第12次全国病毒性肝炎与肝病学术会议征文通知

病毒性肝炎和肝病是严重危害我国人民身体健康的一类常见疾病。近年来，病毒性肝炎的发病率虽有下降趋势，但许多基础和临床问题有待进一步阐明；酒精性肝病和脂肪性肝病等的发病率仍在明显上升；肝纤维化、肝硬化和原发性肝癌等的发病率未得到有效控制；各型病毒性肝炎及肝病的诊断和防治手段有重大进展，终末期肝病的诊治及肝脏移植技术不断成熟，对自身免疫性肝病认识水平不断提高。因此，为了促进学术交流，帮助广大肝病工作者全面了解我国肝病基础和临床研究进展，不断提高病毒性肝     

疑难性肝病诊断的思考

在我国,各型嗜肝病毒所致的急慢性肝炎、肝硬化无疑是最常见的肝病.近年来,随着肝炎病毒预防性疫苗接种的深入普及,病毒性肝炎的发病率呈明显下降趋势;而非感染性肝病如脂肪肝、药物性肝病等正随着社会、自然等因素的变化而逐渐增多.医学科学的飞速发展,虽极大地提高了我们对肝病的诊断和治疗水平,但仍有约10%的疑难性肝病经过各种常规检查仍无法明确诊断.笔者在多年的临床实践中,深深体会到疑难性肝病诊断的艰难,现将其中的体会作一总结,与大家共享.     

与免疫缺陷病感染有关的肝病及处理

经人类免疫缺陷病毒 (ＨＩＶ)感染的患者 ,肝病的发生率较高。据报道 ,在艾滋病 (ＡＩＤＳ)中 ,90 %以上患者有肝功能酶学异常 ,70 %左右伴有肝脏肿大 ,ＨＩＶ感染对肝脏的损害主要是ＨＩＶ对ＣＤ4 +细胞的侵入 ,使ＴＨ细胞数量及功能下降 ,导致细胞免疫功能紊乱所致 ,因而与免疫有关的肝病 ,如病毒性肝炎 ,机会性感染及肿瘤等会乘虚而入 ,并且与ＨＩＶ相互作用 ,使发病过程更加复杂化[1] 。鉴于ＨＩＶ感染在我国呈逐年上升趋势 ,加上我国医务工作者对ＨＩＶ感染有关的肝病诊治经验不多 ,因此有必要对其进行系统认识。为此 ,本文结合有关文…     

近10年肝病住院患者疾病变化趋势分析

目的探讨感染科肝病组住院患者疾病谱的变化,为肝病管理提供循证依据。方法收集2005年1月至2014年12月感染病科收治的所有住院病患,记录患者的性别、年龄、第一出院诊断、治疗转归等。分析近10年来肝病构成比的变化。结果肝病占住院病例的比例逐年下降,最高为2005年59.65%,最低为2013年35.91%,这种分布从2010年起有统计学意义。慢性乙型肝炎仍然是肝病组最主要的住院原因。历年肝病构成比变化差异无统计学意义。急性肝炎最常见的病因为急性甲型肝炎,急性乙型肝炎,急性戊型肝炎,胆源性肝损伤,药物性肝损伤。胆源性肝损伤和药物性肝损伤占急性肝炎的比例有上升趋势:2005年胆源性肝损伤占急性肝病的比例为8.70%,2010年为32.43%,2014年为33.92%;药物性肝损伤占急性肝病比率这3年分别是:13.77%、21.062%和40.35%。慢性乙型肝炎占慢性肝炎的比例历年分布差异无统计学意义。肝病患者的好转率和病死率历年无显著性差异。结论慢性乙型肝炎的构成比有减少趋势,非传染性肝病的构成有上升趋势。从管理层面,肝病的防治涉及到多学科的交叉合作。     

甲胎蛋白检测对肝病患者的临床意义

目的监测肝病患者甲胎蛋白(AFP)变化,判断预后及早期发现癌变。方法随机选择144例慢性肝病患者,按诊断标准分型,观察各型肝病患者的AFP水平、AFP与谷丙转氨酶活力的关系和与肝癌的关系。结果病毒性肝炎、肝硬化患者的AFP含量有不同程度的增高,随着病情好转逐渐下降;肝癌患者的甲胎蛋白含量持续成高滴度,有77%的患者AFP>500μg/L。结论慢性肝病患者发生肝细胞癌的比例(6.9%)明显高于其他正常人群,肝细胞再生、更新、增生被认为是癌变的动因。AFP高滴度患者,肝细胞癌的发生率明显高于AFP低滴度患者。     

老年病毒性肝炎临床特点及防治措施

目的探讨老年病毒性肝炎的临床特点、流行病学和相关的防治方法。方法收集2011年1月至2016年12月在东南大学附属中大医院接受治疗的531例老年肝病患者的资料,应用统计学分析相关趋势。选取其中100例老年病毒性肝炎患者,随机平均分为观察组和对照组,进行全面干预比较分析。结果老年肝病患者整体数量逐年升高,以病毒性肝炎为主,男性患者多于女性(P<0.05)。老年病毒性肝炎的主要病因有乙型肝炎病毒、丙型肝炎病毒及戊型肝炎病毒,分别占老年病毒性肝炎的64.84%、13.28%、16.15%;老年肝病中肝衰竭的发生率(11.68%)也较高,主要以慢性肝衰竭为主,病情好转率低,病死率69.35%。经全面干预治疗后观察组患者谷氨酸氨基转移酶(ALT)水平显著低于对照组(P<0.05),观察组治疗有效率显著高于对照组(P<0.05)。结论老年肝病仍以病毒性肝炎为主,而主要病毒性肝炎类型中乙型和戊型的发病率呈逐年上升趋势。乙型病毒性肝炎还是导致老年肝衰竭、肝病死亡率高的主要原因。对老年病毒性肝炎患者进行全面干预可有效提高治疗效果。     

肝病患者血清肉碱水平的临床研究

目的观察肝病患者血清肉碱水平,探讨其临床意义,为肉碱治疗肝病提供依据。方法用酶循环法检测25例急性病毒性肝炎,34例慢性病毒性肝炎,22例肾功能正常及9例肾功能异常的肝炎后肝硬化患者血清游离肉碱水平,并分别与40名正常人的检测值比较。结果血清游离肉碱:正常人为(48．3±10．2)μmol／L;急性病毒性肝炎患者为(35．2±13．2)μmol／L,明显低于正常对照组,P=0．000。慢性病毒性肝炎患者为(36．5±9．9) μmol／L,明显低于正常对照组,P=0．000。肾功能正常的肝炎后肝硬化患者为(45．0±11．0)μmol／L,比正常对照组略有下降,但差异无统计学意义,P=0．232。肾功能异常的肝炎后肝硬化患者为(83．6±50.4)μmol／L,比正常对照组升高,但差异无统计学意义,P=0．069。结论肝病患者可发生肉碱代谢异常,肝脏疾病是导致继发性肉碱缺乏的原因之一。     

细胞间粘附分子-1在肝病中的表达

细胞间粘附分子-1(ICAM-1)在炎症细胞因子刺激下,在病毒性肝炎、酒精性肝病、肝细胞癌(HCC)和自身免疫性肝病中表达水平明显增高,其表达程度与炎症程度呈正相关,与肝组织病变及病变组织学分级均有关;ICAM-1表达水平的高低可能影响干扰素对慢性病毒性肝炎的治疗;ICAM-1表达与肿瘤的大小、进展、转移也有关,并随病情的缓解而下降。促进ICAM-1表达的细胞因子有IFN-γ、TNF-α、IL-1和HBV X蛋白。     

酒精性肝病患者肝功能评估方法

酒精性肝病的发病率和死亡率在我国呈迅速增长的趋势,成为仅次于病毒性肝炎的第二大肝病。真实、客观地判断酒精性肝病的病情,能为临床医生选择个体化治疗方案及判断预后提供有力的依据。本文介绍了酒精性肝病的各种评估方法。     

住院的酒精性肝病患者临床疾病特点分析

目的：分析住院的酒精性肝病患者临床疾病的特点。方法对近10年收治的4379例各种酒精性肝病患者的疾病构成情况进行分析。结果2002年住院的酒精性肝病患者占住院的肝病患者的比例为1.74%,2006年为2.89%,2011年为4.18%,10年间上升了2.4倍;在酒精性肝病患者中,男性占97.69%（4278/4379）;酒精性肝硬化、酒精性肝病（未分类）、轻症酒精性肝炎为3种最常见的病种,分别占70.66%、10.44%和9.96%,而重症酒精性肝炎、酒精性肝衰竭和酒精性脂肪肝占比为4%左右;酒精性肝硬化患者平均年龄为49.6岁,而酒精性肝病重叠非酒精性脂肪性肝病患者平均年龄为36.9岁,两者差异有统计学意义（P＆lt;0.01）;轻症酒精性肝炎和酒精性脂肪肝治愈率分别为80.28%和91.58%,而重症酒精性肝炎为47.78%,差异有统计学意义（P＆lt;0.01）。结论住院的酒精性肝病患者占住院肝病患者的比例在不断上升,须重视对男性人群和疾病的早期干预。     

Autoimmune liver diseases in systemic rheumatic diseases

Systemic rheumatic diseases (SRDs) are chronic, inflammatory, autoimmune disorders with the presence of autoantibodies that may affect any organ or system. Liver dysfunction in SRDs can be associated with prescribed drugs, viral hepatitis, alternative hepatic comorbidities and coexisting autoimmune liver diseases (AILDs), requiring an exclusion of secondary conditions before considering liver involvement. The patterns of overlap diseases depend predominantly on genetic determinants with common susceptible loci widely distributing in both disorders. In AILDs, it is important to identify the overlapping SRDs at an early stage since such a coexistence may influence the disease course and prognosis. Commonly co-occurring SRDs in AILDs are Sjögren syndrome (SS), rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE) in autoimmune hepatitis (AIH), and SS, RA or systemic sclerosis in primary biliary cholangitis. Owing to different disease complications and therapies, it is imperative to differentiate between SLE liver involvement and SLE-AIH overlap disease. Therapeutic options can be personalized to control coexisting conditions of liver autoimmunity and rheumatic manifestations in AILD-SRD overlap diseases. The collaboration between hepatologists and rheumatologists can lead to significant advances in managing such a complex scenario. In this review, we provide a comprehensive overview on coexisting AILDs in different SRDs and the therapeutic approach in managing these overlap diseases.     

Autophagy in liver diseases

Autophagy is the liver cell energy recycling system regulating a variety of homeostatic mechanisms.Damaged organelles,lipids and proteins are degraded in the lysosomes and their elements are re-used by the cell.Investigations on autophagy have led to the award of two Nobel Prizes and a health of important reports.In this review we describe the fundamental functions of autophagy in the liver including new data on the regulation of autophagy.Moreover we emphasize the fact that autophagy acts like a two edge sword in many occasions with the most prominent paradigm being its involvement in the initiation and progress of hepatocellular carcinoma.We also focused to the implication of autophagy and its specialized forms of lipophagy and mitophagy in the pathogenesis of various liver diseases.We analyzed autophagy not only in well studied diseases,like alcoholic and nonalcoholic fatty liver and liver fibrosis but also in viral hepatitis,biliary diseases,autoimmune hepatitis and rare diseases including inherited metabolic diseases and also acetaminophene hepatotoxicity.We also stressed the different consequences that activation or impairment of autophagy may have in hepatocytes as opposed to Kupffer cells,sinusoidal endothelial cells or hepatic stellate cells.Finally,we analyzed the limited clinical data compared to the extensive experimental evidence and the possible future therapeutic interventions based on autophagy manipulation.     

Orosomucoid in liver diseases

In this editorial, the roles of orosomucoid (ORM) in the diagnoses and follow-up assessments of both nonneoplastic diseases and liver tumors are discussed with respect to the publication by Zhu et al presented in the previous issue of World Journal of Gastroenterology (2020; 26(8): 840-817). ORM, or alpha-1 acid glycoprotein (AGP), is an acute-phase protein that constitutes 1% to 3% of plasma proteins in humans and is mainly synthesized in the liver. ORM exists in serum as two variants: ORM1 and ORM2. Although the variants share 89.6% sequence identity and have similar biological properties, ORM1 constitutes the main component of serum ORM. An interesting feature of ORM is that its biological effects differ according to variations in glycosylation patterns. This variable feature makes ORM an attractive target for diagnosing and monitoring many diseases, including those of the liver. Recent findings suggest that a sharp decrease in ORM level is an important marker for HBV-associated acute liver failure (ALF), and ORM1 plays an important role in liver regeneration. In viral hepatitis, increases in both ORM and its fucosylated forms and the correlation of these increases with fibrosis progression suggest that this glycoprotein can be used with other markers as a noninvasive method in the follow-up assessment of diseases. In addition, similar findings regarding the level of the asialylated form of ORM, called asialo-AGP (AsAGP), have been reported in a follow-up assessment of fibrosis in chronic liver disease. An increase in ORM in serum has also been shown to improve hepatocellular carcinoma (HCC) diagnosis performance when combined with other markers. In addition, determination of the ORM level has been useful in the diagnosis of HCC with AFP concentrations less than 500 ng/mL. For monitoring patients with AFP-negative HCC, a unique trifucosylated tetra-antennary glycan of ORM may also be used as a new potential marker. The fact that there are very few studies investigating the expression of this glycoprotein and its variants in liver tissues constitutes a potential limitation, especially in terms of revealing all the effects of ORM on carcinogenesis and tumor behavior. Current findings indicate that ORM2 expression is decreased in tumors, and this is related to the aggressive course of the disease. Parallel to this finding, in HCC cell lines, ORM2 decreases HCC cell migration and invasion, supporting reports of its tumor suppressor role. In conclusion, the levels of ORM and its different glycosylated variants are promising additional biomarkers for identifying ALF, for monitoring fibrosis in viral hepatitis, and for diagnosing early HCC. Although there is evidence that the loss of ORM2 expression in HCC is associated with poor prognosis, further studies are needed to support these findings. Additionally, investigations of ORM expression in borderline dysplastic nodules and hepatocellular adenomas, which pose diagnostic problems in the differential diagnosis of HCC, especially in biopsy samples, may shed light on whether ORM can be used in histopathological differential diagnosis.     

Genetics in liver diseases

In recent years, few fields in medicine have witnessed discoveries as momentous as those pertaining to the liver. Dramatic advances have been made, particularly in the areas of molecular biology and genetics. A joint EASL/AASLD Monothematic Conference was held on June 23rd-24th, 2006, in Modena, Italy, to bring the latest breakthroughs in different fields of genetics to hepatologists. This article reports the highlights of the conference and summarizes the main conclusions and implications for clinical and experimental hepatology.     

Inflammasomes in liver diseases

Inflammation is a common element in the pathogenesis of most chronic liver diseases that lead to fibrosis and cirrhosis. Inflammation is characterized by activation of innate immune cells and production of pro-inflammatory cytokines IL-1α, IL-1β, and TNFα. Inflammasomes are intracellular multiprotein complexes expressed in both parenchymal and non-parenchymal cells of the liver that in response to cellular danger signals activate caspase-1, and release IL-1β and IL-18. The importance of inflammasome activation in various forms of liver diseases in relation to liver damage, steatosis, inflammation and fibrosis is discussed in this review.