Hepatic Decompensation After Gastric Bypass Surgery

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胆舒胶囊治疗慢性胆囊炎和胆结石的临床效果及安全性

*+,胆舒胶囊治疗慢性胆囊炎和胆结石的临床效果及安全性彭雪莲，徐小青，曹　勤上海市普陀区中心医院消化内科，上海２０００６２摘要：目的　通过一项大样本、多中心、开放性真实世界研究，全面评价胆舒胶囊治疗慢性胆囊炎、胆囊结石的疗效和安全性。

方法　选取２０１７年１月—２０１９年１２月全国３２９家医院的慢性胆囊炎、胆结石患者９５７９例，分为胆结石组（ｎ＝１１４８）、慢性胆囊炎组（ｎ＝５３６０）和慢性胆囊炎伴胆结石组（ｎ＝３０７１）。

所有患者均服用胆舒胶囊，３次／ｄ，１～２粒／次，饭后口服，持续治疗４周。

记录服药前及治疗结束时的腹痛特征、胆源性消化不良症状、中医证候以及胆囊影像学指标，以评价治疗前后用药效果；观察并记录药物不良反应以评价药物安全性。

非正态分布的计量资料治疗前后指标变化比较采用Ｗｉｌｃｏｘｏｎ符号秩和检验，组间比较采用Ｗｉｌｃｏｘｏｎ秩和检验方法。

计数资料治疗前后指标变化比较采用配对χ２检验，多组间比较采用Ｋｒｕｓｋａｌ－ＷａｌｌｉｓＨ法，进一步两两比较采用Ｌｏｇｉｓｔｉｃ回归分析和Ｎｅｍｅｎｙｉ检验。

结果　经胆舒胶囊干预后，所有患者脂餐诱发疼痛总发生率较治疗前明显下降（χ２＝３２．４２２，Ｐ＜０．００１）；疼痛发作频率、疼痛持续时间、疼痛程度评分均明显低于治疗前（Ｚ值分别为－１．９８５、－２．８８７、－３．１７８，Ｐ值均＜００５）；腹胀、饱胀、嗳气、恶心症状评分较治疗前均明显下降（Ｐ值均＜０．００１），胆源性消化不良症状总分明显下降（Ｚ＝－４．１２８，Ｐ＜０．００１）；右上腹痛、口苦、泛酸、胸闷不舒、脘腹胀闷、食少纳呆、肢体困重等中医证候评分均较治疗前明显下降（Ｐ值均＜０．０５），中医证候评分总分明显下降（Ｚ＝３．８６０，Ｐ＜０．００１）。

亚组分析结果显示，胆结石组、慢性胆囊炎组、慢性胆囊炎伴胆结石组疼痛程度、频率、持续时间，以及胆源性消化不良和中医证候评分较治疗前均明显下降（Ｐ值均＜０．０５），治疗后脂餐诱发疼痛的患者占比均明显减少（Ｐ值均＜０．００１）。

乙型肝炎相关慢加急性肝衰竭患者的长期预后及生存质量

乙型肝炎相关慢加急性肝衰竭患者的长期预后及生存质量诸聪妍;卢观婷;祁婷婷;何钦俊;陈永鹏;文维群;周福元;陈金军【摘要】目的探讨乙型肝炎相关慢加急性肝衰竭(HBV-ACLF)存活者长期预后及健康相关的生存质量.方法选取2011年11月～2016年10月在南方医科大学南方医院收治的存活时间超过90d的HBV-ACLF患者,回顾性分析其临床资料,进行随访,记录肝硬化发展、肝硬化失代偿、肝癌发生及死亡等不良事件的发生;并选择同期门诊就诊的慢性乙型肝炎、乙肝肝硬化患者作为对照组,应用SF-36量表对ACLF存活者与常模及对照组的生活质量评分进行比较.结果共入组ACLF患者223例,根据入院时是否合并肝硬化分为乙型肝炎组(CHB-ACLF,n=130)和乙肝肝硬化组(CIR-ACLF,n=93).CHB-ACLF组12个月、24个月、50个月的累计生存率为97％、95.7％和93.9％,高于CIR-ACLF组的91％、86％和74％(P=0.007).CHB-ACLF存活者12个月、24个月、36个月的肝硬化进展率分别是37.9％、58.4％和68.7％.Cox回归结果发现,患者入院时钠水平(HR=0.84,P=0.035)、发病28 d内肌酐最高值(HR=1.015,P=0.026)及INR最高值(HR=2.032,P=0.006)是影响肝硬化发生的独立危险因素.ACLF恢复者SF-36量表的心理健康评分低于常模,其他维度与常模相比无统计学差异;与慢性乙型肝炎、乙肝肝硬化患者相比,ACLF患者在一般健康和躯体疼痛维度得分更高,其余维度差异无统计学意义.结论乙型肝炎疾病基础不同可导致ACLF患者长期预后有所差别.严重的急性打击事件可增加CHB-ACLF患者肝硬化的发生率,可能与肝衰竭时各器官的损害程度有关.ACLF长期存活患者生活、社会能力无显著降低,但心理状态受到一定影响.【期刊名称】《南方医科大学学报》【年(卷),期】2018(038)006【总页数】6页(P736-741)【关键词】乙型肝炎;慢加急性肝衰竭;长期预后;生存质量【作者】诸聪妍;卢观婷;祁婷婷;何钦俊;陈永鹏;文维群;周福元;陈金军【作者单位】南方医科大学南方医院肝病中心,广东广州510515;南方医科大学南方医院肝病中心,广东广州510515;南方医科大学南方医院肝病中心,广东广州510515;南方医科大学南方医院肝病中心,广东广州510515;南方医科大学南方医院肝病中心,广东广州510515;南方医科大学南方医院肝病中心,广东广州510515;南方医科大学南方医院肝病中心,广东广州510515;南方医科大学南方医院肝病中心,广东广州510515【正文语种】中文慢加急性肝衰竭（ACLF）是慢性肝病基础发生急性肝损伤驱动的全身多器官功能障碍。

Hepatitis B

Jaundice
Diagnosis and treatment of hepatitis B
Hepatitis B virus is how to spread?
Blood transmission Iatrogenic transmission
Mother to child transmi ssion
乙肝广泛流行于世界各国主要侵犯儿童及青壮年少数患者可转化为肝硬化或肝癌
Hepatitis B
What is hepatitis B ?
Hepatitis B is caused by hepatitis B virus (HBV).It's a disease which can lead to multiple organ damage.As we all know that hepatitis B is widely popular in the world, mainly affecting children and young adults and a few patients can be transformed into liver cirrhosis（肝硬化） or liver cancer.Therefore, it has become the threat to human health especially in China. Hepatitis B virus has no epidemic period（流行阶段）,that is to say,it happens all year around,but mostly is sporadic（不定时发生的）. The incidence of hepatitis B was significantly increased in recent years.

拉米夫定与阿德福韦酯初始联合治疗慢乙肝失代偿肝硬化46例临床观察

拉米夫定与阿德福韦酯初始联合治疗慢乙肝失代偿肝硬化46例临床观察【摘要】目的通过观察拉米夫定与阿德福韦酯初始治疗慢乙肝失代偿肝硬化的效果，为临床合理用药提供参考。

方法收集46例临床资料进行回顾分析。

结果拉米夫定与阿德福韦酯联合治疗慢乙肝失代偿肝硬化12个月和24个月时患者hbv-dna的下降值要远远大于单用拉米夫定治疗。

结论拉米夫定与阿德福韦酯初始治疗慢乙肝失代偿肝硬化要比单用拉米夫定治疗效果好。

【关键词】拉米夫定与阿德福韦酯；慢性乙型肝炎；失代偿肝硬化阿德福韦酯问世后，拉米夫定与阿德福韦酯初始联合治疗乙肝失代偿肝硬化，通过实验研究和众多循证医学数字显示，经过以上治疗使慢乙肝肝硬化失代偿患者能更好的获得病毒学应答，极大地减少了耐药变异率的发生，使肝功能和child-pugh评分得到显著改善，从而降低了慢乙肝肝硬化失代偿患者的病死率，使乙肝失代偿肝硬化的抗病毒治疗取得了满意的治疗效果[1]。

现报告如下。

1 资料与方法1. 1 一般资料对92例慢乙肝失代偿肝硬化患者随机分拉米夫定单药治疗组（46例）和拉米夫定加阿德福韦酯联合治疗组（46例）进行临床治疗观察，男30例，女16例，年龄42～69岁，所有患者均作腹部b超及经临床诊断为慢乙肝失代偿肝硬化患者。

1. 2 治疗方法对46例慢乙肝失代偿肝硬化患者拉米夫定及阿德福韦酯治疗12个月和治疗24个月，与对照组拉米夫定治疗12个月和24个月进行观察。

1. 3 观察方法包括年龄、性别、肝功能、血清、hbv-dna水平和child-pugh评分，对hbv多聚酶基因给予测序以检测拉米夫定耐药变异在治疗期间检测所有患者临床表现和实验室检查。

2 结果2. 1 治疗效果拉米夫定治疗12个月和治疗24个月后分别有37.0%（11/30）和53.8%（25/46）的患者达到hbv-dna低于检测下线（<1000 copies/ml），而拉米夫定与阿德福韦酯联合治疗组（46例）则分别为41.2% （19/46）和76.67% （33/46）。

慢加急性肝衰竭

GUIDELINESAcute-on-chronic liver failure:consensus recommendationsof the Asian Paciﬁc Association for the Study of the Liver (APASL)2014Shiv Kumar Sarin•Chandan Kumar Kedarisetty•Zaigham Abbas•Deepak Amarapurkar•Chhagan Bihari•Albert C.Chan•Yogesh Kumar Chawla•A.Kadir Dokmeci•Hitendra Garg•Hasmik Ghazinyan•Saeed Hamid•Dong Joon Kim•Piyawat Komolmit•Suman Lata•Guan Huei Lee•Laurentius A.Lesmana•Mamun Mahtab•Rakhi Maiwall•Richard Moreau•Qin Ning•Viniyendra Pamecha•Diana Alcantara Payawal•Archana Rastogi•Salimur Rahman•Mohamed Rela•Anoop Saraya•Didier Samuel•Vivek Saraswat•Samir Shah•Gamal Shiha•Brajesh Chander Sharma•Manoj Kumar Sharma•Kapil Sharma•Amna Subhan Butt•Soek Siam Tan•Chitranshu Vashishtha•Zeeshan Ahmed Wani•Man-Fung Yuen•Osamu Yokosuka•the APASL ACLF Working PartyReceived:4April2014/Accepted:25August2014/Published online:26September2014ÓAsian Paciﬁc Association for the Study of the Liver2014Abstract Theﬁrst consensus report of the working party of the Asian Paciﬁc Association for the Study of the Liver (APASL)set up in2004on acute-on-chronic liver failure (ACLF)was published in2009.Due to the rapid advancements in the knowledge and available information, a consortium of members from countries across Asia Paciﬁc,‘‘APASL ACLF Research Consortium(AARC),’’was formed in2012.A large cohort of retrospective and prospective data of ACLF patients was collated and fol-lowed up in this data base.The current ACLF deﬁnition was reassessed based on the new AARC data base.These initiatives were concluded on a2-day meeting in February 2014at New Delhi and led to the development of theﬁnal AARC consensus.Only those statements which were based on the evidence and were unanimously recommended were accepted.These statements were circulated again to all the experts and subsequently presented at the annual confer-ence of the APASL at Brisbane,on March14,2014.The suggestions from the delegates were analyzed by the expert panel,and the modiﬁcations in the consensus were made. Theﬁnal consensus and guidelines document was pre-pared.After detailed deliberations and data analysis,theS.K.Sarin(&)ÁC.K.KedarisettyÁH.GargÁR.MaiwallÁM.K.SharmaÁK.SharmaÁC.VashishthaÁZ.A.Wani Department of Hepatology,Institute of Liver and Biliary Sciences,New Delhi110070,Indiae-mail:shivsarin@Z.AbbasDepartment of Hepatogastroenterology,Sindh Institute of Urology and Transplantation,Karachi,PakistanD.AmarapurkarDepartment of Gastroenterology and Hepatology,Bombay Hospital and Medical Research,Mumbai,IndiaC.BihariÁA.RastogiDepartment of Pathology,Institute of Liver and Biliary Sciences, New Delhi110070,IndiaA.C.ChanDivision of Hepatobiliary and Pancreatic Surgery,and Liver Transplantation,Department of Surgery,The University of Hong Kong,Hong Kong,China Y.K.ChawlaDepartment of Hepatology,Post Graduate Institute of Medical Education and Research,Chandigarh,IndiaA.K.DokmeciDepartment of Gastroenterology,Ankara University School of Medicine,Ankara,TurkeyH.GhazinyanDepartment of Hepatology,Nork Clinical Hospital of Infectious Diseases,Yerevan,ArmeniaS.HamidÁA.S.ButtDepartment of Medicine,Aga Khan University Hospital, Karachi,PakistanD.J.KimCenter for Liver and Digestive Diseases,Hallym University Chuncheon Sacred Heart Hospital,Chuncheon,Gangwon-Do, Republic of KoreaHepatol Int(2014)8:453–471 DOI10.1007/s12072-014-9580-2original proposed deﬁnition was found to withstand the test of time and identify a homogenous group of patients pre-senting with liver failure.Based on the AARC data,liver failure grading,and its impact on the‘‘Golden therapeutic Window,’’extra-hepatic organ failure and development of sepsis were analyzed.New management options including the algorithms for the management of coagulation disor-ders,renal replacement therapy,sepsis,variceal bleed, antivirals,and criteria for liver transplantation for ACLF patients were proposed.Theﬁnal consensus statements along with the relevant background information are pre-sented here.Keywords Liver failureÁChronic liver diseaseÁCirrhosisÁAscitesÁAcute liver failure and Scute liver failureIntroductionLiver failure is a common medical ailment,and its inci-dence is increasing with the use of alcohol and growing epidemic of obesity and diabetes.It can present as acute liver failure(ALF)(in the absence of any preexisting liver disease),acute-on-chronic liver failure(ACLF)(an acute deterioration of known or unknown chronic liver disease), or an acute decompensation of an end-stage liver disease. Each of these is a well-deﬁned disease entity with a homogenous population of patients with expected out-comes.Due to an overlap and lack of clarity of deﬁnitions and outcomes,entities like late-onset liver failure and subacute hepatic failure have become less relevant and are not often used.The growing interest in ACLF after theﬁrst consensus deﬁnition of ACLF from APASL[1]is evident by the fact that more than200publications as full paper have been published and the trend is surely increasing.A seminal paper from the EASL-CLIF consortium on the deﬁnition and out-come of ACLF has since appeared[2]based on the work of experts from several European and Western countries.The group of investigators working on liver failure in the Asia–Paciﬁc region working for the past decade carefully analyzed the patient characteristics,natural history,and outcome over the years.The group met on yearly basis and collated data on Web site(www.aclf.in)since2009.The data were analyzed at meeting in China and Dhaka in2012,with the setting up of the APASL ACLF Research Consortium(AARC).The ret-rospective and prospective data of patients from different centers were analyzed,and the completed patient records were utilized for deﬁning predictors of mortality and grades of liver failure and incidence of other organ failures.Experts from all over the globe,especially from the Asia–Paciﬁc region,and members of theﬁrst consensus group were requested to identify pertinent and contentious issues in ACLF.Six major contentious issues and unmet needs in the management of ACLF were approached for the update:(1)what constitutes an acute insult;(2)whether chronic liver disease should be included or only cirrhosis of the liver in deﬁning underlying liver disease;(3)the role of SIRS and sepsis as a cause or consequence of liver failure;(4)the incidence and impact of non-hepatic organ failures;(5)the relevance and grades of liver failure,the urgency, and outcome of liver transplant;and(6)an AARC pre-diction model of outcome of ACLF.The process for the development of the recommendations and guidelines included review of all available published literature onP.KomolmitDivision of Gastroenterology and Hepatology,Department of Medicine,Chulalongkorn University,Bangkok,ThailandtaDepartment of Nephrology,Institute of Liver and Biliary Sciences,New Delhi110070,IndiaG.H.LeeDepartment of Gastroenterology and Hepatology,National University Health System,Singapore,SingaporeL.A.LesmanaDivision of Hepatology,University of Indonesia,Jakarta, IndonesiaM.MahtabÁS.RahmanDepartment of Hepatology,Bangabandhu Sheikh Mujib Medical University,Dhaka,BangladeshR.MoreauInserm,U1149,Centre de recherche sur l’Inﬂammation(CRI), Paris,France R.MoreauUMR_S1149,Labex INFLAMEX,Universite´Paris Diderot Paris7,Paris,FranceR.MoreauDe´partement Hospitalo-Universitaire(DHU)UNITY,Service d’He´patologie,Hoˆpital Beaujon,APHP,Clichy,FranceQ.NingDepartment of Infectious Disease,Tongji Hospital of Tongji Medical College,Huazhong University of Science and Technology,Wuhan,ChinaV.PamechaDepartment of Hepatobiliary Surgery,Institute of Liver and Biliary Sciences,New Delhi110070,IndiaD.A.PayawalDepartment of Hepatology,Cardinal Santos Medical Center, Manila,PhilippinesACLF by individual and group of experts;preparation of a review manuscript and consensus statements based on Oxford system of evidence-based approach[3]for devel-oping the consensus statements,circulation of all consen-sus statements to all experts,an effort to deﬁne the acute hepatic insults;the underlying chronic liver disease,a survey of the current approaches for the diagnosis and management of ACLF;discussion on contentious issues; and deliberations to prepare the consensus statement by the experts of the working party.A2-day meeting was held on February22–23,2014,at New Delhi,India,to discuss and ﬁnalize the recommendations and guidelines.These state-ments were circulated to all the experts,posted on the AARC Web site(www.aclf.in),and subsequentlyﬁnalized. These consensus statements and guidelines for the man-agement of such patients are included in this review.A brief background is included providing the available data and published information on each issue.Statements from theﬁrst consensus have been reproduced at places to give a background and continuity.The concept of ACLF and need for a deﬁnitionAcute liver failure is a well-deﬁned medical emergency which is deﬁned as a severe liver injury,leading to coag-ulation abnormality usually with an INR C1.5,and any degree of mental alteration(encephalopathy)in a patient without pre-existing liver disease and with an illness of up to4weeks duration[4].A proportion of patients who present with features mimicking ALF,however,have an underlying chronic liver disease or cirrhosis of the liver. These patients grouped together as acute-on-chronic liver failure(ACLF)also have a poor outcome.These patients are distinctly different from a group of cirrhotic patients who are already decompensated and have a sudden worsening of their condition due to an acute event as liver failure is central.The ACLF is a clinical syndrome manifesting as acute and severe hepatic derangements resulting from varied insults.This term wasﬁrst used in1995to describe a condition in which two insults to liver are operating simultaneously,one of them being ongoing and chronic, and the other acute[5].Over the years,nearly thirteen different deﬁnitions have been proposed,creating confu-sion in theﬁeld[6].Any patient who has an underlying chronic liver disease with superimposed acute insult is being labeled as having ACLF,irrespective of evidence of liver failure per se or evidence of preexisting cirrhotic decompensation.Several investigators were concerned that this would lead to overlap with decompensated liver dis-ease.The main emphasis of the third consensus meeting of the APASL working party was to identify from this large group of patients,a subset of patients who have a relatively homogenous presentation and potentially similar outcome and restrict the use of the term‘‘acute-on-chronic liver failure’’to this subset.The2009APASL deﬁnition had provided a basis to select patients presenting with a distinct syndrome.To cover the entire spectrum of these patients, from mild to most severe,patients with chronic liver dis-ease with or without cirrhosis of the liver were included and carefully analyzed.It is understandable,though not well deﬁned,that the nature and degree acute insult and the status of the underlying chronic liver disease would determine the outcome of the patient(Fig.1).To give clarity to the primary event,a hepatic insult, jaundice and coagulopathy,which deﬁned liver failure was considered essential.In acute liver failure,though hepatic encephalopathy is part of the deﬁnition,it follows liver failure.Encephalopathy in the absence of overt jaundice or liver failure is separately categorized as due to by-pass[7]. Should one wait for deﬁning the outcome of‘‘liver failure’’M.RelaInstitute of Liver Diseases and Transplantation,Global Health City,Chennai,IndiaA.SarayaDepartment of Gastroenterology,All India Institute of Medical Sciences,New Delhi,IndiaD.SamuelINSERM,Centre He´patobiliarie,Hoˆpital Paul Brousse,Villejuif, FranceV.SaraswatDepartment of Gastroenterology,Sanjay Gandhi Post Graduate Institute of Medical Sciences,Lucknow,IndiaS.ShahDepartment of Gastroenterology and Hepatology,Global Hospitals,Mumbai,India G.ShihaDepartment of Internal Medicine,Egyptian Liver Research Institute and Hospital,Cairo,EgyptB.C.SharmaDepartment of Gastroenterology,GB Pant Hospital,New Delhi, IndiaS.S.TanDepartment of Gastroenterology and Hepatology,Selayang Hospital,Kepong,MalaysiaM.-F.YuenDepartment of Medicine,The University of Hong Kong, Hong Kong,ChinaO.YokosukaDepartment of Gastroenterology and Nephrology,Graduate School of Medicine,Chiba University,Chiba,Japantill the time extra-hepatic organ failures set in or not remain contentious.For deﬁnition,the event must be universally present in all patients.From the point of view of intensi-vists,it is well known that with increasing number of organ dysfunction or failure,the mortality would cumulatively increase.Undoubtedly,these events are predictive of the outcome,the basis of SOFA score.It is therefore not sur-prising;the same has been reported in the CANONIC study [2].However,should organ failure be included in deﬁning the clinical syndrome of liver failure needs a thorough analysis.As a corollary,despite decades of extensive experience,renal or circulatory dysfunction has not been included in the deﬁnition of ALF.The issue whether sepsis per se could lead to liver failure or is a result of liver failure had been debated for many years and was again revisited. However,sepsis is an integral part of development of multi-organ failure in any patient,be it of renal,pancreatic, or cardiac origin.The differences between the current deﬁnitions of CLIF consortium and APASL have been recently published[8].While theﬁrst APASL consensus was based on the data of only about200patients,the data of1700patients are now available from14countries.Records of1,363ACLF patients were analyzed.This formed the basis of re-eval-uating the validity of the APASL2009consensus.It was decided that,like in other studies,the analysis of the original data should be sent for separate publications and only the conclusions and recommendations based on these data can be used for the purpose of the consensus.To improve our understanding of the West,Prof Richard Moreau,theﬁrst author of the CANONIC study,kindly consented to join the consensus meeting.The6major issues as mentioned above,and28sub-issues,were deﬁned,and systematic reviews were made available to all participants.These were addressed at length in the meeting.What constitutes an acute insultThis issue was divided into two parts:ﬁrst,what is the time frame for the term‘‘acute,’’and second,what are the cri-teria to deﬁne the nature of an‘‘insult.’’A review of the different published deﬁnitions of acute liver failure and ACLF was done,and the current APASL deﬁnition of ACLF was reassessed.It was clear that the event must be new and acute,and its impact on the patient’s condition should be observable as liver failure within a given time frame.The EASL-AASLD consortium had initially kept the assessment of outcomes at3months[9],but subse-quently revised it to28days in the recent CANONIC study [2].The AARC data were carefully analyzed,and themortality rates were at different time points.A mortality rate of more than33%at4weeks was considered to be signiﬁcant allowing recovery to less than two-thirds of the ing these criteria,the data showed that more than50%patients of ACLF die by week 4.It was, therefore,unanimously agreed that the4-week(28days) period should be maintained as per the initial deﬁnition for deﬁning the impact of an acute event.Efforts were made in light of all the available data on deﬁning the nature of acute event.The acute insult could vary depending on the geographic region and the popu-lation under study.These include both infectious and non-infectious causes.These were well characterized in the past.While Hepatitis B reactivation remains the pre-dominant cause of acute hepatic insult in the East,from the global perspective,the major etiologic agent was alcohol,both in the West and the East.This was a bit unexpected for the Asian countries where alcoholic hep-atitis is emerging as a major acute insult and shows the growing westernization of Asia.The predominant causes of acute hepatic insults are shown in Fig.2.A review of the recent CANONIC study data showed that in the West, the term precipitating event is generally used and proba-bly details of events such as Hepatitis B or superadded Hepatitis A and E are rarely encountered or recorded[2]. However,it was a bit surprising that active alcohol abuse and alcoholic hepatitis were also not the predominant causes.A plausible explanation could be that since the CANONIC study only recorded the acute decompensation of cirrhosis and not the hepatic insults,the major events recorded were only non-hepatic,such as bacterial infec-tions or sepsis.Acute decompensation of cirrhosis is a different entity than ACLF.As the core premise of ACLF is presented as liver failure,the acute insults should be hepatic insults.Both,hepatotropic or non-hepatotropic insults,should manifest in the patientﬁrst with liver failure.Acute hepatic insults of infectious etiology included reactivation of Hepatitis B virus(HBV)as the leading cause of ACLF in the Asian region[10–19].Reactivation of HBV could be either spontaneous or due to intensive chemotherapy or immunosuppressive therapy[10,11], immune restoration after highly active antiretroviral ther-apy for HIV[12,13],treatment-related[14],or reactivation of the occult HBV infection by rituximab(anti-CD20)-based chemotherapy[15–17].Similarly,reactivation of Hepatitis C virus infection has also been reported,espe-cially after immune suppressive therapy[18,19].The other very important infectious etiology of the acute event is super-infection with Hepatitis E virus,predominantly in patients in the Indian subcontinent[20–23].Various bac-terial,parasitic,and fungal infections may affect the liver.Spirochetal,protozoal,helminthic,or fungal organisms may directly infect the liver,whereas bacterial or parasitic infection may spread to the liver from other sites[24]. These infections may lead to liver failure in patients with underlying chronic liver disease.Among the non-infectious etiologies,alcoholic hepatitis is the major cause of acute deterioration in stable known or unknown chronic liver diseases,more often in the western countries[25,26].It was not clear what should be the interval from the last alcoholic drink to be included as acute insult.Since,after the direct hepatic injury,the immunologic injury starts to decline[27],a period of28days was considered adequate for inclusion as the last drink.The issue which remains to be addressed was of binge drinking in patients with ACLF due to recent alcohol intake.It was appreciated that a prospective data collection including the drinking behavior especially in the past6months would help decide the inﬂuence of drinking behavior on the clinical outcome and help in deﬁning the time frame of what should be consid-ered as an acute insult.Hepatotoxic drugs and complimentary and alternative medicines(CAM)are important causes for acute and acute-on-chronic liver failure in the Asia–Paciﬁc region[28]. Hepatitis following the use of anti-tubercular drugs was considered to be an important cause of acute insult leading to ACLF.In a proportion of patients,despite a history of use of CAM,the precise nature and injurious inﬂuence of the agent cannot be determined.The need for further data on the hepatic injury caused by different herbal prepara-tions needs to be studied.Acute variceal bleeding has been included as one of the events to deﬁne hepatic decompensation in the natural history of cirrhosis[29].Variceal bleeding has also been taken as an acute insult for ACLF in some western trials of ACLF.It was extensively debated whether to consider variceal bleed as an acute event of ACLF.Since the deﬁ-nition of ACLF includes liver failure,jaundice,and coag-ulopathy,the variceal bleed should result in liver failure. The liver failure in such patients is mainly due to hepatic ischemia[30]and subsequent bacterial infections[31].It was discussed that for a patient with portal hypertension and cirrhosis of the liver who presents for theﬁrst time with variceal bleed without any previous or present signs or symptoms of chronic liver disease,it would not constitute an acute insult.This is especially relevant if such a patient does not develop any jaundice.The experts discussed the stratiﬁcation of patients based on the stage of underlying liver disease and the severity of variceal bleed.However, since patients with ACLF never decompensated before and are distinct from patients with decompensated cirrhosis,it is unlikely that a variceal bleed would per se lead to sig-niﬁcant liver failure manifesting as jaundice and coagu-lopathy.Based on the data,it was unanimously agreed that acute variceal bleeding is not an acute hepatic insult unless in the patients where it produces jaundice and coagulopa-thy deﬁning ACLF.A scenario may exist that a patient who has already fulﬁlled the criteria of ACLF,and has been diagnosed ACLF,develops a variceal bleed.In such a patient,variceal bleed would be considered as a complication in the natural history of ACLF.The issue of other non-hepatotropic insults which have been considered in other studies such as surgery,trauma, insertion of transjugular intrahepatic porto-systemic shunt, transartrial chemoembolization,or radiofrequency ablation for hepatocellular carcinoma was discussed in detail.While there is an indirect connection with each of these,it was debated that a patient who already has cirrhosis with HCC or a cirrhotic who undergoes surgery,and separate risk scores are already in practice and being utilized.The likely potential for hepatic decompensation would vary depend-ing on the nature of intervention and underlying hepatic reserve.It was agreed that non-hepatotropic insults pro-ducing direct hepatic insult and ACLF in an otherwise compensated liver disease could be considered as acute hepatic insults(2b,C).In a proportion of patients in Asia or even in the west,the precise agent(s)leading to acute hepatic insult is not well recognized on routine assessment. In such patients,this should be recorded as such. RecommendationsDeﬁning the acute event in ACLFThe ACLF can develop from one or more clearly deﬁned acute hepatic insults,which can be due to hepatotropic or non-hepatotropic agents/causes.Acute insults vary depending on the geographic region and the population under study.Major etiologic agents responsible for pre-cipitating ACLF are as follows:1.1Hepatotropic viral infections(1a,A).1.1.1Among these,reactivation of Hepatitis Bvirus(HBV)infection and super-infectionwith HEV are the major causes of acuteinsult in ACLF(1a,A).1.1.2Among the non-infectious causes,activealcohol consumption(within the last28days)remains the commonest cause(1a,A).1.1.3Drug-induced liver injury,consumption ofcomplimentary and alternative medicines(CAM),severe autoimmune hepatitis,andﬂare of Wilson’s disease are other causesof acute insult in ACLF(1a,A).1.2Non-hepatotropic insults like surgery,trauma,andviral infections if producing direct hepatic insultcould lead to ACLF(2b,C).1.3Variceal bleed per se may not qualify as an acuteinsult for ACLF,and we need more data toascertain this(5,D).1.4In a proportion of patients,the acute hepatic insultmay not be identiﬁable by the current routineassessment(5,D).Deﬁning the underlying chronic liver diseaseTwo aspects were carefully analyzed,what constitutes chronic liver disease,cirrhosis alone or non-cirrhotic chronic liver diseases,and the etiology of the chronic liver disease.The degree of hepaticﬁbrosis and the functional hepa-tocellular mass remains heterogeneous in patients with the chronic hepatitis[32,33].Even in patients with stage IV disease,critical mass varies according to the parenchymal reserves.Modiﬁed Laennec Scoring System divides stage IV further,according to the thickness of septa into three, ending up in six stages altogether[34,35].Moreover, ACLF is not equivalent to the acute decompensation of cirrhosis,which is the result of parenchymal extinction. Majority of the ACLF patients present with liver failure without any previous assessment of liver disease.It is not possible to distinguish accurately patients with different degree ofﬁbrosis at this point in time.The liver with any signiﬁcant degree ofﬁbrosis,with activated stellate cells, and inﬁltrated by the inﬂammatory cells,is expected to respond in a different way to the acute insult compared to the liver without inﬂammatory inﬁltrate[36].The NAFLD is the leading cause of donor rejection in liver transplantation[37].Experience from liver trans-plantation centers shows that steatosis[30%in the donor liver is associated with a higher risk of primary non-function and graft initial poor function as compared to grafts with no or\30%steatosis[38].Patients with met-abolic syndrome and fatty liver,diabetics,male patients of age[45–50years,patients with obesity,and dyslipidemia have the increased risk ofﬁbrosis[39].While cirrhosis could be a late event,a large proportion of them may have stage2or3ﬁbrosis.Hence,NASH is indeed an important cause of chronic liver disease[40].Furthermore,in the East,a large proportion of patients do have reactivation of chronic Hepatitis B.In these patients,while liver failure and ACLF-like presentation does develop,cirrhosis is not necessarily present.The AARC data,based on the liver biopsy studies,corroborated the facts that a fair proportion of patients with ACLF do not have underlying cirrhosis, but still carry a poor prognosis,with mortality above33% at4weeks.Based on the available data,the published literature and the validity of the2009consensus on including the non-cirrhotic chronic liver disease were reafﬁrmed.Accurate and reliable assessment of underlying CLD in the setting of ACLF is important for the subsequent man-agement and need for liver transplant in these patients. Diagnosis of chronic liver disease in the setting of ACLF is made by history,physical examination,and previously available or recent laboratory,endoscopic or radiologic investigations[41].Ultrasound and CT abdomen may pick up CLD.However,to assess the degree ofﬁbrosis in an un-shrunken liver would require other radiologic modalities. The current noninvasive tests cannot clearly diagnose the presence of chronic liver disease in the presence of inﬂammation and liver failure.Hence,liver biopsy through the transjugular route remains an important tool to conﬁrm the stage ofﬁbrosis and presence of cirrhotic or non-cir-rhotic liver disease.A liver biopsy through the transjugular route may be of help when the presence of already underlying CLD and the cause of liver disease are not clear.The liver biopsy may highlight the etiology,stage ofﬁbrosis and prognosis,and outcome in patients with ACLF[42].In addition,transju-gular access directly into the hepatic vein allows the hepatic venous pressure gradient to be measured(HVPG). There is a risk of bleeding leading to hemobilia,hemo-peritoneum,and hepatic hematoma in the setting of the deranged clotting proﬁle[43].The need of liver biopsy in ACLF should therefore be individualized.Standardization of liver biopsy assessment would help a uniform approach to the diagnosis and treatment for CLD and the acute insult.There is a need to have reliable noninvasive tools to assess the severity ofﬁbrosis in a previously undiagnosed CLD.Ultrasound and CT abdomen may pick up CLD. However,to assess the degree ofﬁbrosis in an un-shrunken liver would require other radiologic modalities.Transient elastography(ﬁbroscan)is a good modality to detect ﬁbrosis radiologically[44].However,the liver tissue stiffness may also increase with hepatitis,steatosis,and inﬂammation present in the ACLF setting[45].The second issue was about the etiology of chronic liver disease and cirrhosis in the Asian–Paciﬁc region.Experts reviewed the data from the AARC,and the etiologic proﬁle of cirrhosis in ACLF was found to be similar to the etiol-ogy of cirrhosis in general in the respective countries[26, 46,47].With the rising incidence of obesity and NAFLD, proportion of burnt-out NASH presenting as cryptogenic cirrhosis is also increasing[48–50].Viral serology and nucleic acid testing are required to identify viral etiology.Specialized tests to rule to diagnose metabolic and autoimmune diseases would be needed as well. The presence of stigmata of liver disease on clinical exami-nation,low platelets,evidence of synthetic dysfunction in。

Hepatology_Research｜急性失代偿期酒精性肝硬化患者90天生存预后模型的建立和验证

临床肝胆病杂志第40卷第3期2024年3月J Clin Hepatol， Vol.40 No.3， Mar.2024[4]JEPSEN P, OTT P, ANDERSEN PK, et al. Clinical course of alcoholicliver cirrhosis: a Danish population-based cohort study[J]. Hepatol⁃ogy, 2010, 51(5): 1675-1682. DOI: 10.1002/hep.23500.[5]MUMTAZ K, ISSAK A, PORTER K, et al. Validation of risk score inpredicting early readmissions in decompensated cirrhotic patients:a model based on the administrative database[J]. Hepatology,2019, 70(2): 630-639. DOI: 10.1002/hep.30274.[6]BAJAJ JS, HAFEEZULLAH M, HOFFMANN RG, et al. Navigation skillimpairment: Another dimension of the driving difficulties in minimal he⁃patic encephalopathy[J]. Hepatology, 2008, 47(2): 596-604. DOI:10.1002/hep.22032. PMID: 18000989.[7]SUK KT, BAIK SK, YOON JH, et al. Revision and update on clinical prac⁃tice guideline for liver cirrhosis[J]. Korean J Hepatol, 2012, 18(1): 1-21.DOI: 10.3350/kjhep.2012.18.1.1.[8]XU XY, DING HG, LI WG, et al. Chinese guidelines on managementof hepatic encephalopathy in cirrhosis[J]. World J Gastroenterol, 2019, 25(36): 5403-5422. DOI: 10.3748/wjg.v25.i36.5403.[9]UMAPATHY S, DHIMAN RK, GROVER S, et al. Persistence of cognitiveimpairment after resolution of overt hepatic encephalopathy[J]. Am J Gastroenterol, 2014, 109(7): 1011-1019. DOI: 10.1038/ajg.2014.107.[10]HU XP, GAO J. International normalized ratio and Model for End-stage Liver Disease score predict short-term outcome in cirrhotic pa⁃tients after the resolution of hepatic encephalopathy[J]. World J Gas⁃troenterol, 2019, 25(26): 3426-3437. DOI: 10.3748/wjg.v25.i26.3426.[11]TANDON P, KUMAR D, SEO YS, et al. The 22/11 risk predictionmodel: a validated model for predicting 30-day mortality in patients with cirrhosis and spontaneous bacterial peritonitis[J]. Am J Gas⁃troenterol, 2013, 108(9): 1473-1479. DOI: 10.1038/ajg.2013.204. [12]ZAHOREC R. Neutrophil-to-lymphocyte ratio. Sixteen-year-long historysince publication of our article in Bratislava Medical Journal[J]. Bratisl Lek Listy, 2017, 118(6): 321-323. DOI: 10.4149/BLL_2017_062. [13]SHI K, HUANG Y, ZHANG Q, et al. Neutrophil-lymphocyte ratio andthe risk of 30-day mortality in patients with overt hepatic encephalopa⁃thy[J]. Eur J Gastroenterol Hepatol, 2022, 34(5): 529-536. DOI: 10.1097/MEG.0000000000002368.收稿日期：2023-06-02；录用日期：2023-07-31本文编辑：刘晓红引证本文：HUANG YY, SHI K, WANG XB. Influencing factors for death within 30 days in patients with decompensated hepatitis B cirrhosis and hepatic encephalopathy[J]. J Clin Hepatol, 2024, 40(3): 516-520.黄云义, 时克, 王宪波. 失代偿期乙型肝炎肝硬化并发肝性脑病患者30天内死亡影响因素分析[J]. 临床肝胆病杂志, 2024, 40 (3): 516-520.·国外期刊精品文章简介·Hepatology Research｜急性失代偿期酒精性肝硬化患者90天生存预后模型的建立和验证酒精性肝硬化是临床发病率不断升高的慢性肝病之一，首次进展至急性失代偿期作为患者生活质量、住院概率的转折点，表现出更严重的全身炎症及并发症的进展，以及显著升高的短期死亡风险。

乙型肝炎病毒相关肝细胞癌抗病毒治疗的作用和意义

乙型肝炎病毒相关肝细胞癌抗病毒治疗的作用和意义黄罡;周伟平;吴孟超【期刊名称】《腹部外科》【年(卷),期】2017(030)002【摘要】肝细胞癌(hepatocellular carcinoma,HCC)为我国常见恶性肿瘤,虽然肝脏外科技术飞速发展,但近30年来肝癌病人预后无明显改善,大家往往重视局部治疗,对肝癌病人的全身综合治疗关注不够,尤其是忽视了对我国肝癌的最主要致病因素乙型肝炎病毒(hepatitis B virus,HBV)的研究和有效治疗.结合我们自己在这一方面前期的研究结果以及国内外近年来发表的相关文献,系统阐述了HBV相关HCC 抗病毒治疗的作用和意义.抗病毒治疗可有效预防肝癌病人HBV再激活,改善HCC 病人肝脏炎症、肝纤维化,显著降低肝癌术后复发率,提高生存率.并讨论核苷类抗病毒治疗的适应证、药物选择以及治疗疗程等相关问题.研究结果还显示抗病毒应答时间快慢、病毒耐药变异等均是影响HCC术后复发的危险因素,因此选择速效、低耐药核苷类药物.并主张长期抗病毒治疗,以最大限度改善HBV相关HCC病人预后.积极有效的抗病毒治疗应该成为HBV相关HCC病人综合治疗的重要组成部分.%Hepatocellular carcinoma (HCC) is the most common cancer in our country.Hepatitis B virus (HBV) infection is a major risk factor forHCC.Surgical resection is the first-line therapeutic option for patients with resectable tumors and preserved liver function.However,a significant proportion of patients develop tumor recurrence,which together with concomitant hepatic decompensation in a background of cirrhosis,is the main causes of death on long-term follow-up.Thus,the long-termprognosis after liver resection remains unsatisfactory,and prevention of recurrence via adjuvant treatments is important,though unmet medical need,in patients with HCC.HBV infection is responsible for many cases of HCC in our country.Antiviral therapy plays a significant role in the comprehensive treatment of HBV related HCC.Studies showed that antiviral therapy can suppress the replication and reactivation ofHBV,reduce inflammation of the liver,improve hepatic fibrosis,reduce late recurrence after hepatectomy and improve overall survival significantly.So it is very important to choose fast effective and low resistant nucleotide.HCC patients need repeated treatment such asoperation,TACE,radiation and radiofrequency ablation,so long-term antiviral therapy which can prevent the reactivation of HBV isneeded.Nucleotide antiviral therapy is an important part of comprehensive treatment of HBV-related HCC patients,which can reduce the late postoperative recurrence and improve the overall survival.【总页数】4页(P85-88)【作者】黄罡;周伟平;吴孟超【作者单位】200438上海,第二军医大学附属东方肝胆外科医院肝脏外科;200438上海,第二军医大学附属东方肝胆外科医院肝脏外科;200438上海,第二军医大学附属东方肝胆外科医院肝脏外科【正文语种】中文【中图分类】R735.7【相关文献】1.抗病毒治疗对乙型肝炎病毒相关性肝细胞癌患者根治性术后的影响 [J], 周彬;唐德为2.乙型肝炎病毒相关性肝细胞癌抗病毒治疗的研究进展 [J], 姜枫;杨大明;徐克成3.抗病毒治疗对乙型肝炎病毒相关性肝细胞癌患者根治性术后的影响* [J], 柯阳;钟鉴宏;游雪梅;黄盛鑫;梁泳荣;向邦德;黎乐群4.乙型肝炎病毒相关性肝细胞癌抗病毒治疗现状 [J], 袁宝红;钟鉴宏(综述);袁卫平(审校)5.乙型肝炎病毒相关性肝细胞癌病人抗病毒治疗现状及用药教育效果评价 [J], 李悦悦;陈安妮;刘丹丹;战旗;张国庆;王慧因版权原因，仅展示原文概要，查看原文内容请购买。

肝硬化临床研究进展

作者单位:100034北京市北京大学第一医院感染性疾病科第一作者:徐京杭,女,45岁,主任医师,副教授,硕士生导师㊂E-mail:ddcatjh@通讯作者:徐小元,E-mail:xiaoyuanxu6@ ㊃述评㊃肝硬化临床研究进展徐京杭,于岩岩,徐小元㊀㊀ʌ关键词ɔ㊀肝硬化;病因;诊断;治疗㊀㊀DOI:10.3969/j.issn.1672-5069.2024.02.001㊀㊀Liver cirrhosis:Current state of the art㊀Xu Jinghang,Yu Yanyan,Xu Xiaoyuan.Department of Infectious Diseases,First Hospital,Peking University,Beijing100034,China㊀㊀ʌKey wordsɔ㊀Liver cirrhosis;Etiology;Diagnosis;Treatment㊀㊀多种慢性肝病均可导致肝纤维化和假小叶形成,导致肝硬化(liver cirrhosis,LC),成为沉重的疾病负担㊂全球约有1.23亿LC患者[1,2],我国有700万LC及数亿LC高危人群,包括约2.7亿非酒精性脂肪性肝病(non-alcoholic fatty liver disease,NAFLD)㊁6500万慢性HBV感染㊁6200万酒精性肝病(alcoholic liver disease,ALD)和1000万慢性HCV感染者[3]㊂近年来,LC的自然史和临床分期理念逐步在更新,其诊断及评估手段㊁病因治疗㊁并发症管理措施和疾病预防方面也在不断取得进展㊂1㊀肝硬化临床分期与再代偿传统上,LC分为代偿期和失代偿期㊂出现腹水㊁食管胃静脉曲张破裂出血(EVB)和肝性脑病(HE)等并发症前称为代偿期LC;一旦出现上述并发症之一,则诊断为失代偿期LC㊂这种临床分期简单易行,易于临床使用㊂近来,还提出要重视LC失代偿亚临床形式,即轻微肝性脑病㊁超声发现2cm 以下的少量腹水和粪便潜血试验阳性(排除其他原因)等情况㊂分期预测病死率可采用6期法:1期无食管胃静脉曲张或腹水,2期有食管胃静脉曲张但无腹水,3期有腹水伴/不伴有食管胃静脉曲张,4期有食管胃静脉曲张破裂出血伴/不伴有腹水或肝性脑病,5期出现脓毒症㊁难以控制的消化道出血或顽固型腹水㊁急性肾损伤-肝肾综合征及肝性脑病等多器官损伤,6期为肝功能晚期失代偿[4]㊂在LC的分期方面,近年来的研究突出了LC可逆转及再代偿的观点㊂既往认为,一旦发生LC病变则不再可逆,尤其进入失代偿期后病情逐渐加重,难以再回到代偿期㊂随着相关临床证据逐渐丰富,上述传统观念已经被摈弃,失代偿期患者可再代偿的观念也逐渐被接受[5]㊂我国‘慢性乙型肝炎防治指南“已将再代偿列入诊断范畴[6]㊂多个临床研究证实LC可被逆转㊂在有效的抗HCV治疗后, 49%~61%丙型肝炎导致的肝硬化(HCV-LC)可被逆转;在抗HBV治疗5年后,74%乙型肝炎导致的肝硬化(HBV-LC)可被逆转,6年后100%逆转;非酒精性脂肪性肝炎(non-alcoholic steatohepatitis, NASH)导致的LC(NASH-LC)患者接受腹腔镜袖状胃切除术后随访30个月,68%LC被逆转[7]㊂但不同研究中采用的LC逆转组织病理学标准不完全相同,如METAVIR评分或ISHAK评分,有可能导致研究结果的差异[5]㊂即便进入失代偿期,只要积极进行病因治疗和并发症管理,相当部分LC患者可以在较长时间内不再出现失代偿表现,即再代偿㊂120周治疗后56.2%HBV-LC患者达到Baveno VII共识的再代偿标准[8]㊂立即开始抗HBV治疗,约40%在6年抗病毒治疗期间保持稳定的再代偿[9]㊂新近发表的回顾性研究结果显示,196例失代偿期HBV-LC患者接受抗病毒治疗12个月㊁24个月㊁36个月㊁48个月和60个月时,无腹水再代偿比例分别为59.7%㊁70.0%㊁52.3%㊁59.4%和46.2%[10]㊂为尽早识别不能再代偿者,多项研究分析了再代偿的预测因素,发现治疗前较好的肝功能水平㊁治疗早期应答㊁尽早接受病因治疗等因素影响再代偿的实现㊂回顾性多中心研究发现早期再代偿预测因子包括基线较低的血清胆红素水平(ɤ85.5μmol/L)㊁无严重并发症㊁较好的凝血功能,如国际标准化比率(internationalnormalized ratio,INR)ɤ1.5㊁较高的血清甲胎蛋白水平(ȡ50ng/mL)㊁较高的丙氨酸氨基转移酶(alanine aminotransferase,ALT)水平(ȡ200U/L)和较早开始抗病毒治疗的BC2AID模型预测价值优于Child-Pugh㊁MELD和MELD-Na等[11]㊂另一项研究发现,治疗2年时再代偿者可以预测远期的稳定再代偿,远期病死率和肝移植率显著下降[9]㊂LC的再代偿标准中病原㊁临床症状和体征的评估相对清晰,而门静脉压力梯度(HVPG)㊁白蛋白㊁INR和胆红素的改善程度等标准需更多的探讨[5]㊂2㊀肝硬化诊断和评估LC的诊断和评估进展主要表现在病因㊁肝纤维化精准检测和并发症无创评估等方面㊂此外,需鉴别恶性肿瘤肝转移等情况下的假性LC[12]㊂LC的病因分布存在地区差异[13]㊂随着抗HBV治疗的推进和HBV母婴传播阻断措施的开展,HBV的构成比在逐渐下降,而其他原因,如NASH逐渐增加[14]㊂更重要的是,NASH-LC比HBV-LC预后可能更差㊂与HBV-LC腹水患者比,NASH-LC腹水患者稀释性低钠血症㊁难治性腹水㊁LC相关死亡和肝移植累积发生率也更高[15],提示LC防治领域将面临更严峻的挑战,早期诊断和干预NASH-LC非常必要㊂肝组织病理学检查是评估肝纤维化的金标准,治疗前后重复检查可准确判断LC的发展趋势,但其有创性和花费等限制了临床应用㊂我国学者根据肝组织纤维间隔特征变化提出了北京标准 :将治疗后肝纤维化和LC的动态变化分为进展为主型㊁不确定型和逆转为主型,仅依据治疗后肝组织病理学检查结果即可判断LC发展趋势,避免两次肝穿刺带来的风险和经济负担[16]㊂组织病理学评分相同的患者可具有不同的临床特征,亟需对肝纤维化进行精准评估[17]㊂我国学者应用单细胞RNA测序等技术建立了基于肝纤维化特异性基质基因的纤维化分类新方法,揭示了传统组织学评估无法检测到的隐藏信息,将有助于深入了解肝纤维化的发病机制㊂通过非侵入性方法评估门脉高压并发症,如脾硬度测量㊁血小板计数和影像学检查等具有创伤小和可重复等优点的方法,其应用越来越广㊂脾硬度测量在筛查高危静脉曲张(high-risk varices,HRV)㊁减少胃镜检查方面具有重要的价值[18,19]㊂我国多中心研究验证了Baveno VII共识中提出的采用脾硬度测量值(ɤ40kPa)排除HRV的良好价值[20]㊂3㊀肝硬化治疗和并发症预防既重视LC的病因治疗,也应关注其他治疗,如抗纤维化㊁应用非选择性β受体阻滞剂(NSBBs)㊁阿司匹林㊁他汀类药物㊁监测出凝血功能和补充人血白蛋白等㊂抗HBV治疗给HBV-LC患者带来的获益包括抑制HBV复制,促进肝小叶结构恢复,改善肝功能储备,减少失代偿,降低HCC发生风险,逆转LC,促进LC再代偿,降低病死率,减少肝移植需求等[21,22]㊂目前,尚缺乏上市相对较晚的艾米替诺福韦(TMF)在本领域的大样本长疗程治疗数据㊂在抗HBV药物可及性显著提高和抗HBV治疗适应证扩大的背景下,将有更多的临床研究结果涌现,以对临床结局进行更好的分析[21]㊂针对HCV-LC伴临床显著门脉高压者,有效抗病毒治疗后长期随访,少有失代偿发生[23]㊂NAFLD合并肝纤维化和LC者经过治疗可带来肝脏和肝外获益[7,24,25]㊂肝纤维化的消退缓慢[26],且抗病毒联合抗纤维化治疗1年后仍有一定比例患者存在肝纤维化[27],目前认为抗纤维化疗程不能短于1年㊂抗纤维化治疗中成药具有较好的应用证据,研究证实安络化纤丸㊁鳖甲软肝片和扶正化瘀等不仅可改善纤维化本身[28,29],还可改善硬终点[30,31]㊂慢性乙型肝炎(CHB)伴ISHAK纤维化ȡ3分患者在抗病毒治疗的基础上联用鳖甲软肝片可进一步降低肝癌发生风险和肝病相关死亡,联用组7年累积肝癌发生和肝病相关死亡率分别为4.7%和0.2%,均显著低于抗病毒单药治疗组(分别为9.3%和2.2%)[31]㊂此外,多中心㊁随机㊁双盲㊁安慰剂对照的II期临床试验研究显示,恩替卡韦联合口服羟尼酮可促进肝纤维化改善[32]㊂Baveno VII肯定了卡维地洛相对于其他NSBBs 在改善门脉高压方面的优势[33,34]:代偿期HBV-LC 合并中度食管静脉曲张患者在核苷(酸)类(NUCs)抗病毒治疗的基础上联用卡维地洛可进一步改善门脉高压,延缓食管静脉曲张的进展[35]㊂血压㊁脉搏正常的肝硬化腹水患者,特别是顽固性腹水伴急性肾损伤(AKI)患者,在一级或二级预防食管胃静脉曲张出血时,可谨慎使用NSBBs[36,37]㊂临床研究提示非传统肝病药物可使肝病患者获益:CHB患者应用阿司匹林与肝癌发生风险下降相关;他汀可降低NAFLD发生肝纤维化风险[38],降低转氨酶异常率㊁肝脏硬度和失代偿风险[39]㊂重视出凝血功能的动态平衡被用于对门静脉血栓发生风险的监测[40]㊂白蛋白具有重要的生理功能,是LC并发症管理方面的重要药物,不仅要关注其数量,也要关注其质量㊂入院时有效白蛋白(effective albumin, eAlb)水平比总白蛋白水平更能预测LC急性失代偿患者的预后[41],有望成为预测LC结局的新指标㊂期待eAlb检测方法的商业化和便利化,以实现其指导肝硬化患者治疗和管理的价值[42]㊂2023年发表的荟萃分析认为利福昔明可改善轻微肝性脑病患者的生活质量,并可能改善肝性脑病[43],提示其预防肝性脑病的价值㊂ʌ参考文献ɔ[1]Collaborators GC.The global,regional,and national burden of cir-rhosis by cause in195countries and territories,1990-2017:A sys-tematic analysis for the global burden of disease ncet Gastroenterol Hepatol,2020,5(3):245-266.[2]Devarbhavi H,Asrani SK,Arab JP,et al.Global burden of liverdisease:2023update.J Hepatol,2023,79(2):516-537. 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恩替卡韦联合双歧杆菌乳杆菌三联活菌片治疗失代偿期乙型肝炎肝硬化临床疗效观察

恩替卡韦联合双歧杆菌乳杆菌三联活菌片治疗失代偿期乙型肝炎肝硬化临床疗效观察李波;邓存良【摘要】目的探讨恩替卡韦联合双歧杆菌乳杆菌三联活菌片治疗失代偿期乙型肝炎肝硬化患者的临床疗效.方法 2015年3月～2017年8月我院收治的120例失代偿期乙型肝炎肝硬化患者被随机分为对照组60例和观察组60例,分别给予恩替卡韦分散片或恩替卡韦联合双歧杆菌乳杆菌三联活菌片治疗,观察24 w.结果在治疗12 w时,观察组血清TBIL为(16.3±4.2)μmol/L,显著低于对照组的(26.3±5.2)μmol/L(P<0.05),观察组血清ALB为(32.5±4.2)g/L,显著高于对照组的(30.2±5.3)g/L(P<0.05);在治疗24 w时,观察组血清ALB为(37.8±2.3)g/L,显著高于对照组的(34.4±4.2)g/L(P<0.05);观察组血清LN和C-IV分别为(65.2±15.1)ng/ml和(85.5±8.5)ng/ml,显著低于对照组的[(75.3±10.3)ng/ml和(96.2±10.3)ng/ml,P<0.05];观察组血清HBV DNA水平为(1.0±0.1)lg copies/ml,与对照组的(1.7±0.3)lg copies/ml比,无显著性差异(P>0.05),血清HBV DNA转阴率为100.0％,与对照组的90.0％比,无显著性差异(P>0.05);在治疗12 w和24 w,观察组发生自发性细菌性腹膜炎(SBP)5例(8.3％)和2例(3.3％),显著低于对照组的10例(16.7％)和8例(13.3％,P<0.05);在治疗24 w末,观察组死亡3例(5％),而对照组死亡10例(16.7％,P<0.05).结论恩替卡韦联合双歧杆菌乳杆菌三联活菌治疗失代偿期乙型肝炎肝硬化患者能短期改善肝功能指标,降低血清肝纤维化指标水平,减少并发症的发生.【期刊名称】《实用肝脏病杂志》【年(卷),期】2018(021)005【总页数】4页(P669-672)【关键词】肝硬化;乙型肝炎;恩替卡韦;双歧杆菌乳杆菌三联活菌;治疗【作者】李波;邓存良【作者单位】646000 四川省泸州市西南医科大学附属医院感染病科;646000 四川省泸州市西南医科大学附属医院感染病科【正文语种】中文大约有四分之一的慢性乙型肝炎患者可能会发展成为肝硬化[1]。

碱基切除修复抑制剂甲氧胺联合β-榄香烯治疗恶性脑胶质瘤的实验研究

序言β-榄香烯属国家二类非细胞毒性抗肿瘤新药，临床研究证实其对包括脑胶质瘤在内的多种肿瘤疗效确切，且无其他传统化疗药常有的骨髓抑制、肝肾功能损害等毒副作用。

但目前临床应用的榄香烯乳注射液因其存在静脉炎发生率很高、剂型性质不稳定等缺点，其进一步的应用受到了较大的限制。

碱基切除修复抑制剂甲氧胺（Methoxyamine），可通过裂解核酸内切酶破坏DNA碱基切除修复过程，从而抑制肿瘤细胞对损伤作用的修复反应。

据此，可认为抑制DNA 碱基切除修复可能是增强肿瘤细胞化疗敏感性的潜在靶点，目前多项实验报道也已证实了甲氧胺可增强烷化剂和放疗的抗肿瘤效果。

近年来，通过纳米技术构建的纳米脂质体在提高药物溶解度、增加药物稳定性、降低药物副作用、缓控释给药等方面较普通的脂质体有了显著的提高。

研究表明，纳米脂质体对正常细胞和组织无损伤作用，并可长时间吸附于靶细胞周围，因此使药物能充分向靶组织渗透，也可以通过静电吸附效应与细胞膜接触而融合而进入细胞内。

因此将药物包封于纳米脂质体被认为可以改变被包封药物的体内分布，提高药物治疗指数，降低药物毒性。

基于增强β-榄香烯的疗效，减少毒副作用的目的，本课题研究内容分两部分：（一）联合碱基切除修复抑制剂甲氧胺，探讨是否在体内外抗瘤活性上具有协同作用，以期减少榄香烯用量，降低毒副反应，为其在临床的应用提供实验和理论依据。

（二）、利用纳米脂质体技术构建新型的β-榄香烯-纳米脂质体药物传递系统，初步探讨其体外抗瘤活性。

II碱基切除修复抑制剂甲氧胺联合β-榄香烯治疗恶性脑胶质瘤的实验研究中文摘要胶质瘤是成人神经系统最常见的原发性肿瘤，手术全切除率很低，复发率高，当前多种治疗效果仍不理想。

榄香烯属国家二类非细胞毒性抗肿瘤新药，临床研究发现其对多种肿瘤疗效确切，而且还具有提高和改善机体免疫功能，与放化疗协同作用等独特效果。

但是肿瘤细胞具有强大的DNA损伤修复机制，会对化疗药物产生抗性。

因此抑制这种内在的DNA修复过程，如碱基切除修复抑制剂甲氧胺的联合应用有利于提高化疗药物的抗瘤效果。

《2023年美国肝病学会实践指南：+肝硬化门静脉高压和静脉曲张的风险分层及管理》摘译

《2023年美国肝病学会实践指南：肝硬化门静脉高压和静脉曲张的风险分层及管理》摘译雒博晗，韩国宏西安国际医学中心医院消化内科，西安 710100通信作者：韩国宏，139****************（ORCID： 0000-0003-4568-3776）摘要：本实践指南旨在整合最佳实践建议，用于在慢性肝病患者中识别门静脉高压、预防首次肝功能失代偿、管理急性静脉曲张出血以及降低静脉曲张再出血的风险。

该指南中最重要的变化涉及承认代偿期进展性慢性肝病的概念，使用无创评估识别临床有意义的门静脉高压，在发现门静脉高压时建议尽早使用非选择性β-受体阻滞剂，进一步探讨门静脉高压的潜在未来药物治疗选择，阐明优先经颈静脉肝内门体静脉分流术在急性静脉曲张出血中的作用，以及讨论胃底静脉曲张治疗相关的最新数据，并提出了新的主题，如门静脉高压性胃病、经食管超声心动图和抗肿瘤治疗前的内窥镜检查。

关键词：肝硬化；门静脉高压；食管和胃静脉曲张；美国An excerpt of AASLD practice guidance on risk stratification and management of portal hypertension and varices in cirrhosis （2023）LUO Bohan， HAN Guohong.（Department of Gastroenterology， Xi’an International Medical Center Hospital， Xi’an 710100， China）Corresponding author： HAN Guohong，139****************（ORCID： 0000-0003-4568-3776）Abstract：This Practice Guidance intends to coalesce best practice recommendations for the identification of portal hypertension （PH），for prevention of initial hepatic decompensation，for the management of acute variceal hemorrhage （AVH），and for reduction of the risk of recurrent variceal hemorrhage in chronic liver disease. The most significant changes in the current Guidance relate to recognition of the concept of compensated advanced chronic liver disease， codification of methodology to use noninvasiveassessments to identify clinically significant PH （CSPH）， and endorsement of a change in paradigm with the recommendation of early utilization of nonselective beta-blocker therapy when CSPH is identified. The updated guidance further explores potential future pharmacotherapy options for PH，clarifies the role of preemptive transjugular intrahepatic portosystemic shunt in AVH，discusses more recent data related to the management of cardiofundal varices， and addresses new topics such as portal hypertensive gastropathy and endoscopy prior to transesophageal echocardiography and antineoplastic therapy.Key words：Liver Cirrhosis； Portal Hypertension； Esophageal and Gastric Vorrices； United States本实践指南［1］更新并扩展了美国肝病学会（AASLD）于2017年发布的门静脉高压（portal hypertension，PH）和胃食管静脉曲张管理的实践指南，为预防和管理PH提供了数据支持。

肝移植治疗慢加急性肝衰竭研究进展

Vol.41No.2Feb.2021上海交通大学学报（医学版）JOURNAL OF SHANGHAI JIAO TONG UNIVERSITY (MEDICAL SCIENCE)肝移植治疗慢加急性肝衰竭研究进展张天翼，于也萍，夏强，杭化莲上海交通大学医学院附属仁济医院肝脏外科，上海200127［摘要］慢加急性肝衰竭（acute-on-chronic liver failure ，ACLF ）指在慢性肝病的基础上由各种损伤因素引发的急性肝功能失代偿。

该病常伴肝外器官衰竭且短期死亡率极高。

目前ACLF 缺乏有效的治疗手段，肝移植手术是唯一有潜在治愈概率的治疗方式。

肝移植的术前评估十分重要。

我国由于乙型肝炎病毒（hepatitis B virus ，HBV ）感染群体基数较大，需着重考虑HBV 相关ACLF 的术前情况，并根据COSSH-ACLF 、CLIF-ACLF 等评分对患者术前情况进行评估。

手术时机方面，在患者处于ACLF2级时进行肝移植也许能够提高患者生存获益，但相关结论需要进一步的研究讨论。

围手术期主要以病因处理以及多器官衰竭处理为主。

术中则需要注意合理安排供体修整和受体游离的时间安排。

术后除了肝移植常规并发症外，还需注意感染、肝性脑病、器官衰竭等ACLF 相关并发症的处理。

术前与术后的器官衰竭情况均与患者长期预后相关。

该文结合笔者所在科室大量ACLF 肝移植实际工作经验，在查阅大量文献的基础上，就ACLF 肝移植术前评估、手术时机选择、围手术期管理、术中注意事项、术后并发症以及长期预后作一综述。

［关键词］慢加急性肝衰竭；肝移植；多器官衰竭；死亡率；并发症［DOI ］10.3969/j.issn.1674-8115.2021.02.021［中图分类号］R657.3［文献标志码］AResearch progress in liver transplantation for acute -on -chronic liver failureZHANG Tian -yi,YU Ye -ping,XIA Qiang,HANG Hua -lianDepartment of Liver Surgery,Renji Hospital,Shanghai Jiao Tong University School of Medicine,Shanghai 200127,China[Abstract ]Acute-on-chronic liver failure (ACLF),caused by various factors,is a rapid decompensation of liver function based on chronic liver disease,which is often accompanied by multiple organ failure and high short-term mortality.So far,there is no effective treatment except liver transplantation,which is the only possible cure.The evaluation before surgery is critical.Due to the large amount of hepatitis B virus (HBV)patients in our country,the evaluation of HBV-related ACLF (HBV-ACLF)is important.Systems like COSSH-ACLF,and CLIF-ACLF could be used for the evaluation.For the timing of surgery,transplantation at the state of ACLF-2may have more benefit for patients but the conclusion need more research to prove.During the perioperative period,management of organ failure and basic disease is needed.The timing of dissociation of the receptor and trimming of the donor need to be carefully managed during the surgery.After the surgery,beside the usual complication of liver transplantation,events such as infection,organ failure,hepatic encephalopathy should be dealt with.The condition of organ failures before and after liver transplantation is associated with the long-term mortality of patients.This article aims to make review on the assessment before liver transplantation,timing of transplantation,perioperative management,notice during surgery and complication after surgery based on massive clinical experience and plenty of document readings.[Key words ]acute-on-chronic liver failure (ACLF);liver transplantation;multiple organ failure;mortality rate;complication慢加急性肝衰竭（acute-on-chronic liver failure ，ACLF ）是肝衰竭的一种特殊类型。

医学英语常用短语

ICU——intensive care unite保证——vouch for坚持——in adherence to出院——discharge from the hospital违法——violate laws饿死——die of starvation认罪——confess to the crime酗酒——alcohol abuse标准差——standard deviation育龄期——childbearing age专卖店——special stores传染病——infectious disease适应症——indication并发症——complication元分析——meta-analyses无反应——null response肺栓塞——pulmonary embolism危险比——hazard ratio清除杂物——removing clutter精神错乱——mental disorder电气设备——electrical devices集体治疗——group therapy黎明时分——in the predawn hours恳求帮助——plea for help责任分散——diffusion of responsibility集体行为——collective behavior住院患者——hospitalized patients大幅增长——substantial increase前驱症状——prodromal symptom新发皮疹——new-onset cutaneous临床表现——clinical picture影像检查——imaging procedure输血反应——transfusion reaction输血疗法——transfusion practices住院期间——length of hospital stay亚群分析——subgroup analyses多重分析——multivariable analysis治疗强度——intensity of treatment强化治疗——intensive therapy治疗策略——therapeutic strategies复合终点——composite end生存概率——survival probability肝功分级——classification of liver function 肝功测试——liver-function test置信区间——confidence intervals主治医生——attending physician输血指征——transfusion trigger生存曲线——survival curve精算概率——actuarial probability 生存分析——Kaplan-Meier method治疗失效——therapeutic failure补救治疗——rescue therapy有害影响——harmful effects组间差异——between-group difference标准治疗——standard treatment双尾检测——tow-tailed test指示偏差——indication bias混杂因素——confounding factor现行标准——current guidelines治疗靶点——therapeutic targets凝血性质——coagulation properties事后分析——post hoc液体复苏——fluid resuscitation缩短寿命——shorten life随机分配——randomly assigned to疾病恶化——progression of the disease管理机构——regulatory agency不良事件——adverse event派发药物——administer drug治疗期间——treatment duration腹腔血栓——abdominal thrombosis部分反应——partial response冲击治疗——aggressive therapy轻度出血——minor bleeding资格标准——eligible criteria体质指数（BMI）——body-mass index肝部活检——liver biopsy首选药物——the drug of choice初步研究——preliminary study基本特征——baseline characteristics分类变量——categorical variable临床研究——clinical study遵循...原则——in accordance with the principle 危重症病人——critically ill patients等容性贫血——normovolemic anemia突发性贫血——rapid onset of anemia多中心试验——multicenter study进行性疾病——progressive disease肌酐清除率——creatinine clearance实质性肝病——substantial liver disease指导委员会——steering committee浓缩红血球——packed red cells非参数检验——nonparametric test血小板计数——platelet count白细胞计数——leukocyte count再次出血率——the rate of further bleeding连续型变量——continuous variable病例报告表——case-report form实体瘤发作——onset of solid tumor春季大扫除——spring clean真人秀节目——reality program多器官衰竭——multiorgan failure胃肠道出血——gastrointestinal bleeding门静脉高压——portal hypertension消化性溃疡——peptic ulcer血容量不足——intravascular volume depletion随机化实验——randomized trail血栓性疾病——thrombotic events浅静脉血栓——superficial-vein thrombosis癌症复发率——incidence of cancer意向性分析——intention-to-treat analysis开放式研究——open-label study探索性研究——exploratory study观察性研究——observational study回顾性研究——retrospective observation实验性研究——experimental study知情同意书——informed consent流行病学研究——epidemiology study临床试验性研究——pragmatic trial in clinical practice无干扰素治疗——interferon-free treatment主要研究终点——the primary composite end point次要研究终点——secondary end point随即临床试验——randomized clinical trail红细胞增多症——Polycythemia Vera血红蛋白阈值——hemoglobin threshold食管静脉曲张——esophageal varices急性代偿不全——acute decompensation引起某人注意——spark sb. attention患者诊疗协调——coordination of care乙肝表面抗原——hepatitis B surface antigen蛋白酶抑制剂——protease inhibitor正常范围上限——the upper limit of the normal range医学咨询中心——referring medical center假设生成分析——hypothesis-generating analysis周围动脉栓塞——peripheral arterial thrombosis世界卫生组织（WHO）——world health organization药物超敏反应——drug-induced hypersensitivity syndrome获得全部权限——have full access to签署保密协议——sign confidentiality agreements with对数秩和检验——log-rank test基线危险因素——baseline risk factor新鲜冰冻血浆——fresh-frozen plasma急性冠脉综合征——acute coronary syndrome艾滋病病毒抗体——anti-human immunodeficiency virus antibody 桥接纤维化晚期——advanced bridging fibrosis国际标准化比率——international normalized ratio低血容量性休克——hypovolemic shock肝、肾、肺衰竭——hepatic、renal and pulmonary failure意向性分析原则——intention-to-treat principle门静脉压力梯度——portal venous pressure gradient毕业后医学教育——graduate medical education机构审查委员会——institutional review board审查并提供反馈——review and provide feedback并发症总发生率——overall rate of complications堆积如山的旧报纸——a mountain of old newspapers受到某种疾病感染——be affected with a disorder主要复合研究终点——the primary end point持续病毒应答反应——sustained virological response分层随即分配依据——randomization was stratified according to主要疗效判定指标——primary outcome measure次要疗效判定指标——secondary outcome measure进行性血小板增多——progressive thrombocytosis比例风险模型分析——cox proportional-hazards regression model未经校验的危险比——unadjusted hazard ratio内脏血管收缩反应——splanchnic vasoconstrictive response巨噬细胞活化综合征——macrophage activation syndrome口服联合抗病毒治疗——oral-combination antiviral therapy暂时性脑缺血（脑瘫）——transient ischemic attack药品临床试验管理规范——Good clinical practice住院期间并发症发生率——the rate of in-hospital complications只考虑符合病人最大利益——considered only in the best interest of the patients。

肝胆外科文献常用英语单词

文献生词malignancy 恶性,恶性肿瘤hepatectomy 肝切除术bilirubin 胆红素bilirubinemia 胆红素血症Hyperbilirubinemia 高胆红素血症Indocyanine green 吲哚花青绿indocyanine green retention 靛青绿滞留量试验hepatic insufficiency 肝功能不全,肝功能衰退jaundice 黄疸retrospective review 回顾性调查intraoperative 手术中的,术中parameters 参数Logistic Regression Logistic回归prognosis 预后prognostic 预后的hilar 门的,脐的cholangiocarcinoma 胆管上皮癌intrahepatic cholangiocarcinoma 肝内胆管癌anatomic 解剖的,解剖学的hepatic hilus 肝门perioperative 围手术期的indication 适应证,指征curative 治愈的resection 切除术likelihood 可能性liver function 肝功能metastasis 转移hepatocellular carcinoma 肝细胞癌unexpected 意外的,忽然的cholestasis 胆汁淤积biliary drainage 胆汁引流extended hemihepatectomy 扩大半肝切除术Trisegmentectomy 三段切除Chronic viral hepatitis 慢性病毒性肝炎cirrhosis 肝硬化serum 免疫血清,血清on admission 入院时,住医院时percutaneous 经皮的transhepatic 经肝的endoscopic biliary drainage 内镜胆管引流,内镜胆管引流术,endoscopic 内窥镜的;内窥镜检查的drainage tube 引流管,排液管portal vein 门(静)脉embolization 栓塞,栓塞术,栓子形成peritoneal 腹膜的dissemination 播散,散布laparotomy 剖腹手术distant metastasis 远端转移Surgical Procedures 外科手术anastomosis 吻合术enteric 肠的in terms of 以…的观点;以…的方式hemorrhage 出血hemorrhagic 出血性的hemolysis 溶血hemolytic 溶血的hematology 血液学hematological 血液的hemodynamics 血流动力学coagulation status 高凝状态prothrombin time 凝血酶原时间activated partial thromboplastin time 激活部分促凝血酶原激酶时间antithrombin 抗凝血酶thrombolytic 溶血栓药,血栓溶解剂duration 持续时间;期间nonlinear least squares method 非线性最小平方法natural logarithm 自然对数categorize 分类galactose tolerance test 半乳糖耐量试验half life 半衰期computed tomography scan 计算机体层摄影扫描,CT扫描contrast medium 对比剂,造影剂bolus 推注integrated software 集成软件variables 变量continuous variable 连续变量categorical variable 分类变量univariate 单变量multivariate 多变量univariate analysis 单变量分析multivariate analysis 多元分析,多元统计分析stepwise procedure 逐步过程chi square test χ2检验,卡方检验,cutoff value 截断值Odds Ratio 比值比Mann Whitney test 曼-怀二氏检验tailed 有…尾的receiver operating characteristic curve 接受者（机）操作特征曲线morbidity and mortality 并发症和死亡率decompression 减压in regard to 关于,至于living related liver transplantation 活体亲属供肝肝移植术parenchyma 实质liver parenchyma 肝实质excretory 排泄的,分泌的parenchymal 质的,主质的shrinkage 皱缩,皱缩度biotransformation 生物转化adenosine triphosphate 三磷腺苷ammonia 氨Aspartate Aminotransferase 天冬氨酸氨基转移酶Alanine Aminotransferase 丙氨酸氨基转移酶Lactate Dehydrogenase 乳酸脱氢酶alkaline phosphatase 碱性磷酸酶glutamyl 谷氨酰基Inferior Vena Cava 下腔静脉abdominal aorta 腹主动脉Paraaortic 主动脉旁的celiac axis 腹腔干common hepatic artery 肝总动脉proper hepatic artery 肝固有动脉superior mesenteric Artery 肠系膜上动脉Hepatic artery thrombosis 肝动脉血栓形成pseudoaneurysm 假性动脉瘤portacaval shunt 门(静脉与)腔静脉分流术arterialization 动脉化angiography 血管造影术occlusion 闭塞梗塞occluded 闭塞的collateral 侧的,侧支,副的confluence 合流,汇流autologous vein graft 自体静脉移植物porta hepatis 肝门Portal lymph node 肝门淋巴结second order biliary radicles 二级胆管根lobar atrophy 肝叶萎缩caudate lobe 尾状叶falciform ligament 肝镰状韧带periampullary 壶腹周围的Retroduodenal 十二指肠后的jejunum (jejunal) 空肠（的）ileum (ileal) 回肠（的）colon(colonic) 结肠（的）rectum (rectal) 直肠（的）anal canal 肛管oncology 肿瘤学oncological 肿瘤学的neoplasm 肿瘤，新生物neoplastic 肿瘤的，新生物的neoplastic seeding 肿瘤播种papillary tumor 乳头瘤adenocarcinoma 腺癌cystadenoma 囊腺瘤testis 睾丸gastrinoma 胃泌素瘤squamous cell carcinoma 鳞状细胞癌carcinoid tumors 类癌sarcoma 肉瘤focal nodular hyperplasia (FNH) 局灶性结节性增生parenchymal disease 器质性疾病advanced cancer 晚期癌症well differentiated 分化良好nodule 结节nodal metastases 淋巴结转移therapeutic effect 疗效neoadjuvant chemotherapy 新辅助化疗radiofrequency ablation 射频消蚀arterial chemoembolization 动脉化疗性栓塞infiltrating 浸润macroscopically 肉眼[检查]的;目视的carcinoembryonic antigen 癌胚抗原indication 适应症指征contraindication 禁忌证preoperative workup 术前全面评估postoperative morbidity rate 术后并发症发生率operative approach 手术入路radical operation 根治术,根治性手术en bloc 整个地,整块地inoperable 不能手术的,不能做手术的palliative 姑息的diagnostic laparoscopy 诊断性腹腔镜检查non-therapeutic laparotomy 非治疗性剖腹探查术invasive techniques 微创技术procedural complications 手术并发症pancreaticoduodenectomy 胰十二指肠切除术Adrenalectomy 肾上腺切除术thrombectomy 血栓摘除术lymphadenectomy 淋巴结切除术Lymph Node Dissection 淋巴结清扫术lymph node harvest 淋巴结清扫end to side anastomosis 端侧吻合术hepaticojejunostomy 肝空肠吻合术cholecystectomy 胆囊切除术Caudate lobectomy 尾状叶切除术radiopharmaceutical agent 放射性药剂iodized oil 碘化油absolute ethanol 无水乙醇scintigraphy 闪烁扫描术helical 螺旋的,螺旋状,螺旋状的cross sectional imaging 横断层面成像magnetic resonance imaging (MRI) 磁共振成像endoscopy retrograde cholangiopancreatography (ERCP)内镜下逆行胆胰管造影magnetic resonance cholangiopancreatography (MRCP)磁共振胰胆管成像intraoperative ultrasonography 术中超声检查法contrast enhanced computed tomography对比增强扫描CT positron emission tomography PET正电子发射断层扫描cholangiogram 胆管造影Recurrence 复发follow up 随访concomitant 伴发的,附随的comorbidities 并存病bleeding 出血,流血extravasation 外渗,溢出hemobilia 胆道出血biliary fistula 胆瘘pleural effusion 胸腔积液lung edema 肺水肿splenomegaly 脾肿大hypersplenism 脾功能亢进hepatic encephalopathy 肝性脑病ascites 腹水subphrenic abscess 膈下脓肿endotoxaemia 内毒素血症myocardial infarction 心肌梗死pyrexial 发热的hypothermic 低体温的Biliary Stricture 胆管狭窄steatohepatitis 脂肪性肝炎fatty liver 脂肪肝adipose tissue 脂肪组织primary sclerosing cholangitis 原发性硬化性胆管炎angina 心绞痛sepsis 败血症,脓毒症perfusion 灌注ex vivo 离体,在活体外in situ 原位right upper quadrant 右上象限proximal part 近心端perineural 神经周围的bifurcation 二根分叉部,分岔ipsilateral 身体的同侧的,同侧的Institutional Review Board 机构审查委员会Ethics Committees 伦理学委员会predispose to 易患，使易感染、诱发platelet 血小板hyperalimentation 高营养支持cirrhotic 硬变的morbidity 并发症，发病率medications 用药dislodge 移去,逐出,取出gonadal 性腺的,生殖腺的Histologic 组织学的frozen section 冰冻切片atrophy 萎缩hypertrophy 肥大,过度生长proliferation 增生,增殖hyperplasia 增生;数量性肥大Stem cells 干细胞bone marrow derived 骨髓衍生的epithelium 上皮,上皮细胞encased 包裹reconstruction 重建,再造,重构inflammatory 炎症性的broad spectrum antibiotics 广谱抗菌素blood culture 血培养Gram Negative bacillus 革兰阴性[芽胞]杆菌cut surface 切面stent 支架catheter 导管direct cannulation 直接插管spectrophotometer 分光光度计rupture 破裂,vt.(使)破裂somatostatin 生长抑素Extracellular Matrix 细胞外基质cohort 同期组群Length of Stay 住院时间after discharge 出院后stratified 分层的,成层的clear cut 明确的In this regard 在这方面come at a cost 是有代价的progressively 进行性地,渐进地rationale 原理,基础理论homogeneous 同类的同质的heterogeneous 异类的,不同的putative 假定的omnipotent 全能的,无所不能的as controls 作为对照preconditioned 预处理preconditioning 预处理prospectively 前瞻性prospective randomized date 前瞻性随机数据Disease-Specific survival 疾病特异性生存率irreversible 不可逆的references 参考Cochrane 循证医学cholangiopancreatography 胰胆管造影术resolution 分辨率（决心，决议解决）herein 如此,鉴于，在此处iatrogenic 医源性palliation 缓和,减轻running suture 连续缝合orthotopic liver transplantation 原位肝移植chemoradiation 放化疗preneoplastic change 癌前变化carcinogenesis 致癌作用dysplasia 发育不良,不典型增生endoprosthesis 内镜置管术pruritus 瘙痒pruritis 瘙痒症Etiology (aetiology) 病原学etiologic 病原学的epidemiology 流行病学epidemiological 流行病学的pathophysiology 病理生理学lesion 病变Radionuclide 放射性核素nitrosamine 亚硝胺类pathogenesis 发病机制carcinoid 类癌Mucinous Adenocarcinoma 粘液腺癌Clear cell adenocarcinoma 透明细胞腺癌Signet ring cell adenocarcinoma 印戒细胞腺癌Adenosquamous Carcinoma 腺鳞状癌Squamous Cell Carcinoma 鳞状细胞癌Oat Cell Carcinoma 燕麦细胞癌Undifferentiated Carcinoma 未分化癌Papillomatosis 乳头状瘤病Papillary Carcinoma 乳头状癌hepatoblastoma 肝母细胞瘤Haemangioendothelioma 血管内皮瘤neuroendocrine tumour 神经内分泌瘤Leiomyosarcoma 平滑肌肉瘤malignant fibrous histiocytoma 恶化纤维组织细胞瘤nodular tumors 结节性肿瘤cachexia 恶液质sterilize 灭菌,消毒surgical radicality 手术的根治性angiogenetic 血管生成angiogenic 血管源性的，生成血管的antiangiogenic 抗血管生成的chemosensitization 化疗增敏photosensitizer 感光剂,光敏剂irradiation 放射，照射conformational radiotherapy 适形放射治疗brachytherapy 短距离放射治疗stereotactic 立体定位的,立体定向的interventional radiology 介入放射学oxaliplatin 奥沙利铂doxorubicin 多柔比星gemcitabine 吉西他滨immunosuppressant 免疫抑制剂Portography 门静脉造影术contrast agent 对比剂,造影剂lipiodol 碘油Iodophor 碘伏cystic duct 胆囊管choledochal duct 胆总管choledochal cysts 胆总管囊肿Choledocholithiasis 胆总管结石hepatolithiasis 肝内胆管结石病oriental cholangiohepatitis 东方人胆管肝炎Biliary malformation 胆管畸形Liver fluke 肝吸虫protocol 治疗方案therapeutic regimen 治疗方案Palliative Treatment 姑息治疗Signs and Symptoms 体征和症状plethora 多血症,多血质Differential Diagnosis 鉴别诊断Randomized Controlled Trials 随机对照试验enterocinesia 肠动,肠蠕动Ligation 结扎术luminal obstruction 官腔阻塞screening 普检,筛查,筛选predisposing factor 易感因素enhanced susceptibility 增强易感性hyperbaric oxygen treatment 高压氧治疗asymptomatic 无症状的indolent 无痛的Intractable Pain 顽固性疼痛visceral 内脏的steatosis 脂肪变性latency 潜伏期side effects 副作用decompensation 失代偿anoxia 缺养症anoxic 缺氧的anoxemia. 缺氧血症;血缺氧ischemia 局部缺血,缺血Ischemia-Reperfusion Injury 缺血再灌注损伤ischemic change 缺血性改变anemia 贫血pyogenic 化脓的purulent 化脓性,脓性的hepatomegaly 肝肿大umbilical fissure 裂脐cytokine 细胞因子neuropeptide 神经肽neurotransmitter 神经递质fluorescence in situ hybridization 荧光原位杂交necrosis 坏死necrocytosis 细胞坏死apoptosis 凋亡apoptotic 细胞凋亡的desmoplastic reaction 纤维成形性反应oncogene 癌基因Suppressor Genes 抑制基因genetic 遗传的epigenetic change 基因外改变hypermethylation 超甲基化sequential occurrence 顺序发生stepwise 分步的,分段的,逐步的mesenchymal 间质morphology 形态atypia 非典型,异型性Phenotype 表型dehydration 脱水paraffin 石蜡impregnation 浸渍,受精,受孕embedding 包埋,埋植serial section 连续切片anesthesia 麻醉anesthesiology 麻醉学anesthetist 麻醉师palpation 触诊orifice 管口,口,小孔one orifice 一个管口intubate 插管pancreatic secretion 胰腋centrifuge 离心,,离心机cannulation 管子reactive oxygen species 活性氧recanalization 再通，再穿通Celiac Plexus 腹腔丛arteriolar 微动脉的,小动脉的Collateral Circulation 侧支循环intima 内膜subintimal 内膜下的mitochondria 线粒体multifocal 多病灶的endemic 地方性的amenable 适合的more specifically 更具体地说mainstay 主要依据kink 扭折,纽结lethal 致命的peculiarity 特性armamentarium 医疗设备,设备demarcate 划界线,分开,区别paucity 资料贫乏migration 移位interim report 中期报告nihilistic 虚无主义的enigmatic 难理解的，神秘的occult 隐匿的，潜隐的autopsy 尸检detritus 腐屑,腐质,碎屑antegrade 顺行的retrograde逆行的endogenous 内源的,内生的exogenous 外源的,外生的intracorporeal 体内的extracorporeal 体外的autocrine 自分泌paracrine 旁分泌xenogenic 异体的,异种的cryptogenic 隐原性的,原因不明的insidiously 隐袭地congenital 先天的,天生的hereditary 遗传的,遗传性的pitfall 缺陷Biliary anomalies 胆道畸形cholecystolithiasis胆囊结石cholecystitis 胆囊炎choledocholithiasis 胆总管结石total bilirubin总胆红素unconjugated bilirubin 游离胆红素conjugated bilirubin 结合胆红素bile plug 胆栓sinusoid 血窦，窦状隙sinusoidal 血窦的窦状隙的transjugular 经颈静脉的portosystemic shunt 门体分流术hepatic coma 肝昏迷hyperammonaemia 高氨血症hypoalbuminemia 低白蛋白血症neuropsychiatric 神经精神性的confusion 意识错乱,意识模糊disorientation 定向障碍astrocyte 星形胶质细胞inflammatory mediator 炎症介质neutrophil (neutrophilic granulocyte) 嗜中性粒细胞macrophage 巨噬细胞phagocyte 吞噬细胞phagocytosis 吞噬作用mitogen 促细胞分裂原,有丝分裂原reticuloendothelial system 网状内皮系统Synthase 合酶dysregulation 调节异常,失调chromosome 染色体nuclear atypia 核异型nucleotide 核苷酸mitochondria 线粒体mitochondrial 线粒体的microsome 微粒体microsomal 微粒体的detoxify 去毒, 解毒，戒烟毒detoxification 解毒(作用),脱毒,戒毒治疗carcinogen 致癌物mutagen 诱变剂,致突变原carbohydrate antigen 糖类抗原标志物,糖链抗原glycoprotein 糖蛋白extirpation 摘除malignant transformation 恶变,恶性转化forceps biopsy 钳夹活检,钳夹活检术transpapillary 经十二指肠乳头stenosis 狭窄stenotic 狭窄的patency rate 通畅率vasculature 脉管系统diffuse intravascular coagulation 弥散性血管内凝血 (DIC) coagulant and fibrinolytic systems 凝血和纤溶系统circulatory disturbance 循环紊乱Vascular Permeability 血管通透性vasodilatation 血管扩张vasopressor 血管升压类药物vasopressin 加压素endothelin 内皮缩血管肽prostaglandin 前列腺素Saphenous Veins 隐静脉renin 肾素angiotensin 血管紧张素aldosterone 醛固酮oestrogen (estrin) 雌激素progestogen (progestin) 孕激素androgen (androtin) 雄激素testosterone 睾酮acute tubular necrosis 急性肾小管坏死oedema 水肿oliguria 少尿症diuretic(a) 利尿剂haemofiltration 血液滤过dialyse 透析dialysate (Dialysis Solutions) 透析液acute respiratory distress syndrome 急性呼吸窘迫综合征(ARDS)diaphragm 横隔dyspnea 呼吸困难pulmonary oedema 肺水肿ventilatory dysfunction 通气功能障碍Total Parenteral Nutrition 全胃肠外营养enteral nutrition 肠道营养malabsorption 吸收不良venoplasty 血管成形术hematoma 血肿perforation 穿孔paracentesis 穿刺,穿刺术granulomatous inflammation 肉芽肿性炎症Bacterial Translocation 细菌移位the administration of antibiotics 抗生素的应用prophylactic antibiotics 预防性抗生素synbiotic therapy 合生元治疗free radical 自由基lactate 乳酸盐malaise 不适感,全身乏力episode 发作idiopathic 特发性的,自发性的tracer 示踪剂relaparotomy 再手术mild to moderate 轻度到中度multifactorial 多因子的,多因素的iohexol 碘海醇procaine 普鲁卡因lidocaine 利多卡因analgesia 镇痛dehiscence 裂开cryopreserved 冷藏保存的discriminant analysis 判别分析cadaveric 尸体的subjects 受试者obliteration 涂去,抹消,删除milieu 环境,境界potent 有力的,有效的schematic diagram 示意图,原理图misidentification 错误认同,错认algorithm 公式,算法,推导strong echo 强回声acoustic shadow 声影hyperecho(ic) 高回声（的）isoecho(ic) 等回声（的）hypoecho(ic) 低回声（的）anecho(ic) 无回声（的）aseptic technique 无菌术asepsis 灭菌antisepsis 消毒emergency operation 急诊手术confine operation 限期手术selective operation 择期手术evidence-based medicine 循证医学polymerase chain reaction (PCR) 聚合酶链反应inquiry 问诊chief complaints 主诉history collection 病史采集history of present illness 现病史past history 既往史personal history 个人史marital history 婚姻史menstrual history 月经史child bearing history 生育史family history 家族史physical examination 体格检查inspection 视诊palpation 触诊percussion 叩诊auscultation 听诊abdominal pain 腹痛abdominal distension 腹胀diarrhea 腹泻constipation 便秘nausea 恶心vomit 呕吐stool 大便urine 小便aspiration 误吸asphyxia (apnea) 窒息atelectasis 肺不张arrhythmia 心律失常cardiac arrest 心脏骤停ventricular fibrillation 心室纤颤hyperthermia 高热hypothermia 低温Natrium (sodium) 钠Kalium (potassium) 钾Chlorine 氯Calcium 钙Magnesium 镁Phosphorus 磷ion 离子homoeostasis 体内平衡derangement 紊乱isotonic dehydration 等渗性缺水hypotonic dehydration 低渗性缺水hypertonic dehydration 高渗性缺水water intoxication 水中毒hyponatremia 低钠血症hypernatremia 高钠血症hypochloremia 低氯血症hyperchloremia 高氯血症hypokalemia 低钾血症hyperkalemia 高钾血症hypocalcemia 低钙血症hypercalcemia 高钙血症hypomagnesemia 低镁血症hypermagnesemia 高镁血症hypophosphatemia 低磷血症hyperphosphatemia 高磷血症metabolic acidosis 代谢性酸中毒metabolic alkalosis 代谢性碱中毒respiratory acidosis 呼吸性酸中毒respiratory alkalosis 呼吸性碱中毒hematocrit (Hct) 血细胞比容autologous blood transfusion 自体输血salvaged autotransfusion 回收式自体输血predeposited autotransfusion 预存式自体输血hemodiluted autotransfusion 稀释式自体输血cryoprecipitate 冷沉淀furuncle 疖furunculosis 疖病carbuncle 痈acute lymphangitis 急性淋巴管炎erysipelas 丹毒abscess 脓肿dermoid cancer 皮肤癌melanotic 黑痣melanoma 黑色素瘤lipoma 脂肪瘤neurinoma 神经鞘瘤neurofibroma 神经纤维瘤capillary hemangioma 毛细血管瘤angiocavernoma 海绵状血管瘤racemosum hemangioma 蔓状血管瘤sebum cyst 皮脂腺囊肿tetanus 破伤风gangrene 坏疽superinfection 二重感染septicemia 败血症debridement 清创术simple goiter 单纯性甲状腺肿hyperthyroidism 甲亢hypothyroidism 甲减mastitis 乳腺炎mastopathy 乳腺病，乳腺增生症mastectomy 乳房切除术teratoma 畸胎瘤inguinal hernia 腹股沟疝femoral hernia 股疝incisional hernia 切口疝umbilial hernia 脐疝hernia of linea alba 白线疝interloop abscess 肠间脓肿helicobacter pylory (HP) 幽门螺杆菌pyloric obstruction 幽门梗阻vagotomy 迷走神经切断术lymphoma 淋巴瘤duodenal diverticulum 十二指肠憩室intussusception 肠套叠polyps 息肉ulcerative colitis 溃疡性结肠炎rectal prolapse 直肠脱垂anorectal abscess 直肠肛管周围脓肿anal fistula 肛瘘anal fissure 肛裂haemorrhoids 痔internal haemorrhoids 内痔external haemorrhoids 外痔mixed haemorrhoids 混合痔annulus haemorrhoids 环形痔proctocolectomy 直肠与结肠切除术major operation 大手术omentum 网膜pancreaticobiliary 胰胆管的Bile canaliculus 胆小管mediastinum 纵隔quadrate lobe 方叶organic 有机的,器官的interferon 干扰素glomerular filtration rate 肾小球滤过率Fulminant Liver Failure 暴发性肝衰竭Nephrotic Syndrome 肾病综合征enteropathy 肠病,肠病变Esophageal cancer 食管癌gastroesophageal varices 胃食管静脉曲张Supine Position 仰卧位informed consent 知情同意sequelae 后遗症,转归demarcate 划界线,分开,区别postprandial 食后的to date 迄今为止regarding 关于serologic 血清学的Serology 血清学hepaplastin test 肝促凝血活酶试验urea 尿素heme 血红素anionic 阴离子的。

原发性胆汁性胆管炎合并干燥综合征的临床特点

㊃论著㊃通信作者:邓志华,E m a i l :yk d z h @h o t m a i l .c o m 原发性胆汁性胆管炎合并干燥综合征的临床特点王丹丹1,张晓岚2,邓志华1(1.山西医科大学第二医院消化内科,山西太原030001;2.河北医科大学第二医院消化内科,河北石家庄050035) 摘要:目的探讨原发性胆汁性胆管炎(P B C )合并干燥综合征(S S)的临床特点㊂方法收集山西医科大学第二医院2010年11月-2016年6月确诊为P B C 和原发性干燥综合征(pS S )的病历资料,分析患者的临床特点㊂结果 P B C 合并S S 组较单纯P B C 组女性比例高㊁病程长;P B C 合并S S 患者确诊时基线资料中肝损伤相关症状及生化指标较单纯P B C 患者轻;初诊诊断为P B C 而后期合并S S 的患者,较单纯P B C 患者初诊诊断时口干症状明显;抗S S B 抗体阳性率及发热症状在p S S 患者较合并P B C 患者多见㊂P B C 合并S S 患者和单纯P B C 患者第1年和第5年肝硬化及肝功能失代偿进展情况无差异㊂结论 P B C 合并S S 患者同时具有P B C 和p S S 的特点,但又不完全相同,二者合并发生未加速疾病进展㊂关键词:胆管炎;干燥综合征;临床特点;疾病进展中图分类号:R 575.7;R 777.2 文献标志码:A 文章编号:1004-583X (2022)01-0030-05d o i :10.3969/j.i s s n .1004-583X.2022.01.005C l i n i c a l c h a r a c t e r i s t i c o f P r i m a r y b i l i a r y c h o l a n g i t i s c o m p l i c a t i n g S j ög r e n s yn d r o m e W a n g D a n d a n 1,Z h a n g X i a o l a n 2,D e n g Zh i h u a 11.D e p a r t m e n t o f G a s t r o e n t e r o l o g y ,S e c o n d H o s p i t a l o f S h a n x iM e d i c a lU n i v e r s i t y ,T a i yu a n 030001,C h i n a ;2.D e p a r t m e n t o f G a s t r o e n t e r o l o g y ,t h eS e c o n d H o s p i t a l o f H e b e iM e d i c a lU n i v e r s i t y ,S h i j i a z h u a n g 050035,C h i n a C o r r e s p o n d i n g a u t h o r :D e n g Z h i h u a ,E m a i l :yk d z h @h o t m a i l .c o m A B S T R A C T :O b j e c t i v e T o i n v e s t i g a t e t h e c l i n i c a l c h a r a c t e r i s t i c s o f p r i m a r y b i l i a r y c h o l a n g i t i s (P B C )c o m p l i c a t i n g S j ög r e n s y n d r o m e (S S ).M e t h o d s T h e m e d i c a l r e c o r d so f p a t i e n t sd i a g n o s e d w i t h P B Ca n d p r i m a r y S j ög r e n s y n d r o m e (p S S )f r o m N o v e m b e r2010t oJ u n e2016a tS e c o n d H o s p i t a lo fS h a n x iM e d i c a lU n i v e r s i t y we r e c o l l e c t e d t o a n a l y z e t h ec l i n i c a l c h a r a c t e r i s t i c sof t h e p a t i e n t s .R e s u l t s A h igh e r p r o p o r ti o no f f e m a l e sa n da l o n ge r c o u r s e of d i s e a s ew e r e f o u n d i nP B Cc o m p l i c a t i ng S S g r o u p v e r s u sP B C -o n l yg r o u p ;l i v e r i n j u r y -r e l a t e d s y m p t o m s a n d b i o ch e mi c a l i n d i c a t o r s i nt h eb a s e l i n ed a t aw e r e m i l d e r i nP B Cc o m p l i c a t i n g S S g r o u p i nc o m p a r i s o n w i t hP B C -o n l yg r o u p d u r i n g d i a g n o s i s c o n f i r m e d ;p a t i e n t s d i a g n o s e dw i t hP B Ca t t h e i n i t i a l d i a g n o s i s a n d c o m b i n e dw i t hS S a t a l a t e r s t a g eh a d m o r ed r y m o u t hs y m p t o m st h a nt h o s eo fP B C -o n l yp a t i e n t sa tt h ei n i t i a ld i a g n o s i s ;a n t i -S S B a n t i b o d y p o s i t i v i t y r a t e a n d f e v e r s y m p t o m sw e r em o r e c o mm o n i n p a t i e n t sw i t h p S S t h a n t h o s ew i t hP B Cc o m b i n e d .T h e r ew a s n od i f f e r e n c e i nt h e p r o g r e s s i o no fc i r r h o s i sa n dh e p a t i cd e c o m p e n s a t i o nb e t w e e nP B Cc o m p l i c a t i n g SS p a t i e n t sa n d P B C -o n l yp a t i e n t s a t y e a r 1a n d5.C o n c l u s i o n A l t h o u g hP B Cc o m p l i c a t i n g SS i n p a t i e n t sh a v e c h a r a c t e r i s t i c s o f b o t h P B Ca n d p S S ,t h o s e a r e n o t i d e n t i c a l ,a n d t h e c o m b i n a t i o no f t h e t w od i s e a s e s d o e s n o t a c c e l e r a t e d i s e a s e p r o g r e s s i o n .K E Y W O R D S :c h o l a n g i t i s ;S j ög r e n s y n d r o m e ;c l i n i c a l c h a r a c t e r i s t i c ;d i s e a s e p r o gr e s s i o n 原发性胆汁性胆管炎(p r i m a r y b i l i a r yc h o l a n gi t i s ,P B C )是一种慢性㊁血清反应阳性㊁以女性多见的炎症性和胆汁淤积性肝脏疾病[1]㊂P B C 常与其他自身免疫性疾病合并,高达60%的P B C 患者存在自身免疫性肝外疾病,干燥综合征(S j ögr e n s yn d r o m e ,S S )是最常伴发的疾病之一㊂S S 是一种灶性淋巴细胞浸润唾液腺㊁泪腺等外分泌腺,导致的以口干㊁眼干为主要临床表现的慢性自身免疫性疾病㊂约1/3的S S 患者可出现全身表现[2],与多种自身免疫性疾病合并发生,而P B C 是S S 中一种最常见的自身免疫性肝病㊂P B C 与S S 合并发生时表现出不同于二者的特殊的临床和实验室特征[3-4],但仍需大规模㊁多中心研究证实㊂本研究对P B C 合并S S 患者的临床特点进行分析,以提高对疾病的认识㊂1 资料与方法1.1 病例选择选取2010年11月至2016年6月于山西医科大学第二医院就诊的符合入选及排除标准的患者㊂入选标准:P B C 的诊断采用2009年美国肝脏病学会(A A S L D )建议的诊断标准;S S 的诊断采用2002年干燥综合征国际分类(诊断)标准;P B C 合并S S 需同时满足P B C 及S S 的诊断标准㊂排除标准:排除合并病毒性肝炎㊁酒精性肝病㊁α1-抗胰蛋白㊃03㊃‘临床荟萃“ 2022年1月20日第37卷第1期 C l i n i c a l F o c u s ,J a n u a r y 20,2022,V o l 37,N o .1Copyright ©博看网. All Rights Reserved.酶缺乏症㊁自身免疫性肝炎㊁原发性硬化性胆管炎等肝外胆管梗阻及其他肝病,合并类风湿关节炎㊁系统性红斑狼疮等其他自身免疫性疾病,合并肿瘤及死亡者㊂1.2研究方法采用回顾性研究方法,通过查阅患者病历资料,收集患者的临床特点和疾病进展情况㊂按照P B C和S S的诊断标准,将收集的病例分为单纯P B C㊁原发性干燥综合征(p S S)和P B C合并S S组,其中P B C合并S S组又按照初诊诊断分为P B C*(初诊诊断为P B C)㊁S S*(初诊诊断为p S S)和P B C+ S S*(初诊诊断为P B C合并S S)组㊂收集患者一般资料,包括姓名㊁性别㊁年龄㊁病程;基线临床资料,包括临床表现和化验检查结果㊂临床表现主要包括P B C相关表现和S S相关表现;化验检查结果包括肝脏生化指标如丙氨酸氨基转移酶(A L T)㊁天门冬氨酸氨基转氨酶(A S T)㊁碱性磷酸酶(A L P)㊁γ-谷氨酰转肽酶(G G T)㊁总胆红素(T B I L)㊁白蛋白(A L B)㊁总胆固醇(T C),炎性指标如红细胞沉降率(E S R)㊁C反应蛋白(C R P),免疫指标如免疫球蛋白(I g A㊁I g G㊁I g M)㊁抗线粒体抗体(AMA)㊁抗线粒体M2亚型抗体(AMA-M2)㊁抗核抗体(A N A)㊁抗核孔膜蛋白(G P210)抗体㊁抗核体蛋白(S P100)抗体㊁抗干燥综合征A(抗S S A)抗体㊁抗干燥综合征B (抗S S B)抗体,S S相关客观检查指标如基础泪液分泌试验(S c h i r m e r试验)㊁泪膜破裂时间(B U T)㊁角膜染色㊁唾液流率㊁腮腺造影㊂1.3统计学方法应用S P S S22.0软件处理数据㊂计量资料用均数ʃ标准差(x-ʃs)表示,正态分布用t 检验,偏态分布用非参数检验㊂计数资料用例(%)表示,采用χ2检验(根据期望频数情况决定是否采用校正的χ2检验㊁F i s h e r精确概率法)㊂用K a p l a n-M e i e r方法分析肝硬化和肝功能失代偿的进展情况,进展时间的比较用L o g-r a n k检验㊂P<0.05表示差异有统计学意义㊂2结果2.1基本情况本研究共收集病例275例,其中单纯P B C52例,p S S104例,P B C合并S S119例㊂119例P B C合并S S病例中,P B C*15例,S S*12例, P B C+S S*92例㊂与单纯P B C组比较,P B C合并S S 组女性比例较高(P<0.05),且病程较长(P< 0.05),其余各组在性别㊁年龄㊁病程方面差异无统计学意义(P均>0.05)㊂P B C合并S S组腹水㊁肝硬化㊁肝功能失代偿发生率低于单纯P B C组(P均< 0.05),P B C*组肝硬化㊁肝功能失代偿发生率亦低于单纯P B C组(P<0.05),见表1㊂表1各组一般资料及基本情况比较项目P B C合并S S单纯P B C p S S P B C*S S*例数119521041512性别(男/女)2/1175/47#3/1010/150/12年龄(岁)57.15ʃ9.2058.31ʃ11.2354.54ʃ12.3856.22ʃ4.3052.00ʃ6.21病程(月)65.31ʃ74.4626.38ʃ42.75#58.87ʃ69.4042.22ʃ34.9580.22ʃ77.75 E S R(mm/h)43.01ʃ29.9045.14ʃ30.7446.62ʃ36.5841.07ʃ8.5748.08ʃ28.12 C R P(m g/d l)7.07ʃ11.5617.75ʃ27.2513.85ʃ27.0810.97ʃ4.2017.11ʃ45.15静脉曲张[例(%)]28/40(70.00)23/34(67.65)8/14(57.14)上消化道出血[例(%)]3/119(2.52)5/52(9.62)0/15(0.00)腹水[例(%)]16/95(16.84)14/41(34.15)#3/14(21.43)肝硬化[例(%)]62/119(52.10)40/52(76.92)#5/15(33.33)ә肝功能失代偿[例(%)]29/119(24.37)30/52(57.69)#3/15(20.00)ә注:与P B C合并S S组比较,#P<0.05;与单纯P B C组比较,әP<0.052.2临床特点2.2.1主要症状 P B C合并S S与单纯P B C组比较,口干㊁眼干㊁牙齿脱落㊁关节痛㊁口腔溃疡发生率较高(P均<0.05),乏力㊁瘙痒㊁黄疸㊁腹部不适㊁呕血黑便发生率较低(P均<0.05);与p S S组比较,发热症状发生率较低(P<0.05),乏力㊁黄疸㊁腹部不适㊁纳差㊁脾大发生率较高(P均<0.05)㊂P B C*与单纯P B C组比较,口干症状较突出(P<0.05);S S*与p S S组比较,主要症状差异无统计学意义(P均>0.05),见表2㊂2.2.2肝脏生化与免疫指标 P B C合并S S与单纯P B C组肝脏生化指标比较,A L T㊁A S T㊁A L P㊁G G T㊁T B I L较低(P均<0.05),而A L B较高(P<0.05);P B C合并S S与p S S组比较,A L T㊁A S T㊁A L P㊁G G T㊁TB I L㊁T C较高(P均<0.05)㊂P B C*与单纯P B C组及S S*与p S S组比较,肝脏酶学指标㊁胆红素及血脂差异无统计学意义(P均>0.05),见表3㊂㊃13㊃‘临床荟萃“2022年1月20日第37卷第1期 C l i n i c a l F o c u s,J a n u a r y20,2022,V o l37,N o.1Copyright©博看网. All Rights Reserved.P B C合并S S与单纯P B C组免疫指标比较,抗S S A抗体阳性率较高(P<0.05);P B C合并S S与p S S组比较,AMA㊁AMA-M2㊁抗G P210阳性率及I g M水平较高(P均<0.05),抗S S B抗体阳性率较低(P<0.05)㊂P B C*与单纯P B C组及S S*与p S S 组比较,免疫指标差异无统计学意义(P均>0.05),见表3㊂表2各组主要症状比较[例(%)]症状P B C合并S S单纯P B C p S S P B C*S S*口干92/119(77.31)13/52(25.00)#86/104(82.69)9/15(60.00)ә12/12(100.00)眼干60/119(50.42)6/52(11.54)#58/104(55.77)5/15(33.33)9/12(75.00)牙齿脱落32/119(26.89)2/52(3.85)#39/104(37.50)2/15(13.33)3/12(25.00)腮腺肿大4/119(3.36)1/52(1.92)6/104(5.77)1/15(6.67)1/12(8.33)关节痛44/119(36.97)5/52(9.62)#42/104(40.38)1/15(6.67)6/12(50.00)发热6/119(5.04)0/52(0.00)16/104(15.38)#1/15(6.67)0/12(0.00)口腔溃疡14/119(11.76)0/52(0.00)#10/104(9.62)1/15(6.67)2/12(16.67)雷诺现象4/119(3.36)1/52(1.92)6/104(5.77)0/15(0.00)1/12(8.33)乏力39/119(32.77)30/52(57.69)#16/104(15.38)#7/15(46.67)1/12(8.33)瘙痒17/119(14.29)17/52(32.69)#7/104(6.73)2/15(13.33)2/12(16.67)黄疸10/119(8.40)14/52(26.92)#2/104(1.92)#3/15(20.00)0/12(0.00)腹部不适22/119(18.49)17/52(32.69)#2/104(1.92)#4/15(26.67)1/12(8.33)纳差19/119(15.97)6/52(11.54)4/104(3.85)#4/15(26.67)0/12(0.00)呕血黑便2/119(1.68)6/52(11.54)#0/104(0.00)0/15(0.00)0/12(0.00)肝大3/93(3.23)1/40(2.50)1/62(1.61)0/15(0.00)0/12(0.00)脾大52/93(55.91)26/41(63.41)4/62(6.45)#4/15(26.67)0/12(0.00)注:与P B C合并S S组比较,#P<0.05;与单纯P B C组比较,әP<0.05表3各组肝脏生化和免疫指标比较项目P B C合并S S单纯P B C p S S P B C*S S*A L T(U/L)71.56ʃ66.4598.48ʃ94.11#30.35ʃ28.20#76.07ʃ10.0133.50ʃ19.83 A S T(U/L)72.75ʃ54.89117.26ʃ90.31#30.27ʃ18.31#85.07ʃ9.9532.00ʃ17.71 A L P(U/L)228.77ʃ160.33402.36ʃ263.73#76.72ʃ49.93#304.53ʃ71.1171.50ʃ20.68 G G T(U/L)237.52ʃ229.03379.63ʃ325.08#33.60ʃ44.93#207.33ʃ48.3218.75ʃ10.10 TB I L(μm o l/L)23.07ʃ20.6950.80ʃ80.11#12.25ʃ4.94#41.23ʃ29.5910.08ʃ3.18 A L B(g/L)36.97ʃ7.1032.19ʃ6.37#37.22ʃ5.0132.67ʃ3.1539.92ʃ1.56 T C(mm o l/L)5.17ʃ1.954.72ʃ1.694.41ʃ1.06#4.11ʃ0.494.42ʃ0.35 AMA[例(%)]51/69(73.91)20/32(62.50)2/33(6.06)#7/10(70.00)0/10(0.00) AMA-M2[例(%)]106/113(93.81)41/48(85.42)2/38(5.26)#14/14(100.00)0/10(0.00)抗G P210[例(%)]17/91(18.68)11/45(24.44)0/36(0.00)#3/14(21.43)0/10(0.00)抗S P100[例(%)]9/91(9.89)9/45(20.00)1/36(2.78)2/14(14.29)0/10(0.00) A N A[例(%)]93/104(89.42)30/32(93.75)86/95(90.53)7/10(70.00)9/10(90.00)抗S S A抗体[例(%)]74/102(72.55)6/32(18.75)#78/95(82.11)1/10(10.00)9/10(90.00)抗S S B抗体[例(%)]5/102(4.91)0/32(0.00)15/95(15.79)#0/10(0.00)1/10(10.00) I g G(g/L)16.03ʃ5.8215.04ʃ4.4618.21ʃ10.1814.53ʃ2.3915.45ʃ2.89 I g A(g/L)3.27ʃ1.413.36ʃ1.422.99ʃ1.343.38ʃ0.452.70ʃ0.45 I g M(g/L)3.74ʃ2.393.76ʃ1.641.49ʃ0.86#3.55ʃ0.251.42ʃ0.39注:与P B C合并S S组比较,#P<0.052.2.3 S S相关客观指标 P B C合并S S与单纯P B C组比较,S c h i r m e r试验㊁B U T㊁唾液流率及唇腺活检阳性率较高(P均<0.05),P B C合并S S与p S S 组㊁P B C*与单纯P B C组及S S*与p S S组比较,S S相关客观指标差异均无统计学意义(P均>0.05),见表4㊂2.3疾病进展情况P B C合并S S患者第1年和第5年进展至肝硬化比例为0.0%和36.5%,单纯P B C患者为8.3%和43.8%,两组差异无统计学意义(P= 0.545)㊂P B C合并S S患者第1年和第5年进展至肝功能失代偿比例为0.0%和13.2%,单纯P B C患者为0.0%和25.9%,两组差异无统计学意义(P=㊃23㊃‘临床荟萃“2022年1月20日第37卷第1期 C l i n i c a l F o c u s,J a n u a r y20,2022,V o l37,N o.1Copyright©博看网. All Rights Reserved.0.285),见图1~2㊂表4 各组相关客观指标比较项目P B C 合并S S单纯P B CpS S P B C *S S *S c h i r m e r 试验(-/+)53/3120/2#45/304/17/5B U T (-/+)20/6416/6#21/545/05/7角膜染色(-/+)82/222/073/25/012/0唾液流率(-/+)0/8414/8#2/734/10/12腮腺造影(-/+)4/12/07/20/01/1唇腺活检(-/+)5/540/20#5/773/00/12注:与P B C 合并S S 组比较,#P <0.05图1P B C 合并S S 和单纯P B C 患者进展至肝硬化的时间-进展曲线图2 P B C 合并S S 和单纯P B C 患者进展至肝功能失代偿的时间-进展曲线3 讨论P B C 和S S 具有相似的免疫学发病机制,均为自身免疫性上皮细胞炎㊂P B C 被认为是发生在肝脏的S S ,而S S 则是发生在唾液腺的P B C [5]㊂本研究显示,P B C 中S S 发病率为69.6%,据报道P B C 中S S 发病率3.5%~100%[6],发病率的差异可能归因于研究人群以及采用的诊断标准不同㊂P B C 合并S S时男女比例为2ʒ117,与单纯P B C 的5ʒ47差异有统计学意义,提示二者合并发生较单纯P B C 女性比例高,与文献报道一致[7-8]㊂P B C 相关临床特征方面,P B C 合并S S 患者确诊时基线资料中肝损伤相关症状及生化指标较单纯P B C 患者轻,P B C *较单纯P B C 患者肝硬化及肝功能失代偿发生率低,国外也有类似的研究证据[9-10],合并S S 的P B C 患者肝功能失代偿发生率㊁胆汁淤积指标低于单纯P B C 患者,提示其小胆管损伤可能较轻,这可能是由于P B C 早期症状多隐匿,多数因疾病进展至后期出现并发症时就诊,而P B C 合并S S 患者早期口㊁眼干燥症状较明显,利于在疾病早期阶段发现,强调了早期诊断对P B C 预后的重要性㊂S S 相关临床特征方面,P B C *较单纯P B C 患者口干症状明显,提示伴有口干症状的P B C 患者需尽快完善S S 相关检查,以协助诊治㊂S c h i r m e r 试验是S S 的高度特异性试验[11],所有具有S S 可疑症状的P B C 患者都应行此项检查㊂系统症状发热在p S S 较多见,而合并P B C 的S S 仅有口干㊁眼干等局部表现,缺乏系统症状㊂p S S 患者抗S S B 抗体阳性率高于P B C 合并S S 患者,可能与抗S S B 抗体特异性更高和检测方法不同有关[12]㊂疾病进展方面,P B C 合并S S 和单纯P B C 患者第1年和第5年进展至肝硬化及肝功能失代偿的比例差异无统计学意义㊂S S 一般呈慢性经过,预后相对良好,本研究显示,合并S S 并未加速P B C 进展㊂最近一项研究与我们的结论一致,即合并S S 不会影响P B C 的治疗反应和疾病转归[4]㊂然而,C h e n 等[3]开展的一项平均随访8.76年的研究显示,P B C 合并S S 较单纯P B C 患者间质性肺病和自发性细菌性腹膜炎风险高㊁总体存活率低㊂亦有研究提示,S S 合并自身免疫性肝病患者的生存率明显降低[7,13]㊂有学者提出,P B C 的预后可能主要取决于肝脏疾病的严重程度[14]㊂鉴于目前的证据均来源于单中心㊁小样本研究,尚不能明确P B C 和S S 合并发生与单发时疾病转归有无差异㊂本研究存在诸多局限性㊂首先,患者的选择存在偏倚,纳入的病例均为住院患者㊂其次,采用回顾性和描述性研究,限制了P B C 和S S 之间根本关系的探讨㊂最后,样本量较小,随访时间较短,收集的资料相对局限,结果可能存在偏差㊂参考文献:[1] G u l a m h u s e i nA F ,H i r s c h f i e l dGM.P r i m a r y b i l i a r yc h o l a n g i t i s :P a t h o g e n e s i sa n dt h e r a p e u t i co p p o r t u n i t i e s [J ].N a tR e vG a s t r o e n t e r o lH e pa t o l ,2020,17(2):93-110.[2] N o c t u r n eG ,V i r o n eA ,N g W F ,e t a l .R h e u m a t o i df a c t o r a n d d i s e a s ea c t i v i t y a r ei n d e p e n d e n t p r e d i c t o r s o fl y m p h o m ai n p r i m a r y S j ög r e n 'ss yn d r o m e [J ].A r t h r i t i sR h e u m a t o l ,2016,㊃33㊃‘临床荟萃“ 2022年1月20日第37卷第1期 C l i n i c a l F o c u s ,J a n u a r y 20,2022,V o l 37,N o .1Copyright ©博看网. All Rights Reserved.68(4):977-985.[3] C h e n C T,T s e n g Y C,Y a n g C W,e ta l.I n c r e a s e dr i s k so fs p o n t a n e o u s b a c t e r i a l p e r i t o n i t i s a n d i n t e r s t i t i a l l u n g d i s e a s e i n p r i m a r y b i l i a r y c i r r h o s i s p a t i e n t s w i t h c o n c o m i t a n t S jög r e n s y n d r o m e[J].M e d i c i n e(B a l t i m o r e),2016,95(2):e2537.[4] N i P,M e nR,S h e nM,e t a l.C o n c o m i t a n t S jög r e n's s y n d r o m ew a sn o ta s s o c i a t e d w i t h a p o o r e rr e s p o n s e o ro u t c o m e si n u r s o d e o x y c h o l i c a c i d-t r e a t e d p a t i e n t s w i t h p r i m a r y b i l i a r yc h o l a n g i t i s[J].C a n JG a s t r o e n t e r o lH e p a t o l,2019:7396870.[5]S e l m iC,G e r s h w i n M E.C h r o n i ca u t o i mm u n ee p i t h e l i t i si nS jög r e n's s y n d r o m e a n d p r i m a r y b i l i a r y c h o l a n g i t i s:Ac o m p r e h e n s i v e r e v i e w[J].R h e u m a t o l T h e r,2017,4(2):263-279.[6] F l o r e a n i A,C a z z a g o n N.P B C a n d r e l a t e d e x t r a h e p a t i cd i se a s e s[J].B e s t P r a c tR e sC l i nG a s t r o e n t e r o l,2018,34-35:49-54.[7] L i u Y,H a n K,L i u C,e ta l.C l i n i c a lc h a r a c t e r i s t i c sa n dp r o g n o s i s o f c o n c o m i t a n t p r i m a r y b i l i a r y c h o l a n g i t i s a n da u t o i mm u n e d i s e a s e s:A r e t r o s p e c t i v e s t u d y[J].C a n JG a s t r o e n t e r o lH e p a t o l,2021:5557814.[8] F l o r e a n iA,F r a n c e s c h e t I,C a z z a g o n N,e ta l.E x t r a h e p a t i ca u t o i mm u n e c o n d i t i o n s a s s o c i a t e d w i t h p r i m a r yb i l i a r yc i r r h o s i s[J].C l i nR e vA l l e r g y I mm u n o l,2015,48(2-3):192-197.[9]S u nY,Z h a n g W,L iB,e ta l.T h ec o e x i s t e n c eo fS jög r e n'ss y n d r o m e a n d p r i m a r y b i l i a r y c i r r h o s i s:A c o m p r e h e n s i v e r e v i e w[J].C l i nR e vA l l e r g y I mm u n o l,2015,48(2-3):301-315.[10]李文渊,叶超,李磊,等.原发性胆汁性胆管炎患者血清自身抗体和临床特征分析[J].实用肝脏病杂志,2020,23(4): 516-519.[11] P u r o h i t T,C a p p e l l M S.P r i m a r y b i l i a r y c i r r h o s i s:P a t h o p h y s i o l o g y,c l i n i c a l p r e s e n t a t i o na n d t h e r a p y[J].W o r l d JH e p a t o l,2015,7(7):926-941.[12] C h e n t o u f i A A,S e r o v Y A,A l a z m i M,e t a l.I mm u n ec o m p o n e n t s o f l i v e rd a m a g ea s s o c i a te d w i t hc o n n e c t i v et i s s u ed i se a s e s[J].JC l i nT r a n s lH e p a t o l,2014,2(1):37-44.[13] C h e n WQ,D a i X N,Y uY,e t a l.A n a l y s i s o f c l i n i c a l f e a t u r e sa n d p r o g n o s i s i n p a t i e n t sw i t h p r i m a r y S jög r e n's s y n d r o m e a n da u t o i mm u n e l i v e r d i s e a s e[J].B e i j i n g D aX u eX u eB a oY iX u eB a n,2020,52(5):886-891.[14] K i m K A,J e o n g S H,L e eJ I,e ta l.C l i n i c a lf e a t u r e sa n dp r o g n o s i so f p r i m a r y b i l i a r y c i r r h o s i s i n K o r e a[J].K o r e a nJH e p a t o l,2010,16(2):139-146.收稿日期:2021-10-24编辑:张卫国㊃43㊃‘临床荟萃“2022年1月20日第37卷第1期 C l i n i c a l F o c u s,J a n u a r y20,2022,V o l37,N o.1Copyright©博看网. All Rights Reserved.。

肝硬化失代偿与“再代偿”

!,-!.-!/-!肝硬化失代偿与“再代偿”何志颖，王冰琼，尤　红首都医科大学附属北京友谊医院肝病中心，国家消化系统疾病临床医学研究中心，北京１０００５０摘要：肝硬化分期评价体系从关注疾病进展规律到进一步细化急性失代偿时疾病状态分类，提出病因治疗后失代偿期肝硬化可再代偿的概念，系统补充了失代偿期肝硬化分期评价体系，其中门静脉高压、系统性炎症变化等多种因素可影响失代偿期肝硬化的临床转归。

肝硬化再代偿这一新概念的提出，需要更多的临床证据去阐明包括病毒性肝炎等在内的病因治疗后获得“再代偿”患者的临床特征及其潜在的机制。

关键词：肝硬化；失代偿；再代偿基金项目：国家自然科学基金（８２０００５６８）Ｌｉｖｅｒｃｉｒｒｈｏｓｉｓ：Ｄｅｃｏｍｐｅｎｓａｔｉｏｎａｎｄ“ｒｅｃｏｍｐｅｎｓａｔｉｏｎ”ＨＥＺｈｉｙｉｎｇ，ＷＡＮＧＢｉｎｇｑｉｏｎｇ，ＹＯＵＨｏｎｇ．（ＬｉｖｅｒＲｅｓｅａｒｃｈＣｅｎｔｅｒ，ＮａｔｉｏｎａｌＣｌｉｎｉｃａｌＲｅｓｅａｒｃｈＣｅｎｔｅｒｆｏｒＤｉｇｅｓｔｉｖｅＤｉｓｅａｓｅｓ，ＢｅｉｊｉｎｇＦｒｉｅｎｄｓｈｉｐＨｏｓｐｉｔａｌ，ＣａｐｉｔａｌＭｅｄｉｃａｌＵｎｉｖｅｒｓｉｔｙ，Ｂｅｉｊｉｎｇ１０００５０，Ｃｈｉｎａ）Ｃｏｒｒｅｓｐｏｎｄｉｎｇａｕｔｈｏｒ：ＹＯＵＨｏｎｇ，ｙｏｕｈｏｎｇｌｉｖｅｒ＠ｃｃｍｕ．ｅｄｕ．ｃｎ（ＯＲＣＩＤ：００００－０００１－９４０９－１１５８）Ａｂｓｔｒａｃｔ：Ｔｈｅｅｖｏｌｕｔｉｏｎｃｏｎｃｅｐｔｏｆｄｅｃｏｍｐｅｎｓａｔｅｄｃｉｒｒｈｏｓｉｓｒｅｂｕｉｌｄｓｔｈｅｃｌｉｎｉｃａｌｓｔａｇｉｎｇｓｙｓｔｅｍｆｏｒｄｅｃｏｍｐｅｎｓａｔｅｄｃｉｒｒｈｏｓｉｓ，ｗｈｉｃｈｃｈａｎｇｅｓｔｈｅｆｏｃｕｓｆｒｏｍｔｈｅｐａｔｔｅｒｎｏｆｄｉｓｅａｓｅｐｒｏｇｒｅｓｓｉｏｎｔｏｒｅｆｉｎｉｎｇｔｈｅｓｔａｔｕｓｏｆａｃｕｔｅｄｅｃｏｍｐｅｎｓａｔｉｏｎｏｎｓｅｔａｎｄｐｒｏｐｏｓｉｎｇ“ｒｅｃｏｍｐｅｎｓａｔｉｏｎ”ｏｆｄｅｃｏｍｐｅｎｓａｔｅｄｃｉｒｒｈｏｓｉｓ．Ｄｕｒｉｎｇｔｈｅｐｒｏｃｅｓｓ，ｆａｃｔｏｒｓｓｕｃｈａｓｐｏｒｔａｌｈｙｐｅｒｔｅｎｓｉｏｎａｎｄｓｙｓｔｅｍｉｃｉｎｆｌａｍｍａｔｏｒｙｃｈａｎｇｅｓｃａｎａｆｆｅｃｔｔｈｅｃｌｉｎｉｃａｌｏｕｔｃｏｍｅｏｆｄｅｃｏｍｐｅｎｓａｔｅｄｃｉｒｒｈｏｔｉｃｐａｔｉｅｎｔｓ．Ｓｉｇｎｉｆｉｃａｎｔｌｙ，ｍｏｒｅｅｖｉｄｅｎｃｅｉｓｗａｒｒａｎｔｅｄｔｏｅｌｕｃｉｄａｔｅｔｈｅｃｌｉｎｉｃａｌｃｈａｒａｃｔｅｒｉｓｔｉｃｓａｎｄｐｏｔｅｎｔｉａｌｍｅｃｈａｎｉｓｍｓｏｆａｃｈｉｅｖｉｎｇ“ｒｅｃｏｍｐｅｎｓａｔｉｏｎ”ａｆｔｅｒｅｔｉｏｌｏｇｙｃｏｎｔｒｏｌ，ｓｕｃｈａｓｉｎｖｉｒａｌｈｅｐａｔｉｔｉｓｐａｔｉｅｎｔｓ．Ｋｅｙｗｏｒｄｓ：ＬｉｖｅｒＣｉｒｒｈｏｓｉｓ；Ｄｅｃｏｍｐｅｎｓａｔｉｏｎ；ＲｅｃｏｍｐｅｎｓａｔｉｏｎＲｅｓｅａｒｃｈｆｕｎｄｉｎｇ：ＮａｔｉｏｎａｌＮａｔｕｒａｌＳｃｉｅｎｃｅＦｏｕｎｄａｔｉｏｎｏｆＣｈｉｎａ（８２０００５６８）ＤＯＩ：１０．３９６９／ｊ．ｉｓｓｎ．１００１－５２５６．２０２２．０５．００６收稿日期：２０２２－０３－２０；录用日期：２０２２－０４－２１通信作者：尤红，ｙｏｕｈｏｎｇｌｉｖｅｒ＠ｃｃｍｕ．ｅｄｕ．ｃｎ肝硬化是由多种病因长期、反复刺激造成肝脏炎症坏死、弥漫性肝纤维化、假小叶形成的疾病状态，由于肝小叶结构塌陷和血管结构改变等进而导致肝脏储备功能受损和门静脉高压形成［１］。

终末期肝病肝功能评估[1]

第四页，共29页。
第五页，共29页。
2002年2月27日：美国器官共享网/全美器官获取和移植网(Organ Procurement and Transplantation Network, OPTN)确定 MELD为选择肝移植患者的新标准
第六页，共29页。ቤተ መጻሕፍቲ ባይዱ
Perioperative Mortality and long-term survival after
score ≤8 (<0.01).
score
≤8 ≥9
1-Year survival (%)
89
46
3-Year survival (%)
63
34
5-Year survival (%)
51
23
The long-term survival for patients with MELD score ≥9 was significantly shorter than that for patients with MELD score ≤8 (<0.01). .
估计生存率 (%)
分组
一年
A(轻度)
90-100
B(中度)
70~80
C(重度)
40~45
第二页，共29页。
二年 85 60 35
MELD
(Model for End-stage Liver Disease) (终末期肝病模型)
MELD = 9.57 log e(creatine mg/dl) + 3.78 log e （积分） (bilirubin mg/dl) +11.20 log e (INR) + 6.4 3

核黄素结合紫外光灭活血小板细菌及膜糖蛋白的变化

核黄素结合紫外光灭活血小板细菌及膜糖蛋白的变化卫玉芝;许伟;钟涛;张循善【摘要】Aim To explore a photochemical method using riboflavin plus UV light that can inactivate selected model bacteria and to detect its membrane glycoproteins. Methods 500 μmol · L -1 riboflavin(14 ml)was added to the apheresis platelet(125 ml)blood bag,then modelbacteria(Staphylococcus epidermidis ATCC12228 and Escherichia coli ATCC25922)were added to apheresis platelet, and broadband UV light was used illuminate the blood bag, before the bacteria titer was measured. The inactivation effects of UV light plus riboflavin for bacteria was studied. The impact of a new technology for pathogen reduction based on riboflavin plus illumination at 6.2 J ·ml -1 on functional and biochemical characteristics of PLT was evaluated. Its GP CD62p and PAC-1 were detected by flow cytometry. Results With a riboflavin concentration of 50 μmol · L -1 and UV light 265 ～370 nm intensity of 6.2 J · ml -1, mode bacteria in apheresis platelet blood bag could be reduced to less than 1.22 logCFU/ml in 10 minutes. Conclusions Riboflavin plus ultraviolet light could significantly inactivate selected bacteria. Its membrane glycoproteins CD62p and PAC-1 was adequately maintained after treatment and during storage,this was not beyond accepted levels.%目的探讨核黄素光化学法灭活单采血小板污染菌的效果及其膜糖蛋白表达的变化情况.方法将14 ml浓度为500 μmol·L-1核黄素加到125 ml的单采血小板悬液中,再将一定浓度的G+菌(表皮葡萄球菌ATCC12228)和G-菌(大肠埃希氏菌ATCC25922)分别注入上述混悬液中,经(265～370 nm)广谱紫外光(6.2 J·ml-1)照射8～10 min后,测定其浓度,观察灭活效果,并用流式细胞仪检测血小板膜糖蛋白的变化情况.结果经浓度50 μmol·L-1的核黄素结合强度为6.2 J·ml-1紫外光照射8～10 min,可将一定浓度的模型菌灭活至＜1.22 logCFU/ml.结论核黄素结合紫外光照射可以有效灭活细菌,而单采血小板的CD62p、PAC-1的阳性表达率和阴性对照比较差异均无显著性.【期刊名称】《安徽医药》【年(卷),期】2011(015)001【总页数】2页(P80-81)【关键词】核黄素/药理学;光敏感药药理学;细菌灭活;膜糖蛋白【作者】卫玉芝;许伟;钟涛;张循善【作者单位】安徽医科大学第一附属医院输血科,安徽,合肥,230022;安徽医科大学第一附属医院输血科,安徽,合肥,230022;安徽医科大学第一附属医院输血科,安徽,合肥,230022;安徽医科大学第一附属医院输血科,安徽,合肥,230022【正文语种】中文血小板污染细菌的问题在我国一直没有引起足够重视，1998～2000年，美国疾控中心、美国输血协会、美国红十字会和国防部进行了一项细菌污染的研究，有104家采供血机构参加了调查，发放了单采血小板 1 804 725U以及混合血小板1 033 671 U，发生细菌污染 29例，其中 6例死亡。

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Digestive Diseases and Sciences,Vol.49,No.10(October2004),pp.1563–1568(C 2004)CASE REPORTHepatic Decompensation After Gastric Bypass Surgery for Severe ObesitySCOTT J.COTLER,MD,*JOSEPH M.VITELLO,MD,†GRACE GUZMAN,MD,‡GIULIANO TESTA,MD,§ENRICO BENEDETTI,MD,§and THOMAS YDEN,MD*KEY WORDS:gastric bypass;obesity;nonalcoholic fatty liver disease;cirrhosis;hepatic decompensation.Obesity is a pervasive and growing problem in the United States.A Centers for Disease Control and Prevention sur-vey conducted in2000estimated that20%of the U.S.pop-ulation was obese(body mass index[BMI],≥30kg/m2), up from12%in1991(1,2).The prevalence of severe obe-sity(BMI,≥40kg/m2)was2%(1).The rise in obesity has fueled an increasing demand for bariatric surgery. Jejuno-ileal bypass was performed in the late1960s through the early1980s to achieve long-term weight loss (3).The procedure was abandoned due to complications including diarrhea,electrolyte abnormalities,nephrolithi-asis,cholelithiasis,metabolic bone disease,and mortality related to acute liver failure and cirrhosis(4–6).Gastric re-striction procedures such as gastric stapling,gastric band-ing,Roux Y gastric bypass(RNY-GBP),and biliopan-creatic diversion have provided means to achieve weight loss without severe metabolic complications.Roux Y gas-tric bypass is currently the most commonly performed procedure.A study of the Swedish Obese Subjects Co-hort showed that persons who underwent RNY-GBP had a greater weight loss than those who had other gastric restriction procedures or biliopancreatic diversion(7).A number of reports have described the presence of nonalcoholic fatty liver disease(NAFLD)including cir-rhosis in liver biopsy specimens obtained at the time of bariatric surgery(8–12).Hepatic decompensation was re-ported in a patient18months after biliopancreatic di-version(13).However,limited information is available regarding whether RNY-GBP predisposes to progressive liver injury(8).We describe three patients who developed Manuscript received May20,2004;accepted June8,2004.From the*Section of Hepatology,†Division of General Surgery,‡Department of Pathology,and§Division of Transplantation Surgery, the University of Illinois at Chicago,Chicago,Illinois,USA. Address for reprint requests:Scott Cotler,MD,Section of Hepatology (MC787),840South Wood Street,Chicago,Illinois60612,USA; scotler@.hepatic decompensation after RNY-GBP with an extended Roux limb for severe obesity.CASE REPORTSSurgical Technique.Three hundred thirty-two RNY-GBP with an extended Roux limb were performed at our institution for the treatment of severe obesity between January2001and June2003.A225-cm Roux limb was used based on data show-ing superior weight loss with extended versus short Roux limbs in severely obese patients(14).According to standard proce-dure,the stomach was divided,creating a30-ml gastric pouch. The small bowel was divided approximately4ft distal to the lig-ament of Treitz and a225-cm Roux limb was created.A side-to-side jejunojejunostomy was performed to reestablish intestinal continuity.The Roux limb was brought into a retrocolic and ret-rogastric position and an anastomosis was performed to the gas-tric pouch.Three of332patients(0.9%)presented with evidence of severe hepatic dysfunction,7to17months after operation.Patient1.A34-year-old woman with a BMI of86kg/m2 underwent a RNY-GBP with an extended Roux limb.She pre-sented17months later with marked muscle wasting,weakness, fatigue,tender hepatomegaly,and anasarca.Her oral intake was limited to water and small amounts of pureed food.She had lost 128kg since her operation,or51%of her body weight.Laboratory data are listed in boratory tests for viral and autoimmune causes of chronic liver disease were neg-ative.The patient did not drink alcohol.An abdominal ultra-sound showed ascites and splenomegaly.Steatosis with steato-hepatitis and cirrhosis were present on a transjugular liver biopsy (Figures1a and1b).The right atrial-wedged hepatic vein gradi-ent was elevated,at30mm Hg.Parenteral nutrition was provided brieﬂy,followed by nasoen-teral feedings.There was a modest improvement in laboratory parameters(Table1).However,the patient’s course has been complicated by persistent ascites requiring large volume para-centesis every6to8weeks,and two episodes of spontaneous bacterial peritonitis.She is awaiting liver transplantation.Patient2.A37-year-old woman with a history of hyperten-sion and a BMI of61kg/m2underwent a RNY-GBP with an extended Roux limb.She presented7months later with jaun-dice,hepatic encephalopathy,and renal insufﬁciency.The pa-tient had a48-kg weight loss(27%of body weight)from theDigestive Diseases and Sciences,Vol.49,No.10(October2004)15630163-2116/04/1000-1563/0C 2004Springer Science+Business Media,Inc.COTLER ET AL.T ABLE1.L ABORATORY V ALUES FOR P ATIENT1Total bilirubin Direct bilirubin Total Protein Albumin BUN Creatinine Platelets (mg/dl)(mg/dl)(g/dl)(g/dl)INR AST(U/L)ALT(U/L)(mg/dl)(mg/dl)(×103/mm3) Admission 1.60.87.5 1.6 2.17421120.9916mo later0.80.2 4.8 1.6 1.4168110.6157 Note.Normal ranges:total bilirubin(0–1.2mg/dl),direct bilirubin(0–0.2mg/dl),total protein(6.0–8.0g/dl),albumin(3.6–5.0g/dl),INR(0.9–1.2), AST(10–40U/L),ALT(10–50U/L),BUN(6–20mg/dL),creatinine(0.4–1.2mg/dL),and platelets(150–400×103/mm3).No liver enzymes were available from before the time of bariatric surgery.The preoperative platelet count was253×103/mm3.time of her operation and had very limited oral intake during the weeks leading up to her admission.She had severe muscle wasting and tender hepatomegaly.Preoperative and admitting laboratories are listed in Table2.Serologic testing for viral and autoimmune hepatitis was negative.She did not drink alcohol.An abdominal CT scan demonstrated hepatosplenomegaly without ascites.There was massive steatosis and mildﬁbro-sis on a transjugular liver biopsy(Figure2).The right atrial-wedged hepatic vein gradient was elevated to25mm Hg.The patient showed clinical and biochemical improvement with med-ical management including lactulose,volume repletion,and ini-tiation of nasoenteral feedings and metronidazole(Table2).Patient3.A54-year-old woman with a history of non-insulin-dependent diabetes and hypertension and a BMI of 49kg/m2had a RNY-GBP with an extended Roux limb.She presented7months later with jaundice,hepatic encephalopathy, ascites,renal insufﬁciency,muscle wasting,and profound weak-ness.Her history was notable for a35-kg weight loss(25%of body weight).She was achieving very limited oral intake prior to her boratory data are listed in Table3.Tests for viral and autoimmune hepatitis were negative.She had no history of excessive alcohol use.A transjugular liver biopsy showed severe steatosis with steatohepatitis and cirrhosis(Figures3a and3b).The right atrial-wedged hepatic vein gradient was elevated to30mm Hg.The encephalopathy improved with lactulose and treatment of an in-fection.Nasoenteral feedings and metronidazole were started. The patient’s clinical status and laboratories improved transiently (Table3).She then presented with worsening ascites and renal failure.Cytologic evaluation of the ascitesﬂuid showed atypical cells consistent with adenocarcinoma.The patient deteriorated rapidly and died.Gastric carcinoma inﬁltrating the gastric rem-nant with peritoneal metastases was identiﬁed on postmortem examination.DISCUSSIONThe identiﬁcation of three patients who developed hep-atic decompensation after long limb RNY-GBP surgery is alarming.All three were severely obese before the opera-tion,with BMIs ranging from49to86kg/m2.Preopera-tive liver histology was not available for review,although none of the patients was noted to be grossly cirrhotic at the time of surgery.All three patients experienced precipitous weight loss and were achieving only limited oral intake prior to their presentation.They were weak and appeared malnourished,with muscle wasting.An extended,225-cm Roux limb was constructed in all cases.Gastric cancer ap-pears to have precipitated clinical deterioration in patient 3,who had biopsy proven cirrhosis and documented por-tal hypertension.Gastric cancer has been reported rarely after gastric bypass surgery for obesity(15–17).The patients reported here might have been at increased risk for progressive hepatic dysfunction after RNY-GBP due to preexisting NAFLD.In particular,it seems un-likely that patients1and3developed cirrhosis only7to 17months after surgery in the absence of preexisting liver pathology.Studies of liver biopsy specimens obtained at the time of bariatric surgery showed steatohepatitis in2 to35%of cases and bridgingﬁbrosis or cirrhosis in1to 12%of cases(9–12,18).The appearance of the liver at the time of surgery was not found to be predictive of the presence of nonalcoholic steatohepatitis(18).In one re-port,improvements in hepatic steatosis andﬁbrosis were observed with weight loss after RNY-GBP(19).How-ever,another study showed that steatohepatitis worsened in some patients with rapid weight loss after gastric re-striction procedures(20).Based on ourﬁndings and the available literature,we recommend that bariatric surgery candidates,who are known to have a high prevalence of NAFLD(9–12,18), should have a thorough evaluation for liver disease.A survey detailing outcomes in91patients found to be cir-rhotic at the time of bariatric surgery reported a periop-erative mortality rate of4%,a late death rate due to liver disease of7%,and that11%of patients were alive with progressive hepatic dysfunction(8).Another series de-tailed30patients who underwent RNY-GBP and were felt to have cirrhosis on gross inspection of the liver,al-though histologic features of cirrhosis were present in only 13(43%)cases(21).No liver-related deaths occurred,but complications including acute tubular necrosis,prolonged intubation,and need for blood transfusion were observed (21).Patients with relative thrombocytopenia suggesting the possibility of portal hypertension should be consid-ered for a preoperative liver biopsy.An intraoperative liver biopsy with evaluation of a frozen section might be con-sidered in other cases.Due to the increased risk of ce-liotomy in patients with cirrhosis and the potential for1564Digestive Diseases and Sciences,Vol.49,No.10(October2004)HEPATIC DECOMPENSATION AFTER GASTRIC BYPASSFig1.(A)A medium-power view of a liver core from patient1displays cirrhosis with extensive mixed micro-and macrovesicular steatosis involving more than50%of liver parenchyma.(Hemotoxylin and eosin stain;original magniﬁcation,×100.)(B)A high-power view of the biopsy from patient1shows microvesicularand macrovesicular steatosis with steatohepatitis(black arrow),ballooning degeneration,and Mallory hyaline(white arrow).(Hemotoxylin and eosin stain;original magniﬁcation,×400.)Digestive Diseases and Sciences,Vol.49,No.10(October2004)1565COTLER ET AL.T ABLE 2.L ABORATORY D ATA FOR P ATIENT 2Total bilirubin Direct bilirubin Total Protein Albumin BUN Creatinine Platelets Ammonia (mg/dl)(mg/dl)(g/dl)(g/dl)INR AST (U/L)ALT (U/L)(mg/dl)(mg/dl)(×103/mm 3)(µg/dl)Preoperative0.41824396Admission 13.38.15.81.5 1.91377043.11122103mo later1.62.51.56521Note.Normal ranges:total bilirubin (0–1.2mg/dl),direct bilirubin (0–0.2mg/dl),total protein (6.0–8.0g/dl),albumin (3.6–5.0g/dl),INR (0.9–1.2),AST (10–40U/L),ALT (10–50U/L),BUN (6–20mg/dl),creatinine (0.4–1.2mg/dl),platelets (150–400×103/mm 3),ammonia (<56µg/dl).progression of liver injury after RNY-GBP,we favor non-operative management of obesity in patients with precir-rhosis or cirrhosis.As demonstrated by patient 2,hepatic decompensation can also occur after RNY-GBP in the absence of cirrhosis.It is possible that the severity of steatosis or steatohepati-tis,or the use of an extended Roux limb,might predispose to progressive hepatic dysfunction after gastric bypass.We plan to use a shorter Roux limb in patients with mod-erate to severe NAFLD until prospective dataregarding Fig 2.A low-power view of a liver core from patient 2displays severe diffuse macrovesicular steatosis involving up to 95%of the liver parenchyma with focal mild ﬁbrosis.There is no signiﬁcant steatohepatitis.(Hemotoxylin and eosin stain;original magniﬁcation,×40.)risk factors for hepatic complications after RNY-GBP are available.Protein malnutrition and bacterial overgrowth have been implicated in the pathogenesis of liver disease af-ter jejunoileal bypass (22–24).Both of these factors could have contributed to the development of hepatic decompen-sation in our series.All three patients had considerable weight loss and muscle wasting and appeared malnour-ished at the time of presentation.Patients 2and 3showed substantial clinical improvement with enteral feeding and1566Digestive Diseases and Sciences,Vol.49,No.10(October 2004)HEPATIC DECOMPENSATION AFTER GASTRIC BYPASST ABLE3.L ABORATORY V ALUES FOR P ATIENT3Total bilirubin Direct bilirubin Total Protein Albumin BUN Creatinine Platelets Ammonia (mg/dl)(mg/dl)(g/dl)(g/dl)INR AST(U/L)ALT(U/L)(mg/dl)(mg/dl)(×103/mm3)(µg/dl) Admission11.7 6.9 5.9 2.7 2.0502610 1.91361112mo later0.90.47.5 1.8 1.1402727 1.13044mo later 2.70.97.9 1.9 1.5544095 4.1392Note.Normal ranges:total bilirubin(0–1.2mg/dl),direct bilirubin(0–0.2mg/dl),total protein(6.0–8.0g/dl),albumin(3.6–5.0g/dl),INR(0.9–1.2), AST(10–40U/L),ALT(10–50U/L),BUN(6–20mg/dl),creatinine(0.4–1.2mg/dl),platelets(150–400×103/mm3),ammonia(<56µg/dl).No liver enzymes were available from before the time of bariatric surgery.The preoperative platelet count was270×103/mm3.Fig3.(A)A low-power view of the liver biopsy from patient3shows cirrhosis withmacrovesicular fat replacement in up to85%of hepatic parenchyma.(Hemotoxylinand eosin stain;original magniﬁcation,×40.)(B)High-power view of liver histologyfrom patient3displays extensive mixed vesicular steatosis with ballooning degener-ation(white arrow)and steatohepatitis(black arrow).(Hemotoxylin and eosin stain;original magniﬁcation,×400.)Digestive Diseases and Sciences,Vol.49,No.10(October2004)1567COTLER ET AL.metronidazole therapy.The fact that all three patients had an extended Roux limb raises the possibility that this pro-cedure may increase the likelihood of malnutrition and bacterial overgrowth in patients undergoing RNY-GBP. Patients who develop hepatic decompensation after obesity surgery present a difﬁcult management problem. In one report,22%of patients who underwent reversal of jejuno-ileal bypass for cirrhosis died in the perioperative period(4).Consequently,we have followed a conserva-tive management strategy in our patients consisting of en-teral feeding and empiric antibiotic therapy for bacterial overgrowth.Patient1remains on the liver transplant wait-ing list.We do not plan to reverse the RNY-GBP unless graft dysfunction develops posttransplant,based on the experience with liver transplantation for cirrhosis due to jejuno-ileal bypass(5).In conclusion,the cases presented here demonstrate that hepatic decompensation can occur after RNY-GBP.A careful assessment for liver disease is indicated in can-didates for gastric bypass,based on the high prevalence of NAFLD including cirrhosis in this population.Ourﬁnd-ings raise the possibility that creation of a225-cm ex-tended Roux limb might place a subset of patients under-going RNY-GBP at risk for developing progressive hep-atic dysfunction.Further studies 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