2019.02.021
Abstract:
Objective To evaluate the clinical efficacy and safety of transjugular intrahepatic portosystemic shunt ( TIPS) versus endoscopic cyanoacrylate injection in the treatment of gastric variceal bleeding through a meta-analysis. Methods Pub Med, Embase, the Cochrane Library, ScienceDirect, CNKI, and Wanfang Data were searched for the randomized controlled trials ( RCTs) of the efficacy of TIPS versus endoscopic cyanoacrylate injection in the treatment of gastric variceal bleeding published up to June 30, 2018. We assessed study quality and extracted data from the included studies. RevMan 5. 3 software was used to statistically analyze the data. Results Six RCTs were included, involving366 cases in the TIPS group and 255 cases in the cyanoacrylate group. The meta-analysis showed no significant difference in the early rebleeding rate between the TIPS group and the cyanoacrylate group ( odds ratio [OR]= 1. 05, 95% confidence interval [CI]: 0. 53-2. 06, P = 0. 89) , but the postoperative late rebleeding rate of the TIPS group was significantly lower than that of the cyanoacrylate group ( OR =0. 33, 95% CI: 0. 19-0. 57, P < 0. 000 1) . There was no significant difference in the mortality between the TIPS group and the cyanoacrylate group ( OR = 1, 95% CI: 0. 65-1. 55, P > 0. 05) . The TIPS group had a significantly increased incidence of postoperative hepatic encephalopathy compared with the cyanoacrylate group ( OR = 4. 09, 95% CI: 1. 59-10. 58, P = 0. 004) . Conclusions In the long term, the rebleeding rate of gastric variceal bleeding is significantly lower in patients treated with TIPS than in those treated with endoscopic cyanoacrylate injection, so TIPS is an effective method to treat gastric variceal bleeding.
Original articles_Others
Clinical features of autoimmune hepatitis and primary biliary cholangitis: A comparative analysis
Shu YanYun, Pan XiaoLi, Song YuHu, Ye Jin
2019, 35(2): 354-358. DOI: 10.3969/j.issn.1001-5256.2019.02.022
Abstract:

Objective To compare the clinical features of autoimmune hepatitis ( AIH) and primary biliary cholangitis ( PBC) , and to provide a reference for differentiation and early diagnosis of these two diseases. Methods A retrospective analysis was performed for the clinical data of 83 patients with AIH and 108 patients with PBC who were diagnosed and treated in Union Hospital Affiliated to Tongji Medical College of Huazhong University of Science and Technology from January 2010 to February 2018, including age, sex, serum biochemical parameters, immunological indices, and liver pathology. The clinical features of AIH and PBC were compared. The independent samples t-test was used for comparison of normally distributed continuous data between two groups, and the Mann-Whitney U test was used for comparison of continuous data with skewed distribution between two groups; the chi-square test or the Fisher's exact test was used for comparison of categorical data between two groups. Results Most of the patients with AIH or PBC were female, with a peak age of onset of 40-60 years. There was no obvious specificity in the clinical features of AIH or PBC, with cardinal symptoms and signs of weakness, abdominal distension, jaundice, and poor appetite, and compared with the PBC group, the AIH group had a significantly higher proportion of patients with poor appetite ( 25% vs 14%, X2= 6. 52, P = 0. 011) . Compared with the PBC group, the AIH group also had significantly higher proportions of patients with liver cirrhosis ( 59. 0% vs 40. 7%, X2= 6. 23, P = 0. 012) and rheumatic diseases ( 23. 5% vs 15. 7%, X2= 7. 46, P = 0. 006) . Compared with the PBC group, the AIH group had significantly lower platelet count ( PLT) , alkaline phosphatase ( ALP) , gamma-glutamyl transpeptidase ( GGT) , immunoglobulin M, erythrocyte sedimentation rate ( ESR) , and complement C3 and significantly higher prothrombin time ( PT) , international normalized ratio ( INR) , and immunoglobulin G ( all P < 0. 05) . Compared with the AIH group, the PBC group had significantly higher positive rates of anti-mitochondrial antibody M2 ( 78. 8% vs 14. 8%, X2= 74. 70, P<0. 001) , anti-gp210 antibody ( 46. 4% vs 5. 3%, X2= 7. 31, P = 0. 007) , and anti-BCOADC-E2 PDC-E2 OGDC-E2 ( anti-3 E-BPO) antibodies ( 75. 0% vs 31. 6%, X2= 8. 73, P = 0. 003) . As for liver histological features, PBC was characterized by bile duct injury, including small cholangitis, biliary granuloma, absence of bile duct, and reactive hyperplasia of bile capillaries, while AIH was characterized by interface hepatitis ( X2= 31. 00 and 5. 88, P < 0. 001 and P = 0. 015) . Conclusion AIH and PBC often occur in women and lack specific clinical manifestations. PLT, ALP, GGT, PT, INR, ESR, complement, and immunoglobulins on admission, type of serological antibodies, and liver pathological features can be used for the differential diagnosis of AIH and PBC, and anti-3 E-BPO antibody can help with the diagnosis of PBC.

Clinicopathological features of drug-induced liver injury or primary biliary cholangitis with vanishing bile duct syndrome
Ye LiHong, Wang ChongKui, Jin Peng, Zhao LiangLiang, Zhang HaiCong, Liu ZhiQuan, Tang YaFang
2019, 35(2): 359-363. DOI: 10.3969/j.issn.1001-5256.2019.02.023
Abstract:

Objective To investigate the clinical features of patients with drug-induced liver injury ( DILI) and vanishing bile duct syndrome ( VBDS) and patients with primary biliary cholangitis ( PBC) and VBDS. Methods A retrospective analysis was performed for the clinical data of 42 DILI patients and 43 PBC patients who visited Shijiazhuang Fifth Hospital from January 2003 to January 2018 were diagnosed with VBDS by liver biopsy, including general information, clinical symptoms and signs, and serological markers, and pathomorphological features were observed. The Mann-Whitney U rank sum test was used for comparison between two groups; the chi-square test was used for comparison of categorical data between groups. Results Most of the patients in the two groups were female patients aged 40-50 years. The D-VBDS group had a significantly higher incidence rate of yellow staining of skin and sclera than the P-VBDS group ( X2=5. 683, P = 0. 017) . Comparison of the peak values of liver biochemical indices showed that compared with the P-VBDS group, the D-VBDS group had significantly higher total bilirubin ( Z =-2. 020, P = 0. 043) and direct bilirubin ( Z =-2. 910, P = 0. 004) . According to the results of pathomorphological analysis and morphological scores of the portal area, the P-VBDS group had significantly higher morphological scores of portal inflammation, fibrosis, and granuloma than the D-VBDS group ( Z =-3. 136, -2. 710, and-2. 913, P =0. 002, 0. 007, and 0. 005) . The morphological scores of the hepatic lobules showed that compared with the P-VBDS group, the D-VBDS group had significantly higher morphological scores of intralobular inflammation, bile thrombus in bile capillary, and activated phagocytes ( Z =-3. 255, -2. 455, and-4. 398, P = 0. 001, 0. 014, and < 0. 001) . Conclusion Pathomorphological features of the liver are objective and accurate indices for the differentiation between DILI with VBDS and PBS with VBDS and have great significance in making a definite diagnosis, understanding the degree of injury, and predicting prognosis.

Protective effect of hepatocyte growth-promoting factor against liver ischemia-reperfusion injury in rats and its mechanism of action
Luo YanQing, Feng ChunLin, Mei Yong, Du Chao, Ceng PengFei, Wang Jun, Wang GuoXing, Zhao Liang, Leng Kai
2019, 35(2): 364-367. DOI: 10.3969/j.issn.1001-5256.2019.02.024
Abstract:

Objective To investigate the protective effect of hepatocyte growth-promoting factor ( PHGF) against liver ischemia-reperfusion injury in rats and its mechanism of its action. Methods A total of 80 healthy male Sprague-Dawley rats were randomly divided into experimental group ( PHGF group) and control group ( NS group) , with 40 rats in each group. A rat model of liver ischemia-reperfusion injury was established by 70% liver ischemia caused by the occlusion of blood flow in the middle and left lobes of the liver, with an ischemia time of 21 minutes. The rats in the PHGF group were given intraperitoneal injection of PHGF for intervention before surgery, and those in the NS group were given an equal volume of normal saline. Serum and liver tissue samples were collected before surgery and on days 1, 3, 5, and 7 after surgery, and the levels of alanine aminotransferase ( ALT) , aspartate aminotransferase ( AST) , and total bilirubin ( TBil) were measured; HE staining was used to observe pathological changes; real-time PCR was used to measure the mRNA expression of mitochondrial transcription factor A ( TFAM) in the liver. The independent samples t-test was used for comparison of continuous data between two groups. Results HE staining showed that compared with the NS group, the PHGF group had significantly lower degrees of hepatocyte swelling, inflammatory cell infiltration, and hepatocyte necrosis under a light microscope. Liver biochemistry showed that on days 1, 3, 5, and 7 after surgery, the PHGF group had significantly lower serum levels of ALT, AST, and TBil than the NS group ( t = 11. 879, 16. 019, 22. 168, 10. 235, 9. 041, 12. 936, 18. 759, 8. 142, 10. 108, 11. 014, 13. 245, and 9. 968, all P < 0. 001) . Real-time PCR showed that on days 1, 3, and 5 after surgery, the PHGF group had a significantly higher mRNA level of TFAM in the liver than the NS group ( t =7. 998, 14. 764, and 13. 861, all P < 0. 001) . Conclusion PHGF preconditioning exerts a protective effect against liver ischemia-reperfusion injury in rats, possibly by upregulating the expression of TFAM to alleviate liver ischemia-reperfusion injury.

Expression of Mindin, a pattern recognition molecule, in a mouse model of acute liver injury induced by carbon tetrachloride
Zhang Xin, Wang WenJun, Zhai Song, Li YaPing, Shi JuanJuan, Jia XiaoLi, Dang ShuangSuo
2019, 35(2): 368-371. DOI: 10.3969/j.issn.1001-5256.2019.02.025
Abstract:

Objective To investigate the dynamic expression of Mindin protein in mice with acute liver injury induced by carbon tetrachloride ( CCl4) and its mechanism of action. Methods A total of 48 male C57 B1/6 mice were selected and divided into experimental group ( n= 40) and control group ( n = 8) . The mice in the experimental group were given intraperitoneal injection of CCl4 olive oil to induce acute liver injury, and the liver tissue was collected for pathological observation at 6, 12, 24, 48, and 72 hours after modeling. The mice in the control group were given intraperitoneal injection of olive oil. Western blot was used to measure the protein expression of Mindin and its change trend, and quantitative real-time PCR was used to measure the mRNA expression of Mindin. The t-test was used for comparison of continuous data between two groups. Results Abnormal liver structure was observed after liver injury was induced by CCl4, with the most significant pathological change at 48 hours. There was a low protein expression level of Mindin within 12-72 hours after the injection of CCl4. The mRNA expression of Mindin reached the lowest level at 12 hours after CCl4 injection and there was a significant difference between the experimental group and the control group at this time point ( 0. 183 ± 0. 105 vs 1. 023 ± 0. 247, t = 8. 841, P < 0. 01) ; then there was a gradual increase in the mRNA expression of Mindin, and at 48 and 72 hours, the mRNA expression of Mindin in the experimental group was more than 2 times that in the control group ( 48 hours: 2. 548 ± 0. 775 vs 1. 023 ± 0. 247, t = 5. 428, P < 0. 01; 72 hours: 2. 699 ± 0. 995 vs 1. 023± 0. 247, t = 4. 621, P < 0. 01) . Conclusion There is a significant change in Mindin protein during the process of acute liver injury induced by CCl4 in mice, which is characterized by the downregulation of protein expression and the regulation of post-transcriptional mRNA level, suggesting that Mindin may play an important role in the process of acute liver injury induced by CCl4.

Case reports
Neonatal intrahepatic cholestasis caused by Citrin deficiency with hepatic cirrhosis ascites as the main manifestation:A case report
Zhang JianLing, Shu SaiNan, Cai ZaiSheng, Luo XiaoPing, Dong Chen
2019, 35(2): 372-375. DOI: 10.3969/j.issn.1001-5256.2019.02.026
Abstract:
A case of arterio-biliary fistula during transjugular intrahepatic portosystemic shunt
Xi XiaoTan, Luo XueFeng, Zhu YongJun, Wang XiaoZe, Yang Li
2019, 35(2): 376-378. DOI: 10.3969/j.issn.1001-5256.2019.02.027
Abstract:
Primary biliary cholangitis-autoimmune hepatitis overlap syndrome with Wilson's disease: A case report
Pang XiangJun, Xin GuiJie, Zhang Juan, Yan Qi
2019, 35(2): 379-381. DOI: 10.3969/j.issn.1001-5256.2019.02.028
Abstract:
A case of acute hepatic venular occlusive disease caused by Gynura segetum
Qu WeiGe, Cai YanJun, Sun XiaoFeng, Qi Yue
2019, 35(2): 382-383. DOI: 10.3969/j.issn.1001-5256.2019.02.029
Abstract:
A case of Pneumocystis carini pneumonia after liver transplantation
Zhang DaLi, Gao YinJie, Feng DanNi, Zhang LiJuan, He Xi, Liu ZhenWen, Liu HongLing
2019, 35(2): 384-385. DOI: 10.3969/j.issn.1001-5256.2019.02.030
Abstract:
Glucocorticoid treatment of intrahepatic cholestasis caused by infectious cholangitis: A case report
Zhao YouYou, Zhang Duan, Yin Xin, Wen XiaoYu, Gao PuJun
2019, 35(2): 386-387. DOI: 10.3969/j.issn.1001-5256.2019.02.031
Abstract:
A case of IgG4-related autoimmune pancreatitis
Han Lin, Yu Fan, Qin ShaoYou, Zhou ZhangYu
2019, 35(2): 388-389. DOI: 10.3969/j.issn.1001-5256.2019.02.032
Abstract:
Child pancreatoblastoma: A case report and review of the literature
Wang Kun, Liu Feng, Abudureyimu Tuerhong, Yang Fan, Liu YaHui, Zhang Wei
2019, 35(2): 390-391. DOI: 10.3969/j.issn.1001-5256.2019.02.033
Abstract:
Primary pancreatic signet ring cell carcinoma: A case report and literature review
Zhang JiaQi, Yao XiaoXiao, Tian Xuan, Zhang LiFu, Fang He, Jia MingKu, Zhang Dan
2019, 35(2): 392-394. DOI: 10.3969/j.issn.1001-5256.2019.02.034
Abstract:
Reviews
Research advances in the role of lipid metabolism in hepatitis C virus infection and life cycle
Xu Chu, Zhang PingAn
2019, 35(2): 395-398. DOI: 10.3969/j.issn.1001-5256.2019.02.035
Abstract:
Hepatitis C virus ( HCV) infection is one of the leading causes of liver cirrhosis, end-stage liver disease, and even liver cancer. Patients with HCV infection tend to have insulin resistance and dyslipidemia, which may lead to a series of metabolic syndromes and greatly threaten human health. At present, there are still no effective vaccines to prevent HCV infection, and therefore, the mechanism of HCV infection remains a hot topic in clinical research. Many studies have shown that there is a complex relationship between HCV infection and lipids, but the role of lipids in HCV infection remains unclear. This article reviews the current research status of the role of lipid metabolism in HCV infection and life cycle, in order to understand the mechanism of abnormal fat metabolism in the liver and the pathogenesis of fatty liver disease.
Mechanism and current status of carvedilol in treatment of cirrhotic portal hypertension
He Bo, Zhang ChunQing
2019, 35(2): 399-401. DOI: 10.3969/j.issn.1001-5256.2019.02.036
Abstract:
The formation of cirrhotic portal hypertension depends on the increase in intrahepatic vascular resistance and the state of hyperdynamic circulation. The specific effect of carvedilol in reducing intrahepatic vascular resistance has a better effect in alleviating portal hypertension in theory. This article summarizes the known and possible mechanisms of carvedilol in reducing portal hypertension and reviews the latest research advances in the role of carvedilol in the treatment of cirrhotic portal hypertension. It is pointed out that carvedilol is expected to become the core drug in the treatment of cirrhotic portal hypertension, and statins may be their best partner.
Mechanism and current status of simvastatin in treatment of cirrhotic portal hypertension
Wu Huan, Wu Long, Yang Jing
2019, 35(2): 402-405. DOI: 10.3969/j.issn.1001-5256.2019.02.037
Abstract:
Besides related etiologies, portal hypertension ( PHT) is considered an important physiological link in promoting liver dysfunction. Literature review has shown that compared with the conventional drugs for the prevention and treatment of PHT, simvastatin can induce the expression of Kruppel-like factor-2 and nitric oxide to improve liver function and reduce cirrhotic portal venous pressure. Related analysis shows that simvastatin can be widely used in clinical practice to improve portal vein hemodynamics in cirrhotic patients.
Noninvasive diagnosis of progressive nonalcoholic fatty liver disease
Gong Hang, Li LiangPing
2019, 35(2): 406-410. DOI: 10.3969/j.issn.1001-5256.2019.02.038
Abstract:
Nonalcoholic fatty liver disease ( NAFLD) is characterized by the pathological feature of hepatocyte fatty degeneration and lipid accumulation, and liver histopathology evolves from simple liver fatty degeneration to steatohepatitis with hepatocellular injury and finally progresses to liver fibrosis, liver cirrhosis, and even liver cancer. NAFLD is closely associated with metabolic syndrome and colorectal tumors and can even lead to disability and death, and therefore, it is of great importance to diagnose nonalcoholic steatohepatitis ( NASH) as early as possible and clarify liver fibrosis degree. As the gold standard for determining the liver histopathological grade and stage of NAFLD, liver biopsy has always been a main method for the diagnosis of liver fibrosis. However, the limitations of liver biopsy have greatly promoted the rapid development of noninvasive diagnostic techniques in recent years. The sensitivity and specificity of serology models and imaging tests in the diagnosis of NASH and early-stage liver fibrosis need to be improved. This article reviews the advances in noninvasive diagnostic methods for progressive NAFLD.
The association between interleukin-8 and autoimmune liver diseases
Lei YunJie, Yang JinHui
2019, 35(2): 411-413. DOI: 10.3969/j.issn.1001-5256.2019.02.039
Abstract:
Interleukin-8 ( IL-8) is an inflammatory cytokine with chemotaxis and there is a significant increase in the expression of IL-8 in autoimmune liver diseases. It participates in disease progression by binding to its receptors CXCR1 and CXCR2, promoting chemotaxis of inflammatory cells, angiogenesis, and fibrosis, and inducing cell proliferation. This article reviews the research advances in the association between IL-8 and autoimmune liver diseases.
Influencing factors for short-term prognosis of liver failure in pregnancy
Zhang BaoZhong, Zhou PengZhi
2019, 35(2): 414-418. DOI: 10.3969/j.issn.1001-5256.2019.02.040
Abstract:
Liver failure in pregnancy is one of the most serious complications that greatly threaten the safety of pregnant women and parturients, with a high mortality rate and poor prognosis. The short-term prognosis of liver failure in pregnancy can be predicted based on etiology, clinical type and stage of liver failure, dynamic changes of laboratory markers, liver ultrasound, type and number of complications, selection of obstetric treatment, and whether artificial liver support therapy was performed. It is pointed out that it is necessary for clinicians to comprehensively evaluate the short-term prognosis of liver failure in pregnancy, which helps to guide clinical treatment, optimize medical resource allocation, and improve resource utilization.
Clinical features of patients with liver failure and fungal infections and influencing factors for prognosis
Wang Yu, Hu JinHua
2019, 35(2): 419-423. DOI: 10.3969/j.issn.1001-5256.2019.02.041
Abstract:

Liver failure is severe liver injury due to a variety of causes and has complex and diverse complications. Fungal infection is one of the serious complications of liver failure which often occurs in the advanced stage of liver failure, greatly affects prognosis, and leads to a significant increase in mortality, and therefore, it has become a difficult problem in clinical practice. This article introduces the research advances in high-risk factors, clinical features, diagnostic methods, and prognostic factors in patients with liver failure and fungal infections and provides a theoretical basis for improving the level of clinical diagnosis and treatment, in order to reduce the mortality of such patients and improve their quality of life.

Effect of various cells on the activation of hepatic stellate cells in liver microenvironment
Xu Ying, Zhang DingQi, Chen JiaMei, Liu Wei, Liu Ping
2019, 35(2): 424-430. DOI: 10.3969/j.issn.1001-5256.2019.02.042
Abstract:
Liver fibrosis is a dynamic pathological process characterized by excessive deposition of extracellular matrix ( ECM) or hyperplasia of scar tissue. The activation of hepatic stellate cells ( HSCs) is generally considered the central link in the formation of liver fibrosis. HSC activation is regulated by various factors in liver microenvironment, including physical and chemical stimulations and intercellular interactions. Intrinsic cells and immune cells in the liver and HSCs together establish a complex regulatory system to regulate HSC activation and regression. This article introduces the regulatory effect of the cells in liver microenvironment on HSC activation, in order to expand thinking for the research on new diagnosis and treatment methods for liver fibrosis.
Bile formation, secretion, and excretion and the pathogenesis of cholestasis
Shen Hong, Hu Meng, Wei ZeHui, Zhang Dong, Zhang JunChang, Tian GuangJun
2019, 35(2): 431-437. DOI: 10.3969/j.issn.1001-5256.2019.02.043
Abstract(1607) PDF (292KB)(1277)
Abstract:
Normal bile formation, secretion, and excretion are important physiological processes in human body. Bile plays an important role in promoting lipid digestion and absorption, eliminating metabolic waste, and regulating cholesterol metabolism. Disorders in bile formation, secretion, or excretion due to various causes may lead to acute or chronic cholestatic diseases. A deep understanding of the role of bile formation, secretion, and excretion and the pathogenesis of cholestasis is of great significance in the research on cholestatic liver diseases and clinical practice.
Current status of clinical research on hematobilia
Ma Min, Zhou ZhongYin
2019, 35(2): 438-440. DOI: 10.3969/j.issn.1001-5256.2019.02.044
Abstract:
Hematobilia is one of the rare causes of upper gastrointestinal bleeding. It is difficult to diagnose in clinical practice, due to its atypical clinical manifestations, rare Quikle triad ( abdominal pain, jaundice, and upper gastrointestinal bleeding) , and a lack of specificity.At present, it is believed that iatrogenic injury is the main cause of hematobilia, selective hepatic arteriography is the preferred choice for the diagnosis of hematobilia, and interventional embolization is the main treatment method. With reference to related articles, this article mainly elaborates on the current status of the research on the etiology, clinical manifestations, diagnosis, and treatment of hematobilia.
Epidemiology of polypoid lesions of the gallbladder and related risk factors
Chen ShanPeng, Wang ZhiXiang, Zhang XiaoDi, Shen NaiYing, Wei ZhiLi
2019, 35(2): 441-443. DOI: 10.3969/j.issn.1001-5256.2019.02.045
Abstract:

Polypoid lesions of the gallbladder ( PLG) is a common gallbladder disease in clinical practice. Most patients have non-adenomatous polyps, while adenomatous polyps are observed in a small number of patients. This article summarizes the epidemiology of PLG and related risk factors and points out that PLG is caused by the combined effect of various factors including sex, hepatitis B virus infection, metabolic syndrome, visceral obesity, a low level of low-density lipoprotein, gallbladder wall thickening, and diabetes. With the gradual increase in the incidence rate of PLG, epidemiological data should be used for health screening among the high-risk population, and standardized follow-up should be performed for patients with a confirmed diagnosis. PLG which may progress to cancer should be identified and intervention should be given as early as possible.

Establishment and application of animal models of cholestasis
Du LiNa, Yang Yan
2019, 35(2): 444-447. DOI: 10.3969/j.issn.1001-5256.2019.02.046
Abstract(1188) PDF (199KB)(750)
Abstract:
Cholestatic liver disease is one of the common diseases in children aged < 1 year and has a complex etiology and different outcomes. Various animal models have been established to further investigate the pathogenesis of cholestatic liver disease and related treatment strategies. A model of obstructive cholestasis is established by surgery or external physical and chemical damage; a model of intrahepatic cholestasis is induced by chemicals or endotoxins, including α-naphthyl isothiocyanate, lipopolysaccharide, 3, 5-diethoxycarbonyl-1, 4-dihydrocollidine, estrogen, chlorpromazine, rifampicin, and lithocholic acid; a model of parenteral nutrition-associated cholestasis is established by a combination of intestinal damage and parenteral nutrition. These models reflect different causes and development processes.This article reviews the characteristics, mechanisms, and indications of animal models of cholestasis commonly used in medical research.
Research advances in the epidemiological features, pathogenesis, and diagnosis and treatment of alcoholic pancreatitis
Hu JiangFeng, Lu LunGen
2019, 35(2): 448-450. DOI: 10.3969/j.issn.1001-5256.2019.02.047
Abstract:
There has been a significant increase in the number of patients with alcoholic pancreatitis in recent years, and the pathogenesis of alcoholic pancreatitis is associated with various factors including genetic factors, smoking, and gut microbiota. Alcoholic pancreatitis is different from other types of pancreatitis in epidemiological features and clinical manifestations. This article reviews the research advances in the epidemiological features, pathogenesis, clinical manifestations, treatment, and prognosis of alcoholic pancreatitis.
Features of infection secondary to severe acute pancreatitis and related control strategies
Tian Hao, Li FuXing, Song ShaoWei
2019, 35(2): 451-456. DOI: 10.3969/j.issn.1001-5256.2019.02.048
Abstract:
Severe acute pancreatitis ( SAP) is an acute abdominal disease and a critical illness commonly seen in clinical practice. Infection complications in the middle and late stages of SAP have a great impact on the prognosis of SAP and are often difficult to avoid. This article introduces the pathogenesis of secondary pancreatic and extra-pancreatic infections and summarizes the pathogen spectrum of infections secondary to SAP in the past 10 years. This article also summarizes and evaluates the current strategies for preventing secondary infections and briefly describes the advances in surgical interventions for SAP secondary infections. These analyses show that the pathogenesis, pathogenic features, and immunological features of SAP secondary infection remain unclear. There are various control strategies for such infection, but there are still no effective measures to prevent infection except early enteral nutrition. Conclusions will be achieved on the issues including the timing of percutaneous catheter drainage, and surgical interventions have developed rapidly on the basis of the STEP-UP approach. Endoscopic STEP-UP approach is slightly superior to conventional STEP-UP approach in the treatment of critically ill patients with SAP.