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Adenovirus infection can occur in all regions or countries of the world, with no obvious seasonality, but pandemics mostly occur in winter or early spring. Adenovirus infection is self-limited among immunocompetent host with supportive care, however fatal infection can occur among immunocompromised patients, mainly affecting respiratory, gastrointestinal tract and adjunctiva and very rarely causing hepatitis, cholecystitis, pancreatitis, hemorrhagic cystitis, myocarditis, meningitis or encephalitis. Adenovirus hepatitis mainly occur in malignant tumors or organ transplantation patients, but acute severe hepatitis can occur even in immunocompetent children or adults. On 5 April 2022, WHO was notified of 10 cases of severe acute hepatitis of unknown etiology in children. As of 21 April 2022, at least 169 cases of acute hepatitis of unknown origin have been reported from 12 countries (including 11 WHO European Region countries and the United States). Adenovirus has been detected in at least 74 cases; SARS-CoV-2 was identified in 20 cases of those that were tested. Furthermore, 19 were detected with a SARS-CoV-2 and adenovirus co-infection. At present, the etiology has not been fully elucidated. The leading hypotheses center around adenovirus, and the relationship with SARS-CoV-2 needs to be further ruled out.腺病毒感染在全球各地区均可出现，无明显季节性，但大流行多发生在冬季或早春。腺病毒在免疫功能正常的人中常引起轻度、自限性感染，主要累及呼吸道、消化道、眼结膜等，偶尔可导致肝炎、胆囊炎、胰腺炎、出血性膀胱炎、心肌炎、脑膜炎或脑炎。一般预后良好，但在免疫功能缺陷者，可发生严重或致命的感染。腺病毒肝炎主要见于恶性肿瘤及组织器官移植等处于免疫功能抑制状态的人群，但也有在免疫功能正常的小儿或成人引起急性肝炎的个案报道。2022年4月5日，世界卫生组织收到英国通报10例原因不明的儿童严重急性重症肝炎病例，至4月21日增至169例，遍及12个国家（11个世界卫生组织欧洲区国家及美国），其中74例腺病毒阳性、20例新型冠状病毒阳性，19例新型冠状病毒和腺病毒同时阳性。其病因尚未完全阐明，但病因假说主要围绕腺病毒感染，与新型冠状病毒的关系也需进一步排除。.

Connective tissue disease (CTD) are closely related to liver abnormality. CTD can affect the liver causing various degrees of liver injury, coexist with other liver diseases, especially autoimmune liver disease (ALD). Medications for CTD can also lead to liver injury or reactivate the hepatitis B virus. CTD patients can also be positive for ALD-related autoantibodies without corresponding manifestation; and vis versa. The diagnosis and differential diagnosis should be made on integrating clinical presentation, laboratory, imaging, and histological studies, not solely relying on autoantibody positivity.结缔组织病（CTD）与肝脏关系密切。CTD可以累及肝脏并导致不同程度的肝损伤，也可以合并其他肝脏疾病尤其是自身免疫性肝脏疾病（ALD）。此外，治疗CTD的药物也可以引起肝脏损伤或激活乙型肝炎病毒。需要注意的是，ALD可出现CTD相关的自身抗体阳性，而无CTD的其他表现；反之亦然。因此，其诊断和鉴别诊断需综合分析患者的临床表现、实验室检查、影像学检查，甚至组织病理学检查，不能仅凭相应的自身抗体阳性就下结论。.

As a secondary endocrine organ, the liver is closely related to the endocrine system. Liver involvement is not uncommon in endocrine diseases, such as hyper/hypothyroidism, diabetes, dysfunction of adrenal and gonadal. It can be manifested in a variety of forms, including hepatocyte injury (elevated transaminase), bile duct injury (cholestasis), hepatocyte steatosis, vascular injury and liver tumor. Direct and indirect liver injury caused by abnormal hormone levels and side effects of drugs for the treatment of endocrine diseases are common pathogenesis. In addition, endocrine diseases can be concomitant with liver diseases, such as autoimmune thyroiditis and autoimmune hepatitis. Systemic diseases can also involve the endocrine system and liver at the same time, such as systemic lupus erythematosus and IgG4 related diseases. For patients with unexplained liver injury, endocrine system diseases should be considered as the differential diagnosis.肝脏作为次级内分泌器官，与整个内分泌系统之间存在密切联系。多种内分泌系统疾病可影响到肝脏，如甲状腺功能亢进/减退症、糖尿病、肾上腺、性腺相关疾病等，并可表现为肝细胞损伤（转氨酶升高）、胆管损伤（胆汁淤积）、肝细胞脂肪变性、血管损伤及肝占位等多种形式。激素水平异常引起的直接、间接肝损伤、治疗内分泌疾病药物的不良反应是其常见的机制。此外，内分泌疾病可同时合并肝脏疾病如自身免疫性甲状腺炎易合并自身免疫性肝炎；全身系统性疾病也可同时累及内分泌系统和肝脏，如系统性红斑狼疮、IgG4相关疾病等。临床上遇到不明原因肝损伤的患者，需注意内分泌系统疾病的甄别。.

Liver have complex functions with a high workload. Various liver diseases are the result of the interaction of diverse genetic and environmental factors. Moreover, other systemic diseases may also affect liver, producing corresponding manifestations, such as abnormal liver function tests, portal vein or hepatic vein thrombosis, portal hypertension, hepatosplenomegaly and liver space-occupying lesions. Therefore, it is extremely important for hepatologists to have an in-depth understanding of other systemic diseases of hepatic manifestations, especially hematologic, connective tissue, endocrine, and circulatory, in order to improve the level of clinical diagnosis and treatment.肝脏功能复杂、工作负荷繁重，各种遗传及环境因素的相互作用可导致各种肝脏疾病。而且，其他系统的疾病也可能累及肝脏并产生相应的表现，如肝功能试验异常、门静脉或肝静脉血栓形成、门静脉高压症、肝脾肿大及肝占位等。深入理解其他系统特别是血液、结缔组织、内分泌及循环系统疾病的肝脏表现，对于提高肝病医生的临床诊疗水平极为重要。.

Liver involvement is often observed in hematological disorders, resulting in liver abnormality, including unconjugated hyperbilirubinemia, monoclonal hyperglobulinemia, portal vein, or hepatic vein thrombosis or portal hypertension, hepatosplenomegaly, or iron accumulation in the liver. Here we summarize the major hematological diseases that often affect the liver: hemolytic anemia, defect in coagulation or anti-coagulation factors, myeloproliferative neoplasm, hemophagocytic lymphohistiocytosis, multiple myeloma, leukemia, and lymphoma. We hope this review will help clinicians diagnose and manage the patients with liver involvement by hematological disorders.多种血液系统疾病可累及肝脏，并导致复杂多样的临床表现，如高非结合型胆红素血症、单克隆性免疫球蛋白升高、门静脉或肝静脉血栓形成/门静脉高压、肝脾肿大及肝脏铁沉积等临床表现。现简要论述常见溶血性疾病、凝血和抗凝因子缺陷、骨髓增殖性肿瘤、噬血细胞综合征、多发性骨髓瘤、白血病、淋巴瘤等血液系统疾病的肝脏表现，以帮助临床医生更好诊治此类疾病。.

原发性胆汁性胆管炎（PBC）是一种由自身免疫介导的慢性胆汁淤积性肝病，其发病机制尚未完全阐明。PBC在亚太地区的流行率呈逐年上升趋势，疾病负担日益加重。对此，亚太肝病学会邀请了多位知名肝病学家和方法学家共同制定了《原发性胆汁性胆管炎临床诊疗指南》。PBC常见于中年女性，主要疾病特点为血清学胆汁淤积性指标升高、PBC特异性自身抗体阳性，以及组织学显示非化脓性破坏性胆管炎。熊去氧胆酸13～15 mg·kg(-1)·d(-1)是所有PBC患者的标准一线治疗，而二线治疗药物(苯扎贝特/非诺贝特、奥贝胆酸或布地奈德)可用于治疗对熊去氧胆酸单药应答不佳的患者。取得良好生化应答的PBC患者预后良好，但诊断较晚或应答不佳的患者仍有可能发展为肝硬化、肝衰竭，终末期肝病PBC患者仍需肝移植治疗。.

The《中华肝脏病杂志》2020年核心影响因子为1.807，名列消化病学类期刊第1名，入选中国科学技术协会高质量科技期刊分级目录T1级。2021年获重庆市新闻出版局出版专项资金、重庆市科学技术协会高品质科技期刊资助项目、国家教育部产学研合作协同育人项目支持；获"川渝一流科技期刊"、"重庆市高品质科技期刊"等多项殊荣，实现了期刊"质与量"的双效发展。2022年我们将着力于吸引高水平研究成果，及时、高效、精准传播学术成果，重视数字化传播，建设一流学术期刊。.

Long term antiviral therapy with nucleos(ti)ide analogues could suppress HBV viral load thereby prevent the progression to cirrhosis and hepatocellular carcinoma. Interferon-based therapy could result in sustained virological response in a fair proportion of patients and even HBsAg loss in a small proportion of them. Novel therapies aiming at functional cure (loss of HBsAg) are under active development. Among the categories of many, HBV core protein inhibitors are safe and could suppress the HBV DNA and HBV RNA, but only with modest effect on the level of HBsAg; silencing of HBV mRNA by siRNA or antisense oligonucleotides could produce meaningful and sustainable declining in HBsAg levels; immune modulators with different mode of action showed modest effect on the reduction of HBsAg, but with noticeable adverse event (especially transaminase flares) related to the mode of action. Novel clinical trial design on the combination or sequential use of innovative molecules will ultimately lead to the functional cure of CHB in the near future.长期口服抗病毒治疗可以有效抑制HBV DNA复制从而阻断和延缓进展为肝硬化和肝细胞癌，基于干扰素的治疗可以在部分患者实现持续病毒学应答，在少部分患者甚至可以达到HBsAg消失。目前国内外以慢性乙型肝炎临床治愈（HBsAg消失）为目标新药包括：口服核心蛋白抑制剂，耐受性和安全性良好，能有效降低HBV DNA和HBV RNA,但单用不能有效降低HBsAg水平；注射用干扰RNA或反义RNA，可以有效地降低HBsAg水平，且持续时间较长；免疫调节剂只能带来轻微的HBsAg水平下降，但同时也可能带来免疫相关的不良事件。在不远的将来,通过设计新颖的临床试验，探索不同机制的抗HBV新药联合或序贯应用，有可能实现慢性乙型肝炎的临床治愈。.

Hepatitis B virus (HBV) infection is a serious global public health issue. At present, clinical cure is the ideal endpoint for hepatitis B treatment. That is to say, after the completion of treatment, the serum hepatitis B virus surface antigen (HBsAg) is negative, with or without the presence of antibody against hepatitis B virus surface antigen (anti-HBs), undetectable HBV DNA, liver biochemical indicators within normal range, and improved liver tissue lesions. However, it is difficult to achieve a satisfactory clinical cure effect based on the existing therapeutic drugs. To this end, scientists have conducted many explorations, whether it is a combination of nucleos(t)ide analogues and pegylated interferon therapy strategies, or timely termination of antiviral drug treatment, or accelerate the research and development of innovative drugs. The road to clinical cure of hepatitis B is obstructive and long, with full of opportunities and controversies, but the lead is about to come. We always believe that through unremitting efforts, the dream of helping chronic hepatitis B patients to obtain clinical cure or even complete cure will eventually come true.乙型肝炎（乙肝）病毒（HBV）感染是严重的全球公共卫生问题。目前临床治愈是乙肝治疗的理想终点，即患者完成治疗后血清乙肝病毒表面抗原阴性，伴或不伴乙肝病毒表面抗体出现，HBV DNA检测不到，肝脏生物化学指标正常，肝脏组织病变得到改善。然而，基于现有的治疗药物难以获得令人满意的临床治愈效果，为此，科学工作者们进行了诸多探索，不论是联合核苷（酸）类似物和聚乙二醇干扰素的治疗策略，还是适时终止抗病毒药物治疗，抑或是加速创新药物的研发，目前都充满着机遇与争议。乙肝临床治愈之路道阻且长，但行则将至，我们始终相信，经过不懈努力，帮助慢性乙肝患者获得临床治愈甚至完全治愈的梦想终会实现。.

The discovery of hepatitis B virus (HBV) has provided a scientific basis for the diagnosis, prevention and treatment of chronic hepatitis B (CHB). The universalization of neonatal hepatitis B vaccine has greatly reduced the HBsAg positive load rate of the Chinese population. Antiviral therapy based on interferon and / or nucleos(t)ide analogues had effectively inhibited HBV replication, improved liver inflammation, liver fibrosis, and reduced the incidence of liver cirrhosis and hepatocellular carcinoma. However, the existing treatment methods can achieve the clinical cure goal of negative HBsAg. In recent years, direct antiviral drugs for HBV life cycle and immunomodulatory drugs for antiviral response have entered an active stage of research and development. Clinical trials that are well-designed, standardized, analyzed, and interpreted are the key to the success of the research and development of a clinical cure for hepatitis B. It is hoped that the experts in hepatology, clinical pharmacology and methodology will work together to promote the research and development process of new drugs for clinical cure of hepatitis B by adopting new clinical trial design, new endpoint indicators, new data management and quality control technology.乙型肝炎病毒（HBV）的发现为慢性乙型肝炎（CHB）的诊断、预防和治疗提供了科学基础。新生儿乙型肝炎疫苗的普种极大地降低了我国人群乙型肝炎表面抗原（HBsAg）阳性率，基于干扰素和/或核苷（酸）类似物的抗病毒治疗，可有效抑制HBV复制、改善肝脏炎症坏死和肝纤维化，从而减少肝硬化和肝细胞癌的发生。然而，现有治疗手段很难实现到HBsAg转阴的临床治愈目标。近年来，针对HBV生命周期的直接抗病毒药物及针对机体抗病毒应答的免疫调节药物进入研发活跃期。设计良好、执行规范、分析正确、解读恰当的临床试验，是决定乙型肝炎临床治愈新药能否研发成功的关键。希望肝脏病学、临床药理学及方法学专家通力合作，采用新型临床试验设计、新型终点指标、新型数据管理和质控技术，共同促进乙型肝炎临床治愈新药研发进程。.

为进一步规范我国慢性乙肝的预防诊断和治疗，中华医学会感染学分会和肝病学分会发表了《慢性乙型肝炎防治指南（2019年版）。本文介绍了本版指南在流行病学、自然史、预防、诊断和治疗方面的十大亮点。其最突出的变化是放宽了慢性乙型肝炎及肝硬化的抗病毒治疗适应证；进一步明确推荐高效低耐药的恩替卡韦、替诺福韦酯或丙酚替诺福韦；推荐高病毒载量的孕妇于妊娠中晚期开始服用替诺福韦酯或替比夫定以进一步提供母婴阻断率。.

Hereditary hemochromatosis is a kind of hereditary metabolic liver disorders. It is caused by mutations in genes related to hemochromatosis, which leads to over deposition of iron in the liver, pancreas, skin, hypophysis, gonad and other organs and tissues of the whole body and is manifested as cirrhosis, diabetes, skin pigmentation, and low libido. Physicians of our country have inadequate understanding and familiarity with this disorder. Both the European Association for the Study of the Liver and the American Association for the Study of Liver Diseases have issued guidelines for the diagnosis and treatment of hemochromatosis, but these two guidelines are complicated and difficult for Chinese clinical physician to comprehend. In 2018, Hepatology International published therapeutic recommendations in遗传性血色病是一种遗传代谢性肝病，是由血色病相关基因突变导致过多的铁沉积在肝脏、胰腺、皮肤、垂体、性腺等全身多个器官组织，表现为肝硬化、糖尿病、皮肤色素沉着、性功能低下等。我国医师对该病的认知度及熟悉度不够。欧洲肝病学会及美国肝病学会均已发布血色病诊断和治疗指南，但是这两个指南内容繁杂，我国临床医师掌握较为困难。2018年，

To elucidate the regulatory effect of miRNA-1236-3p on the cellular behaviors of osteosarcoma (OS) cells, and to provide novel hallmarks and therapeutic targets for the diagnosis, treatment, and prognosis of OS.Relative level of miRNA-1236-3p in OS tissues and cell lines was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Regulatory effects of miRNA-1236-3p on the proliferative ability of HOS and U-2OS cells were evaluated by cell counting kit-8 (CCK-8) assay. Through flow cytometry, the potential influences of miRNA-1236-3p on cell cycle progression and apoptosis of OS cells were examined. Subsequently, the dual-luciferase reporter gene assay was conducted to explore the binding of KLF8 (Krüppel-like factor 8) to miRNA-1236-3p. Regulatory effects of KLF8 on cellular behaviors of OC cells were also evaluated.MiRNA-1236-3p was downregulated in OS tissues relative to controls. Meanwhile, miRNA-1236-3p was lowly expressed in OS with worse TNM stage or distant metastasis. The overexpression of miRNA-1236-3p in HOS and U-2OS cells suppressed the proliferative ability, arrested the cell cycle in the G0/G1 phase and induced apoptosis. Conversely, miRNA-1236-3p knockdown obtained the opposite trends. KLF8 was verified to bind to miRNA-1236-3p, and its expression was negatively regulated by miRNA-1236-3p in OS cells. A series of functional experiments displayed the oncogenic role of KLF8 in OS.MiRNA-1236-3p is downregulated in OS tissues and cell lines. The overexpression of miRNA-1236-3p suppresses the proliferative ability and induces apoptosis of OS cells via downregulating KLF8.

Idiosyncratic (unpredictable) drug-induced liver injury (iDILI) is one of the most challenging liver diseases encountered by hepatologists due to its diverse clinical and pathological manifestations and lack of specific diagnostic markers. An increasing awareness of iDILI diagnosis and carefully excluding liver damage induced by other causes is the key to a proper diagnosis of iDILI. However, delayed diagnosis, inappropriate monitor and care leads to serious clinical consequences, such as acute liver failure or even liver-related death. In addition, there is presently no effective treatment for iDILI. Herein, we presented the main recommendations of the recent EASL published first DILI guidelines into Chinese language to facilitate liver disease authors and health workers to understand the latest research progress of DILI.特异质性（不可预测性）药物性肝损伤（DILI）是肝病医师所面临的最具挑战性的肝脏疾病之一。临床实践所用药物种类繁多，现有的草药和膳食补充剂也具有潜在的肝毒性，其临床和病理表现多种多样，而且目前尚缺乏特异性的生物标志物，这使得DILI的诊断具有很大的不确定性。临床医师需要提高对DILI诊断的意识，并仔细排除其他原因导致的肝病。特异质性肝毒性可以很严重，导致各种特别严重的急性肝衰竭，目前尚无有效的治疗方法。.

This study detected the expressions of microRNA-26a (miR-26a), miR-146a and miR-31 in lung tissues and BALF (bronchoalveolar lavage fluid) of asthma mice and children. Besides, cytokine levels of interleukin-5 (IL-5), IL-8, IL-12 and tumor necrosis factor-α (TNF-α) were detected as well. We aim to provide an experimental basis for clinical treatment of asthma.Forty female BALB/c mice were randomly assigned into control group and asthma group, respectively. Mice in asthma group (n=20) were immunized by intraperitoneal injection of OVA (ovalbumin) and provoked by atomization inhalation of OVA from the 15th day for 10 days. Mice in control group (n=20) were immunized and provoked with isodose saline during the same period. At the 26th day, mice were sacrificed for collecting lung tissues and BALF. Besides, we enrolled 17 cases of asthma children and 13 cases of children with airway foreign body as controls. BALF of each subject was collected. Total cellular score and differential counting in BALF were recorded. Expression levels of miR-26a, miR-146a, and miR-31 were detected by reverse transcription-polymerase chain reaction (RT-PCR). Levels of IL-5, IL-8, IL-12, and TNF-α were detected by enzyme-linked immunosorbent assay (ELISA).The total cellular score in BALF of asthma mice and asthma children was higher than that of controls (p0.05). Percentages of eosinophils, neutrophils, and lymphocytes in BALF of asthma mice and asthma children were higher than those of controls, whereas the percentage of macrophages was lower (p0.05). Levels of IL-5, IL-8, IL-12, and TNF-α in lung tissues of asthma mice were markedly elevated compared with those of controls (p0.05). Similarly, levels of IL-5, IL-8, IL-12, and TNF-α were higher in BALF of asthma children than controls (p0.05). RT-PCR data showed higher mRNA levels of miR-26a, miR-146a, and miR-31 in lung tissues of asthma mice than controls (p0.05). The mRNA levels of miR-26a, miR-146a, and miR-31 in BALF of asthma children were highly expressed compared with those of controls as well (p0.05).MiR-26a, miR-146a, and miR-31 are involved in asthma progression mainly through regulating inflammatory factors and cells.

Hepatolenticular degeneration (HLD) is an autosomal recessive inherited disorder of copper metabolism. The mutations in the ATP7B gene on chromosome 13 leads to the functional defect of ATP7B, which produces pathological deposits of copper in liver, brain, cornea and kidney, with diverse clinical manifestations in various forms of liver disease, nervous system disease and corneal disease (Kayser-Fleischer rings). Early diagnosis and proper treatment can improve the prognosis of hepatolenticular degeneration. Conversely, it may progress to end-stage liver disease or severe motor dysfunction, which seriously affects patient quality of life.肝豆状核变性是常染色体隐性遗传的铜代谢障碍性疾病，由于13号染色体上ATP7B基因突变，导致其编码产物ATP7B的功能缺陷，引起铜在肝脏、脑、角膜、肾脏等病理性沉积，临床表现多样，最常见为肝病、神经系统疾病、角膜色素环。早期诊断及正确治疗可以改善肝豆状核变性预后，反之则可进展至终末期肝病或严重运动功能障碍，严重影响患者生存质量。.

Gastroesophageal variceal bleeding is one of the major complications of cirrhosis and also the leading causes of death in patients with decompensated cirrhosis. Terlipressin is a triglycyl-lysine vasopressin, a synthetic vasopressin analogue that is mainly used for the treatment of acute variceal hemorrhage. This article aims to review the current status of treatment of gastroesophageal variceal bleeding with terlipressin from the perspective of evidence-based medicine.食管胃静脉曲张出血是肝硬化的主要并发症之一，也是肝硬化失代偿期患者的主要死亡原因之一。特利加压素系三甘氨酰-赖氨酸血管加压素，是一种人工合成的血管加压素类似物，主要用于治疗急性静脉曲张破裂出血。现从循证医学角度回顾特利加压素治疗食管胃静脉曲张出血的当前现状。.

Primary biliary cholangitis (PBC) is a chronic cholestatic disease with unknown pathogenesis. Positive anti-mitochondrial antibody has high sensitivity and specificity in the diagnosis of this disease. Ursodeoxycholic acid is mainly used for the treatment of PBC, but 40% of patients have an unsatisfactory biochemical response to this drug. 6-Ethylchenodeoxycholic acid is a new drug approved for the treatment of PBC, and liver transplantation remains the only effective method for the treatment of patients with end-stage PBC.原发性胆汁性胆管炎（PBC）是一种慢性胆汁淤积性疾病。其发病机制尚不完全清楚。抗线粒体抗体阳性对诊断具有很高的敏感性和特异性。熊去氧胆酸是治疗PBC最主要的药物，但是大约40%的患者对熊去氧胆酸生物化学应答欠佳。奥贝胆酸是最新批准的用于PBC治疗的药物，肝移植是疾病终末阶段唯一有效的治疗手段。.

Hepatitis B core antibody (anti-HBc) targets viral core protein and is produced in patients with hepatitis B virus (HBV) infection, and seroconversion occurs in the early stage of infection and often lasts for a lifetime. Qualitative detection of anti-HBc has been used in clinical practice for many years, while the clinical significance of its quantitative level remains unclear. A novel anti-HBc immunoassay based on double-antigen sandwich ELISA has been developed in recent years and lays a foundation for illustrating the change in the quantitative level of anti-HBc (qAnti-HBc) in HBV infection and its clinical significance. Several recent studies have revealed that qAnti-HBc is associated with the degree of hepatitis activity and response to pharmacotherapy and may become an important basis for selecting antiviral drugs, optimizing therapeutic regimen, and predicting treatment outcome.乙型肝炎病毒核心抗体（抗-HBc）是乙型肝炎病毒（HBV）感染者产生的针对病毒核心蛋白的抗体，在感染早期即发生阳转，且常持续存在终生。抗-HBc的定性检测已在临床实践中应用多年，但其定量水平的临床意义尚不十分清楚。近年发展起来的基于双抗原夹心法的抗-HBc检测技术，为阐释抗-HBc定量水平（qAnti-HBc）在HBV感染中的变化规律及其临床意义奠定了基础。近年多项研究表明，qAnti-HBc与肝炎活动程度及药物治疗应答高度相关，有望成为抗病毒治疗药物选择、方案优化及疗效预测的重要依据。.

Portal hypertension is one of the main performance of liver cirrhosis, in addition to anatomical factors, hyperdynamic circulatory status caused by abnormal splanchnic vascular tension is also very important in this procession. We summarised the mechanism and treatment strategies of hyperdynamic circulation in cirrhosis, so as to provide some recommendation for clinical practice.门静脉高压是肝硬化的主要表现之一，在其形成过程中，除解剖因素外，内脏血管床张力异常引起的高动力循环状态也起到重要作用。现就肝硬化时高动力循环的发生机制及其治疗策略进行总结，以期为临床治疗提供参考。.

Tenofovir disoproxil fumarate (TDF) has demonstrated long-term efficacy and a high barrier to resistance in multiple chronic hepatitis B (CHB) populations outside of China. This study aimed to evaluate the efficacy and safety of TDF compared with adefovir dipivoxil (ADV) in Chinese patients with CHB during 48 weeks of treatment (ClinicalTrial.gov number, NCT01300234). A Phase 3, multicentred, randomized, double-blind, controlled trial compared the efficacy and safety of TDF with ADV in Chinese patients with CHB. The primary endpoint was the proportion of patients with HBV DNA400 copies/mL in each treatment group at Week 48, using an unpooled Z-test for superiority. Secondary endpoints included viral suppression, serologic response, histological improvement, normalization of alanine aminotransferase (ALT) levels and the emergence of resistance mutations. A total of 509 patients, 202 hepatitis B e antigen (HBeAg)-positive and 307 HBeAg-negative, with HBV DNA ≥10(5) copies/mL received either TDF 300 mg od or ADV 10 mg od. At Week 48, TDF demonstrated superior viral suppression compared with ADV in both HBeAg-positive (76.7% vs 18.2%, P0.0001) and HBeAg-negative (96.8% vs 71.2%, P0.0001) patients. The majority of patients in both treatment arms achieved ALT normalization (85%). No resistance to TDF was observed. The frequency of adverse events was comparable between treatment arms (TDF 3.9% vs ADV 4.8%). In this double-blind, randomized, clinical trial, TDF demonstrated superiority over ADV with respect to viral suppression in Chinese patients with CHB at 48 weeks of treatment and without the development of resistance.

Immunoglobulin G4 (IgG4)-associated autoimmune hepatitis (AIH) was recognized as a new disease entity; however, IgG4-associated de novo AIH after the liver transplantation had not been reported yet. Herein we have described a 56-year-old man who developed IgG4 de novo AIH as 1 year-post liver transplantation after receiving pegylated interferon alpha-2a and ribavirin therapy for hepatitis C virus recurrence. The histopathologic evidence showed an aggressive lymphoplasmacytic interface hepatitis with centrilobular necrosis (plasma cells > 30%) and IgG4-positive plasma cells (>10 per high power field). Serum IgG (9220 mg/dL) and IgG4 (3289 mg/dL) were also elevated. Improvement of liver function tests (LFTs) by prednisone and azathioprine therapy are manifested as normalized alanine aminotransferase and IgG levels. IgG4 relates to more severe histological activity; however, it is believed to be a good prognostic predictor of a response to prednisone plus azathioprine therapy especially with early diagnosis and timely management.

Previous studies suggested that a finite course of peginterferon alfa-2a may offer an alternative rescue therapy for patients with lamivudine resistance. However, because of the limitation of study design and small sample size, it is difficult to make definitive conclusion.To explore the role of peginterferon alfa-2a, in the rescue treatment of HBeAg-positive chronic hepatitis B patients with lamivudine resistance.In this randomised study, chronic hepatitis B patients with lamivudine resistance were treated with peginterferon alfa-2a for 48 weeks (n=155) or adefovir for 72 weeks (n=80). All enrolled patients were treated with lamivudine for the first 12weeks.At 6 months posttreatment, 14.6% (18/123) of peginterferon alfa-2a-treated patients achieved HBeAg seroconversion, in contrast to 3.8% (3/80) of adefovir-treated patients after 72 weeks continuous therapy (P=0.01). For peginterferon alfa-2a-treated patients, the rate of HBeAg seroconversion at week 72 was significantly higher in patients who had HBsAg decline0.5 Log(10) IU/mL from baseline at week 24, compared with patients with HBsAg decline ≤0.5 Log(10) IU/mL from baseline at week 24 (25.5% vs. 7.7%, P=0.01). After 72 weeks continuous adefovir treatment, 22.5% of patients achieved HBV DNA80 IU/mL, compared with 10.6% in peginterferon alfa-2a-treated patients at 6months off-treatment (P=0.02).Overall, the response to peginterferon alfa-2a among patients with lamivudine resistance was suboptimal. HBeAg seroconversion rate at week 72 by 48 weeks peginterferon alfa-2a treatment was higher than continuous adefovir therapy. Monitoring HBsAg levels can help to predict response to peginterferon alfa-2a.

A variety of adverse stimuli, such as hepatotoxins, hepatotropic viruses, immune reactions to the liver, metabolic diseases, and biliary stasis can trigger liver fibrogenesis, i.e., the excess synthesis and deposition of extracellular matrix (ECM). Whereas in acute liver diseases, such as self-limited viral hepatitis, fibrogenesis is balanced by fibrolysis, i. e., the removal of excess ECM, repeated insults of sufficient severity, as occur in many chronic liver diseases, tilt the balance in favor of fibrogenesis, finally resulting in morphologically apparent fibrosis or cirrhosis. In fibrogenesis, damage to the hepatocyte or the bile duct epithelium leads to mononuclear cell activation, release of fibrogenic factors and activation of mesenchymal cells. It is the activated Kupffer cell, the macrophage and the proliferating bile duct epithelium that are thought to be the primary sources of the potentially fibrogenic cytokines and growth factors [1, 16–18, 26, 30, 33, 34, 37, 39] that finally target the hepatic stellate cell (HSC, the novel denomination for the perisinusoidal lipocyte or Ito cell) and the portal fibroblast (PF), those cell types that are responsible for excess ECM deposition in the liver [15, 17, 18, 22, 35, 36, 42, 46, 68].