长期饮酒对老年脑萎缩发生的影响及头颅CT特征

目的观察长期饮酒对老年脑萎缩发生的影响并分析头颅CT特征。方法接受检查或治疗的长期饮酒患者75例作为观察组;无长期饮酒史的受试者80例作为对照组。结果观察组脑萎缩发生率显著高于对照组(84.0%,63/75 vs 45.0%,36/80;χ~2=25.510,P0.001)。Logistics回归分析显示:每日饮酒次数、每日饮酒量及饮酒年限均为老年长期饮酒人群发生脑萎缩的独立危险因素(P0.05)。观察组第三脑室宽度及哈氏值显著高于对照组(P0.05);观察组侧脑室体部指数、侧脑室体部宽度指数及前角指数均显著低于对照组(P0.05)。结论长期饮酒是导致老年脑萎缩的独立危险因素,应当劝导老年酗酒者戒酒。     

酒精性肝病患者戒酒失败原因分析

目的 探讨酒精性肝病(ALD)患者戒酒失败的原因。方法 2021年2月～2022年6月我院诊治的ALD或ALD合并其他肝病男性患者149例,在初次门诊就诊时采取劝戒方法戒酒。采用酒精应用障碍筛查量表(AUDIT)调查,应用二元多因素Logistic回归分析影响戒酒失败的因素。结果 在149例ALD患者中,单纯ALD 88例,合并慢性乙型肝炎(CHB)49例,合并其他慢性肝病12例;轻症肝病27例,脂肪肝36例,酒精性肝炎14例和肝硬化/原发性肝癌72例;在随访3个月时,戒酒失败53例(35.6%),戒酒成功96例(64.4%);戒酒成功组年龄、饮酒≥30年、合并肝病和酒精依赖占比分别为(54.8±11.3)岁、56.3%、50.0%和16.7%,与戒酒失败组比[分别为(49.6±11.5)岁、28.3%、24.5%和60.4%],差异显著(P<0.05);戒酒成功组轻症肝病、脂肪肝、肝炎和肝硬化/肝癌占比分别为17.7%、15.6%、6.3%和60.4%,与戒酒失败组(分别为18.9%、39.6%、15.1%和26.4%)比,差异显著(P<0.05);二元Logistic回...     

老年慢性乙型肝炎合并酒精性肝病临床预后分析

嗜酒和肝炎病毒感染是导致慢性肝病的主要原因,临床上两者往往合并存在.老年慢性乙型活动性肝炎合并酒精性肝病预后差,危险因素明显增高,应引起重视.本文对其临床预后影响因素进行分析,报道如下. 资料与方法 一般资料 收集本院感染科与消化内科2008年1月～2012年12月诊治的老年酒精性肝病(aleoholic liver disease,ALD)患者108例,均为男性,年龄60 ～ 76岁,平均64.5 ±8.3岁.其中慢性乙型肝炎(hepatitis virus B,HBV)合并酒精性肝病患者56例(简称合并组),其余52例为单纯酒精性肝病患者(简称酒精性肝病组).     

还原型谷胱甘肽联合硫普罗宁治疗酒精性肝炎34例

自2001年11月-2004年8月,我院用还原型谷胱甘肽(GSH)联合硫普罗宁(MPG)治疗酒精性肝炎患者34例,取得了较好的疗效,现总结如下. 1 资料与方法 1.1 一般资料 68例患者的诊断符合2002年中华医学会肝脏病学分会脂肪肝和酒精性肝病学组制订的酒精性肝病诊断标准.全部为男性,平均日饮酒量＞50g.将患者随机分为两组,治疗组34例,年龄35～72岁,平均51.5岁,饮酒时间平均为10年;对照组34例,年龄36～71岁,平均52岁,饮酒时间平均为9.5年.两组患者在年龄、饮酒时间、日均摄入量、治疗前实验室指标等方面比较,差异无显著性意义,具有可比性(P＞0.05).     

全国酒精性肝病的多中心调查分析

目的对全国酒精性肝病发病情况、临床特征等进行多中心回顾研究。方法按酒精性肝病诊疗指南标准，将全国7家医院2000—2004年902例确诊为酒精性肝病患者纳入研究。回顾调查酒精性肝病患者占同期住院肝病患者的构成比，分析酒精性肝病的易感因素。结果2000-2004年,酒精性肝病患者占同期住院肝病患者的病例构成比分别为2．4％、2．7％、2．8％、3．4％和4．3％；酒精性肝病以40～49岁者居多，每日摄入乙醇量为80～159g。饮酒年限以20～29年者居多；轻症酒精性肝病101例（11．2％）。酒精性脂肪肝204例（22．6％），酒精性肝炎260例（28．8％），酒精性肝硬化337例（37．4％）。酒精性肝硬化组的饮酒量、饮酒年限与其他三组差异有统计学意义（P〈0．05）。酒精性肝病患者常见临床表现为乏力、纳差、黄疸、腹胀、腹痛等；血清学改变以天冬氨酸转氨酶、丙氨酸转氨酶、了谷氨酰转肽酶、胆红素升高为主。约19．7％患者出现乙醇相关性精神障碍表现，11．9％出现乙醇戒断综合征．10．8％有乙醇性肌病表现；乙醇性心肌和胰腺损害分别占4．6％和3．1％；0．3％有乙醇性性功能障碍表现。结论酒精性肝病占同期住院肝病患者构成比呈逐年上升趋势,肝脏损害程度与饮酒量、饮酒年限相关．长期大量饮酒可造成多器官功能受损。     

戒酒互助小组对酒精性肝病患者饮酒行为自我管理的影响

目的观察戒酒互助小组对酒精性肝病患者饮酒行为自我管理的影响.方法 79例酒精性肝病患者随即分成2组:治疗组39例,对照组40例.两组患者均给予酒精性肝病常规治疗及健康教育,治疗组在此基础上给予戒酒互助小组辅导干预,1次/wk,持续12 wk.比较干预前后酒精依赖调查量表(Michigan Alcoholism Screening Test,MAST)、动机调查问卷(Motivation Assessment Questionnaire,MAQ)、法尼亚酒精渴求量表(Pennsylvania Alcohol Craving Scale,PACS)及3 mo后的复饮率.结果最终共有75例患者完成了本研究(治疗组37例,对照组38例).干预前,两患者组各量表评分差异均无统计学意义(P0.05).干预后,治疗组MAST评分、MAQ评分、PACS评分及复饮率均较对照组明显下降(P0.01,P0.05).结论戒酒互助小组干预可明显改善酒精性肝病患者对酒精的依赖和渴求程度,降低复饮率,值得临床推广应用.     

肝癌组织中HBV感染与甲基化转移酶表达的相关性研究

目的:探讨肝癌组织中乙型肝炎病毒感染与甲基化转移酶表达的相关性。方法:以2012年1月到2017年2月在我院诊治的原发性肝癌患者178例作为研究对象,根据乙型肝炎病毒感染检出情况分为感染组78例与非感染组100例,两组患者都进行甲基化转移酶MGMT的活性检测与基因型分布PCR检测,同时进行临床资料的调查与相关性分析。结果:感染组患者MGMT活性为(3.45±1.46)U/ml,对照组患者为(5.14±1.89)U/ml,观察组明显低于对照组(t=8.341,P0.05)。178例肝癌患者中MGMT(+)基因型65例,MGMT(-)基因型113例,两组患者MGMT型分布频率比较差异有统计学意义(χ2=4.985,P0.05)。单因素分析显示肝癌患者合并乙型肝炎病毒感染主要与吸烟、MGMT活性、MGMT(+)基因型、糖尿病史等明显相关(P0.05);多因素Logistic回归分析显示吸烟、MGMT活性、MGMT(+)基因型、糖尿病史为肝癌患者合并乙型肝炎病毒感染发生的独立危险因素(P0.05)。结论:肝癌组织中乙型肝炎病毒感染比较常见,多伴随有甲基化转移酶MGMT表达活性下降,MGMT(+)基因型减少,吸烟、MGMT活性、MGMT(+)基因型、糖尿病史为肝癌患者合并乙型肝炎病毒感染发生的独立危险因素。     

饮酒对慢性乙型病毒性肝炎患者肝脏炎症和纤维化的病理影响

目的:从病理角度研究饮酒对慢性乙型病毒性肝炎(CHB)患者肝脏炎症和纤维化的影响.方法:回顾性分析84例有肝活检的患者,分为单纯饮酒组、单纯CHB组、CHB合并饮酒组.以半定量的方法分析并评价肝穿活检病理的炎症活动度、纤维化程度及脂肪变性程度.结果:在饮酒的CHB患者的病理下炎症活动度、纤维化程度及脂肪变性程度(8.73±6.93,7.67±5.34,43.58±21.80)均显著高于单纯CHB组(5.20±3.41,5.40±3.94,6.83±12.81,P均<0.05).多元线性逐步回归分析显示,每日饮酒量分别与病理下炎症活动度及脂肪变性程度的加重相关(R2=0.673,P=0.000;R2=0.559,P=0.000),每日饮酒量和累积饮酒量与病理下纤维化程度的加重相关(R2=0.650,P=0.000).结论:饮酒、尤其每日饮酒量与肝细胞损害程度有关,可明显加重CHB的病情.     

男性高血压病患者长期饮酒与阻塞性睡眠呼吸暂停综合征

目的 探讨男性高血压病患者长期饮酒与阻塞性睡眠呼吸暂停低通气综合征(OSAHS)的相关关系.方法 以男性高血压患者304例为研究对象,经标准多导睡眠呼吸监测后分为OSAHS组220例和非OSAHS对照组84例.采用回顾性问卷调查所有研究对象的饮酒史,包括饮酒种类、平均饮酒频率、平均每次饮酒量、饮酒年限等,计算平均每月饮酒量及累积饮酒量,分析长期酒精摄入与OSAHS的相关关系.结果 1)OSAHS组和非OSAHS对照组的平均每次饮酒量(白酒)、平均每月饮酒量及累积饮酒量的差异无统计学意义(P＞0.05).2)以平均每月饮酒量≥50 g定义为饮酒者,将研究对象分为饮酒组244例和非饮酒组60例,饮酒组和非饮酒组的睡眠呼吸监测参数及OSAHS患病状况的差异无统计学意义(P＞0.05).3)将所有研究对象按睡眠呼吸暂停低通气指数(AHI)水平分层,在AHI＜20次/h的样本中,均衡了年龄、体质量指数及血压等危险因素后,与非饮酒组比较,饮酒组的AHI增大、平均及最长呼吸暂停时间延长,差异有统计学意义(P＜0.05).4)进一步以累积饮酒量的中位数(108 kg)将饮酒组划分为少量饮酒组和大量饮酒组,与非饮酒组进行睡眠呼吸监测参数的比较;在AHI＜20次/h的样本中,大量饮酒组(累积饮酒量＞108 kg)的最低血氧饱和度(SaO2)、平均、最长呼吸暂停持续时间比非饮酒组明显加重,差异有统计学意义(P＜0.05);但在AHI≥20次/h的样本中比较未见上述结果.结论 在AHI＜20次/h的男性高血压患者中,长期大量饮酒与阻塞性睡眠呼吸暂停的频率、时程及缺氧程度有关.     

酒精性肝病患者肝移植后生存及再饮酒研究

目的初步明确我国酒精性肝病(alcoholic liver disease,ALD)肝移植患者术后生存及再饮酒情况,明确术前不同戒酒时间及不同类型ALD患者生存及再饮酒的差异。方法入组2016年10月至2019年10月于首都医科大学附属北京朝阳医院因ALD(包括重症酒精性肝炎、酒精性肝硬化及酒精性肝癌)首次行肝移植的36例患者。收集患者人口学指标(年龄、性别等)、移植前饮酒时间及戒酒时间、合并肝硬化并发症(食管胃底静脉曲张出血等)、合并精神疾病及是否退休等,随访患者移植后生存及再饮酒情况。根据入组患者移植前戒酒时间将其分为移植前戒酒时间≥6个月组(13例)与移植前戒酒时间6个月组(23例);根据入组患者酒精性肝病类型将其分重症酒精性肝炎组(9例)与酒精性肝硬化/肝癌组(27例)。采用Fisher检验比较各组患者的再饮酒率。采用Log-rank法比较各组患者生存情况差异。结果本研究共入组ALD相关肝移植患者36例,术后随访时间为3～41.5个月,共3例(8.3%)患者病死。随访6个月、1年及2年累积生存率分别为97.2%、91.7%与91.7%。重症酒精性肝炎组患者与酒精性肝硬化/肝癌组患者生存曲线差异无统计学意义(Log-rank χ~2=1.039,P=0.308)。移植前戒酒≥6个月组与戒酒6个月组患者累积生存情况差异无统计学意义(Log-rank χ~2=0.019,P=0.891)。36例患者累积随访至1年再饮酒率为2.8%(1/36),移植前戒酒≥6个月患者与戒酒6个月患者随访至1年的再饮酒率差异无统计学意义(0%vs 4.35%,P=1.000)。重症酒精性肝炎组患者与酒精性肝硬化/肝癌组患者再饮酒率差异无统计学意义(11.1%vs 0%,P=1.000)。结论初步证据提示ALD相关肝移植患者术后生存情况良好,暂无证据提示重症酒精性肝炎与酒精性肝硬化/肝癌患者移植前戒酒时间≥6个月与移植前戒酒时间6个月患者的生存及再饮酒有差异,需扩大队列并延长随访时间进一步验证。     

A Preliminary Study of Hepatitis B Virus Replication during Short-Term (7-Day) Social Drinking

The purpose of this study is to determine the effect of short-term social drinking on hepatitis B virus (HBV) replication as measured by serum levels of hepatitis B virus DNA (HBV-DNA). We studied five male carriers of hepatitis B e antigen who were social drinkers. Levels of HBV-DNA, blood alcohol, and aspartate aminotransferase (AST) were measured during abstinence from alcohol, before and during a test dose (29.8 g) of alcohol which followed one week of abstinence, and before and during the same test dose which followed social drinking for one week. We observed no significant changes in HBV-DNA or AST levels. These data suggest that a single one-week period of social drinking in patients with chronic HBV infection does not cause enhanced viral replication. The risks of repeated ingestion of moderate amounts of alcohol by such patients have not been established. Interpretation of our data is limited by the small number of subjects, and further studies are needed. Nevertheless, our results are consistent with published recommendations that social drinking by nonalcoholic HBV carriers should be restricted but need not be totally forbidden.     

Hepatitis B virus multiplication in the absence of usual serological markers. A study of 146 chronic alcoholics

The possible role of HBV infection in the progression of alcoholic liver disease remains debated. However, serum HBV markers in alcoholics, although present with a high frequency, mainly consist of anti-HBs and/or anti-HBc antibodies. In order to detect an HBV multiplication that could be missed by the usual markers, we looked for HBV-DNA in the serum of 146 chronic alcoholics; the results were compared with those of the usual serological HBV markers. Sixty-eight of the 146 patients could be studied for HBV-DNA both in the liver and the serum. The 146 alcoholics were divided in 48 with normal liver function (group I); 67 with non-cirrhotic alcoholic liver disease (group II); 31 with alcoholic cirrhosis (group III). Among the 146 patients, 17 had a viral multiplication reflected by serum positive HBV-DNA, as against none of 100 healthy controls (P less than 0.01). Six of the 17 had a normal liver function (6/48 = 12.5%), 7 were of group II (7/67 = 10.4%) and 4 had cirrhosis (4/31 = 12.9%). Serum HBV-DNA was associated with HBsAg in 3 occasions; in addition serum HBV-DNA was also present in 5 HBsAg-negative patients with anti-HBc and/or anti-HBs and even in 9 without any usual HBV marker. The overall prevalence of HBV markers in the 146 patients went from 30.8% to 37.0% when serum HBV-DNA was taken into account; it was similar in the 3 groups studied. Eight patients, of the 68 studied, were liver HBV-DNA-positive.(ABSTRACT TRUNCATED AT 250 WORDS)     

Long-term survival and predictors of relapse and survival after liver transplantation for alcoholic liver disease

Objective: Studies of predictive factors of alcohol recidivism and survival post-LT are not up-to-date. With evolving LT activity and with longer-term outcomes becoming increasingly available, re-evaluating post-LT outcomes is imperative. We analyzed recent data on survival, alcohol recurrence and predictive factors.

Methods: We compared long-term survival among 159 consecutive ALD patients transplanted 2003–2016 with 159 propensity-score matched controls transplanted for non-ALD. Alcohol ‘slips’ (occasional lapse) and relapse to moderate or harmful drinking were assessed from medical records and structured forms filled in by home-district physicians, and analyzed by competing-risk and multivariate Cox regression analyses.

Results: Patient and graft survival at 10 years were 75 and 69% in the ALD group and 65 and 63% in the control group (p=.06 and .36). In ALD patients, the 10-year cumulative rate of alcohol slip was 52% and of relapse, 37%. Duration of pre-LT abstinence (HR 0.97, 95% CI 0.94–0.99) and a history of prior alcohol relapses (HR 3.05, 95% CI 1.41–6.60) were significant predictors of relapse, but failed to predict death/graft loss. Patients with <6 months abstinence relapsed sooner than those with 7–24 months abstinence, but 10-year relapse rates were similar (40–50%). Ten-year relapse rate with 2–5-year pre-LT abstinence was 21%, and with >5-year abstinence, 0%. In patients with <6 months pre-LT abstinence, years of heavy drinking, prior addiction treatments, and lack of children predicted inferior survival.

Conclusions: Although 37% of our ALD patients relapsed to drinking by 10 years post-LT, 14-year survival was not significantly different from survival in non-ALD patients. Short duration of pre-LT abstinence and prior relapses predicted post-LT relapse.     

Occult hepatitis B virus infection and its clinical implications

Occult hepatitis B virus (HBV) infection is characterized by presence of HBV infection with undetectable hepatitis B surface antigen (HBsAg). Serum HBV level is usually less than 10⁴ copies/mL in these patients. Diagnosis of occult HBV infection requires sensitive HBV-DNA PCR assay. Several possibilities have been hypothesized as the mechanisms of occult HBV infection. These include: (i) mutations of HBV-DNA sequence; (ii) integration of HBV-DNA into host's chromosomes; (iii) infection of peripheral blood mononuclear cells by HBV; (iv) formation of HBV-containing immune complex; (v) altered host immune response; and (vi) interference of HBV by other viruses. The precise prevalence of occult HBV infection remains to be defined. The clinical implications of occult HBV infection involve different clinical aspects. First of all, occult HBV infection harbours potential risk of HBV transmission through blood transfusion, haemodialysis, and organ transplantation. Second, it may serve as the cause of cryptogenic liver disease, contribute to acute exacerbation of chronic hepatitis B, or even fulminant hepatitis. Third, it is associated with development of hepatocellular carcinoma. Fourth, it may affect disease progression and treatment response of chronic hepatitis C. Most of the previous studies utilized retrospective observation without control groups, and lacked direct association of occult HBV infection with specific pathological changes and disease progression. Highly sensitive, quantitative, and functional molecular analyses of HBV, combined with a well-designed prospective clinical assessment will provide the best approach for the future study of occult HBV infection.     

Lack of association between occult hepatitis B virus DNA viral load and aminotransferase levels in patients with hepatitis C virus-related chronic liver disease

BACKGROUND AND AIM: Occult hepatitis B virus (HBV) infection in hepatitis C virus (HCV)-infected patients might enhance the severity of chronic liver disease (CLD). To elucidate the correlation between occult HBV infection and the clinical course of HCV-related CLD, we evaluated whether the fluctuation of occult HBV-DNA directly affects the serum alanine aminotransferase (ALT) level. METHODS: Forty-one patients with HCV-related CLD who received regular outpatient treatment and 42 age-, sex-, and antibody to hepatitis B core antigen positivity-matched healthy volunteers were enrolled. Serum HBV-DNA was quantitatively detected using real-time detection polymerase chain reaction (RTD-PCR). Serial serum samples in three patients were measured for HBV-DNA, ALT and HCV core antigen. RESULTS: Hepatitis B virus DNA was amplified in eight of the HCV-related CLD patients (19.5%), which was significantly higher than that of healthy volunteers (2.4%). No significant difference between the genotype 1 HCV-related CLD group and the genotype 2 group was found. Based on the analyses using serial serum samples, the elevation of HBV-DNA did not occur before the ALT flares, but occurred at the same time or after the ALT flares. CONCLUSIONS: The prevalence of occult HBV infection of HCV-related CLD is significantly higher than that of control. Occult HBV infection has no influence on ALT flares among patients with HCV-related CLD.     

High viral load is a risk factor for hepatocellular carcinoma in patients with chronic hepatitis B virus infection

BACKGROUND AND AIMS: Hepatitis B virus (HBV) is considered a major risk factor for the progression to liver cirrhosis and hepatocellular carcinoma (HCC). The serum level of HBV-DNA is correlated with progression of the disease. The aim of the present study was to determine the relationship between the level of HBV-DNA and hepatocarcinogenesis in patients with chronic HBV infection. METHODS: The authors studied 73 patients who were diagnosed with chronic HBV infection at Nagasaki University Hospital (Nagasaki, Japan) between January 1980 and December 1999. The significance of age, sex, habitual drinking, serum alanine aminotransferase level, HBV viral load, interferon treatment, hepatic fibrosis and hepatic inflammation on the development of HCC were examined using univariate and multivariate analyses. RESULTS: The cumulative incidence rates of HCC were 14%, 29% and 48% at 5, 10 and 15 years after liver biopsy, respectively. Multivariate analysis identified high viral load, together with age and severe fibrosis, as independent and significant risk factors (P = 0.045, 0.047 and 0.013, respectively) for HCC. CONCLUSIONS: The present findings indicate that high viral load is a risk factor for HCC in patients with chronic HBV infection. Patients with a high HBV viral load should be carefully monitored for HCC.     

Histochemical Study of Hyaluronate in Alcoholic Liver Disease

Recently, it has been reported that serum hyaluronate (hyaluronic acid; HA) concentrations increase in various liver diseases, especially in alcoholic liver disease (ALD), and serum HA concentration has been used as a marker for hepatic fibrosis. However, it is unknown whether hepatic HA contents in ALD increase by alcohol or not. In this study, we histochemically stained HA in liver biopsy specimens obtained from ALD patients while actively drinking and after abstinence to clarify the effects of alcohol on hepatic HA contents. Liver biopsy specimens were obtained from 13 patients with ALD and 10 patients with non-ALD. In ALD patients, liver biopsy was performed twice within 3 days, and 4 to 8 weeks after abstinence when serum levels of AST and ALT normalized. HA in biopsy specimens was stained histochemically with biotinylated HA binding protein. Staining intensity of HA in liver tissue was also determined by computer-assisted imaging analyzer. HA staining was clearly observed in sinusoidal wall and fibrous regions around the portal tract and central vein in liver diseases. HA staining intensities in patients actively drinking with ALD increased markedly, compared with those in patients with non-ALD, and these intensities decreased with abstinence. These results clearly suggest that hepatic HA contents in ALD may be increased by alcohol in addition to hepatic fibrosis, and, therefore, increased HA deposition in the liver may be reversible by abstinence of alcohol.     

The Reluctance of Liver Transplant Participants with Alcoholic Liver Disease to Participate in Treatment for Their Alcohol Use Disorder: An Issue of Treatment Matching?

Liver transplantation (LT) has increased the survival for participants with end-stage alcoholic liver disease (ALD), however more than 50% of ALD transplant patients return to alcohol use after LT. Despite medical referral and a number of clinical trials of standard alcohol interventions, participants who are ALD transplant patients are reluctant to use specialist alcohol programs to support their required abstinence. The aim of this study was to identify those factors contributing to treatment reluctance by participants who are ALD transplant patients. The authors conducted a prospective case-control study comparing 40 ALD transplant patients matched for age and sex with 40 alcohol treatment seekers on a number of demographic and clinical predictors associated with treatment seeking. The authors found that lengthy abstinence and a progressive stage of change profile by participants who are ALD transplant patients contributed toward alcohol treatment being perceived as unwarranted or not needed. Furthermore, the ALD group differed significantly to those who would typically utilize alcohol treatment on a number of other clinical variables suggesting that standard alcohol interventions are not well tailored to the ALD transplant population. Two major barriers to help seeking among ALD transplant patients included the potential for stigma and limited access to alcohol services. Based on these findings, an individualized stepped-care alcohol treatment approach taking into account the clinical characteristics and needs of ALD transplant participants is required. Alcohol treatment needs to be integrated with the medical transplant program and is recommended for responsiveness to the ongoing psychological and social needs of those at risk of relapsing.     

原发性胆汁性肝硬化失代偿期的临床特征

目的了解原发性胆汁性肝硬化(PBC)失代偿期的临床特征。方法回顾性分析204例PBC患者(包括代偿期113例,失代偿期91例)的人口统计学、实验室检查、临床表现及预后模型积分等,研究失代偿期PBC的临床特征,并且与乙型肝炎肝硬化失代偿期(乙肝组,51例)、丙型肝炎肝硬化失代偿期(丙肝组,20例)、酒精性肝硬化失代偿期(ALD组,51例)患者的临床特征进行比较。统计学处理采用t检验、方差分析及χ2检验。结果 (1)PBC失代偿期患者往往高龄,血细胞计数、血脂水平、白蛋白、胆碱酯酶及凝血酶原活动度明显降低,国际标准化比值、总胆红素及直接胆红素水平显著升高,Child-Pugh分级、终末期肝病模型、Mayo等模型积分均明显升高(P<0.05)。(2)与乙肝、丙肝及ALD组失代偿期肝硬化相比,PBC失代偿期患者女性比例较多,血清碱性磷酸酶显著升高,凝血酶原时间延长较少,更常见瘙痒症状(与ALD、丙肝组相比,P<0.05),上消化道出血发生率较高(与乙肝、丙肝组相比,P<0.05),更常合并干燥综合征、骨质疏松,但肝细胞癌发生率较低。结论 PBC多发于中老年女性,与其他病因所致肝硬化失代偿期患者相比,失代偿期PBC有一些显著不同的临床特征。