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Copyright of Journal of Clinical Hepatology / Linchuang Gandanbing Zazhi is the property of Journal of Clinical Hepatology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Autoimmune liver disease is a group of diseases mainly caused by autoimmune abnormalities, including autoimmune hepatitis dominated by hepatocellular injury, primary biliary cholangitis and primary sclerosing cholangitis dominated by bile duct injury, and overlap syndrome with the main features of the above two diseases. Recently, IgG4 - related hepatobiliary diseases have also been included in this category, and without timely diagnosis and treatment, it can progress to liver cirrhosis and even liver failure. Different autoimmune liver diseases have their own features, and with the popularization of the knowledge on autoimmune liver diseases, physicians have gradually increased their understanding of such diseases and can achieve the early diagnosis and timely treatment of most typical autoimmune liver diseases. However, some patients may have atypical manifestations or laboratory markers, which may easily delay the diagnosis, and therefore, it is of great importance to identify atypical autoimmune liver disease and give timely diagnosis and treatment as soon as possible. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Clinical Hepatology / Linchuang Gandanbing Zazhi is the property of Journal of Clinical Hepatology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Hepatology / Linchuang Gandanbing Zazhi is the property of Journal of Clinical Hepatology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Hepatology / Linchuang Gandanbing Zazhi is the property of Journal of Clinical Hepatology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Hepatology / Linchuang Gandanbing Zazhi is the property of Journal of Clinical Hepatology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Hepatology / Linchuang Gandanbing Zazhi is the property of Journal of Clinical Hepatology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Autoimmune hepatitis (AIH) is a chronic liver inflammatory disease with unknown etiology, and at present, both genetic and environmental factors are thought to be involved in the pathogenesis of AIH. Environmental exposure has an important impact on the development of AIH. Autoimmune ecology is the study of the interactions between individuals and their environment, the development of imbalance between individuals and environment, and the mechanism of such imbalance in promoting the development of autoimmune disease. This article reviews the research advances in the role of autoimmune ecology in the pathogenesis of AIH. [ABSTRACT FROM AUTHOR]

Overgrowth of intestinal bacteria. change in intestinal flora, translocation between bacteria and their products. and bile acid metabolism are the important pathways for the development and progression of liver diseases. Hepatocytes are persistently exposed to intestinal metabolites and various antigens and antibodies via the portal vein system, and the constituents or metabolites of some intestinal bacteria can activate the autoimmune mechanism targeting hepatocytes through several mechanisms, including molecular mimicry. Therefore, intestinal flora plays an important role in the development/progression and treatment of autoimmune liver diseases, including autoimmune hepatitis, primary biliary cholangitis, and primary sclerosing cholangitis. This article reviews the related research advances in recent years. [ABSTRACT FROM AUTHOR]

Prognostic evaluation of patients with primary biliary cirrhosis (PBC) and how to improve the prognosis have attracted much attention. Further therapeutic regimens for PBC patients with poor prognosis has become the direction of clinical and scientific studies. This article summarizes the association between baseline indices and prognosis and prognostic evaluation of patients undergoing ursodeoxycholic acid (UDCA) treatment, introduces the current status of UDCA combined with budesonide, fibrates, and obeticholic acid for patients with poor response to UDCA and the drugs being developed, and analyzes the influencing factors for prognosis and efficacy of UDCA. It is pointed out that prognosis and efficacy should be evaluated before and during UDCA treatment, and that therapeutic regimens should be adjusted in time to improve prognosis. [ABSTRACT FROM AUTHOR]

Objective To investigate the correlation between clinical data and pathological stage in patients with primary biliary cirrhosis (PBC) and to provide guidance for clinical diagnosis and treatment. MethodsThe clinical data of 54 PBC patients were collected for analyzing the correlation between the clinical data and pathological stage. The clinical data included biochemical parameters, immunological markers, and autoantibodies. Biopsy of the liver was used for the pathological staging of PBC. For the continuous data of normal distribution, analysis of variance was applied for comparisons between groups; for continuous data of skewed distribution, Wilcoxon rank sum test was used. For categorical data, chi-square test was used. Correlation analysis was performed by Pearson correlation and logistic regression. ResultsAmong the 54 patients, the male-to-female ratio was 1.5; the mean age was 48.9±9.3 years; pathological stage was identified in 15 cases, stage in 18 cases, stage in 12 cases, and stage in 9 cases, and patients with stage disease were significantly older than the other patients (P＜0.05). Total bilirubin (TBil), alkaline phosphatase, prothrombin time, IgA, IgG, and SP200 were positively correlated with pathological stage (r=0.592, 0.343, 0.281, 0.388, 0.274, and 0.320, respectively, P＜0.05), while a negative correlation was found between albumin and pathological stage (r=-0.569, P=0.000). Multivariate analysis revealed an independent correlation between TBil level and pathological stage (P=0.039). Patients with the same pathological stage might have different clinical stages, while those with the same clinical stage might have different pathological stages. ConclusionsThe same pathological stage may appear in different clinical stages. TBil level is an independent predictive factor for pathological stage in PBC patients. [ABSTRACT FROM AUTHOR]