失代偿期肝硬化患者并发医院内感染病原菌类别及其耐药特点分析*

目的 探讨失代偿期肝硬化患者并发医院内感染病原菌类别及耐药特点,为失代偿期肝硬化患者医院内感染的防治提供参考依据。方法 2018年1月～2020年1月我科诊治的失代偿期肝硬化患者67例,分析67例患者并发医院内感染发生情况,采用VITEK-2Compact全自动微生物分析系统鉴定感染病原菌种类,采用K-B纸片琼脂扩散法对病原菌进行药敏试验。结果 在本组67例失代偿期肝硬化患者中,发生医院内感染者24例(35.8%),其中腹腔感染占比为45.8%、肺部感染占比为33.3%和泌尿道感染占比为20.8%;感染组年龄≥60岁、消化道出血、住院时间长和Child C级占比显著高于未感染组(P＜0.05),而血清白蛋白水平和预防性应用抗生素占比显著低于未感染组(P＜0.05);Logistic回归分析发现年龄(OR=1.16,95%CI:1.09～1.24)、住院时间(OR=1.13,95%CI:1.05～1.93)、消化道出血(OR=1.50,95%CI:1.09～2.09)、血清白蛋白(OR=1.11,95%CI:1.02～1.20)、是否预防性应用抗生素(OR=1.48,95%CI:1.21～1.81)为失代偿期肝硬化患者并发医院内感染的影响因素(P＜0.05);在24例感染患者标本中培养出37株病原菌,其中革兰阴性菌21株(56.8%),革兰阳性菌11株(29.7%),真菌5株(13.5%);大肠埃希菌对氨苄西林和哌拉西林耐药率高,肺炎克雷伯菌对抗菌药物的耐药率均低于16.7%,金黄色葡萄球菌对庆大霉素的耐药率为60.0%。结论 失代偿期肝硬化患者并发医院内感染风险高,其影响因素多且复杂,病原菌分布以革兰阴性菌为主,但病原菌耐药现象明显,临床上需加强对高危感染人群的重视,必要时预防性应用敏感性抗菌药物,对减少并发医院内感染的发生尤为重要。     

乙型肝炎肝硬化患者肠道菌群变化研究*

目的 分析乙型肝炎肝硬化患者肠道菌群的分布情况及其临床意义。方法 2018年 7月～2019年4月我院收治的乙型肝炎肝硬化患者103例(代偿期肝硬化41例和失代偿期肝硬化62例)和同期健康人群20例,采集粪便,采用Illumina Miseq测序法分析肠道菌群结构差异和物种多样性。结果 在健康人,巨单胞菌属、拟杆菌属和粪杆菌属分别为14.8%、11.4%和9.8%,在代偿期肝硬化组,拟杆菌属、粪杆菌属和巨单胞菌属比例分别为15.2%、11.5%和11.2%,在失代偿期肝硬化组,拟杆菌属、粪杆菌属和韦荣球菌属比例分别为16.9%、9.6%和9.2%;健康人Chao指数为(1250.5±283.7),显著高于代偿期肝硬化组【(1111.5±277.1),P＜0.05】或失代偿期肝硬化组【(910.2±369.6),P＜0.05】,健康人Shannon指数为(3.7±0.6),显著高于代偿期肝硬化组【(3.5±0.1),P＜0.05】或失代偿期肝硬化组【(3.3±0.4),P＜0.05】,健康人Simpson指数为(0.3±0.1),显著高于代偿期肝硬化组【(0.2±0.1),P＜0.05】或失代偿期肝硬化组【(0.1±0.4),P＜0.05】。结论 乙型肝炎肝硬化患者肠道菌群丰度和多样性降低,失代偿期肝硬化患者肠道菌群变化更为明显,即存在随着病情进展肠道菌群多样性减少现象,其临床意义值得探讨。     

长期核苷(酸)类抗病毒治疗的乙型肝炎肝硬化患者肝癌发生相关因素研究

目的 探讨长期接受核苷酸抗病毒治疗的乙型肝炎肝硬化患者肝癌发生的相关危险因素。方法 2002年5月～2015年5月接受核苷(酸)类抗病毒治疗的乙型肝炎肝硬化患者417例,平均抗病毒治疗时间为(9.11±2.09)年。记录观察期内原发性肝癌发生情况。采用多元Logistics回归分析导致肝癌发生的危险因素。结果 在观察期内,本组417例乙型肝炎肝硬化患者发生原发性肝癌57例(13.7)%;肝癌组在有肝癌家族史、长期饮酒、Child-Pugh C级、未应用一线抗病毒药物、抗病毒治疗后血清HBV DNA水平仍大于20 IU/ml的比率显著高于未发生肝癌组(P<0.05);多因素Logistic分析显示存在肝癌家族史(OR=1.568,95%CI为1.074～2.289,P=0.020)、长期饮酒史(OR=1.791,95%CI为1.227～2.615,P=0.003)、Child-Pugh C级(OR=1.598,95%CI为1.095～2.333,P=0.016)、未应用一线抗病毒药物(OR=1.476,95%CI为0.997～2.168,P=0.047)和抗病毒治疗后血清HBV DNA水平仍未转阴(OR=1.480,95%CI为1.014～2.160,P=0.043)为肝癌发生的独立危险因素。结论 本研究经过长期随访观察,发现有肝癌家族史、长期饮酒、Child-Pugh分级C级、未应用一线抗病毒药物治疗和抗病毒治疗后血清HBV DNA仍大于20 IU/ml是导致乙型肝炎肝硬化患者发生肝癌的危险因素,选择一线抗病毒药物治疗、戒酒、改善肝功能状态可能减少肝癌的发生,值得认真对待。     

血清-腹水白蛋白梯度对失代偿期乙型肝炎肝硬化患者发生EVB风险的预测价值*

目的 研究血清-腹水白蛋白梯度(SAAG)预测失代偿期乙型肝炎肝硬化患者并发食管静脉曲张破裂出血(EVB)的临床价值。方法 2017年4月～2019年10月我院收治的失代偿期乙型肝炎肝硬化患者84例,根据是否发生EVB分组,计算SAAG和校正的SAAG值。采用Logistic多因素分析患者并发EVB的独立影响因素,采用受试者工作特征曲线(ROC)并计算曲线下面积(AUC)分析各指标预测EVB风险的临床价值。结果 在随访的6个月内,本组发生EVB 18例,未发生66例;EVB患者年龄≥65岁的比例为72.2%,显著大于肝硬化患者(43.9%,P<0.05);EVB患者血清白蛋白水平为(35.8±2.7)g/L,显著低于肝硬化患者【(37.7±3.3)g/L,P<0.05】,血小板计数为(52.3±10.7)×10⁹/L,显著低于肝硬化患者【(59.4±12.5)×10⁹/L,P<0.05】,部分凝血酶原时间(APTT)为(45.8±5.9)s,显著长于肝硬化患者【(41.1±7.4)s,P<0.05】,SAAG为(18.7±5.1),显著大于肝硬化患者【(16.1±4.2),P<0.05】,矫正的SAAG为(9.2±2.4),显著大于肝硬化患者【(7.6±1.8),P<0.05】;脾脏厚度为(5.2±1.3)cm,显著大于肝硬化患者【(4.5±0.8)cm,P<0.05】,门静脉血流速度为(15.2±2.9)cm/s,显著慢于肝硬化患者【(17.0±3.3)cm/s,P<0.05】;Logistic多因素分析显示血清白蛋白(OR=0.435,95%CI=0.287～0.659)、腹水白蛋白(OR=1.845,95%CI=1.063～3.202)、APTT(OR=1.469,95%CI=1.272～1.697)、MELD评分(OR=3.285,95%CI=1.697～6.359)和矫正的SAAG(OR=2.917,95%CI=1.337～6.364)是影响失代偿期乙型肝炎肝硬化患者并发EVB的独立因素(P<0.05);采用校正的SAAG和MELD预测EVB的AUC分别为0.827和0.791,其敏感度分别为0.889和0.787,特异度分别为0.636和0.612。结论 采用矫正的SAAG有助于预测失代偿期乙型肝炎肝硬化患者并发EVB的风险,因其简单,值得临床应用验证。     

肝移植术后缺血型胆道病变发生危险因素分析

目的 探讨肝移植术后缺血型胆道病变(ITBL)发生的危险因素。方法 2015年1月～2019年2月我院收治的接受肝移植术治疗患者312例,根据肝功能、胆道造影和影像学检查结果诊断术后ITBL的发生,采用单因素和多因素Logistic 回归分析。结果 本组312例接受肝移植术患者原发疾病以原发性肝癌为主(占45.8%),术后发生ITBL者37例(11.9%);经Logistic回归分析显示输入血浆的量(OR=1.2,P=0.01)、术后1周肝动脉阻力指数(RI,OR=8.9,P=0.03)、急性排斥反应(OR=7.0,P=0.02)、冷缺血时间≥11.5 h(OR=1.1,P=0.01)为影响患者发生ITBL的独立影响因素。结论 肝移植术后患者易发生ITBL,需针对诱发因素给予针对性的预防处理,以提高肝移植效果。     

乙型肝炎肝硬化患者并发急性肾损伤危险因素分析*

目的 分析探讨乙型肝炎肝硬化患者并发急性肾损伤(AKI)的危险因素。方法 2018年3月～2020年3月于我院进行治疗的乙型肝炎肝硬化患者136例,通过电子病历收集一般资料和实验室指标,根据相关标准诊断诊断并发AKI者40例,无AKI者96例。应用Logistic回归分析影响AKI发生的危险因素。结果 单因素分析结果表明,并发AKI患者失代偿期肝硬化占比为52.5%,显著高于无AKI患者的31.3%(P<0.05),腹水发生率为55.0%,显著高于无AKI患者的29.2%(P<0.05),并发肝性脑病发生率为22.5%,显著高于无AKI患者的4.2%(P<0.05),而两组性别、年龄、病程、Child-Pugh分级差异无统计学意义(P>0.05);多元Logistic回归分析结果显示肝硬化分期、腹水和并发肝性脑病是乙型肝炎肝硬化患者发生AKI的独立危险因素(P<0.05)。结论 乙型肝炎肝硬化患者发生肝功能失代偿、腹水或并发肝性脑病容易诱发AKI,临床需要行针对性的预防措施,以提高生存率。     

合并MAFLD的乙型肝炎肝硬化患者血清瘦素水平变化特点分析*

目的 探讨合并代谢相关脂肪性肝病(MAFLD)的乙型肝炎肝硬化患者血清瘦素(LP)水平变化特点。方法 在我院中法肝癌项目收集的标本库中,选择186例乙型肝炎肝硬化患者(Child-Pugh A级95例,B级51例和C级40例),在Child-Pugh A级患者中,合并MAFLD患者49例,未合并46例。采用ELISA法检测血清LP水平,采用多因素Logistic回归分析。结果 合并MAFLD的乙型肝炎肝硬化组血清甲胎蛋白(AFP)和LP水平分别为(2.1±1.3)ln ng/ml和(0.9±1.2)ng/ml,显著高于乙型肝炎肝硬化组[分别为(1.5±1.1)ln ng/ml和(0.5±1.1)ng/ml,P＜0.05];以是否合并MAFLD为因变量,进行多因素Logistic回归分析,结果最终进入模型的因素有血清LP和AFP,发现LP每增加1个单位,发生MAFLD乙型肝炎LC的风险增加2.3倍(P＜0.05,OR=2.3),而血清AFP每增加1个单位,合并MAFLD的风险增加1.8倍(P＜0.05,OR=1.8);Child-Pugh A级、B级和C级乙型肝炎肝硬化患者血清LP水平无显著性差异(P＞0.05),而三组间血清AFP水平差异显著(P＜0.05)。结论 合并MAFLD的乙型肝炎肝硬化患者血清LP水平升高,未发现血清LP水平与乙型肝炎肝硬化严重程度相关,提示乙型肝炎肝硬化患者血清LP水平升高可能与合并代谢性因素相关。     

肝细胞癌发病危险因素Logistic回归分析*

目的 探讨肝细胞癌发病的危险因素。方法 2019年1月～2021年1月青海省第四人民医院消化科和青海大学附属医院介入科确诊为肝细胞癌(HCC)患者150例,收集患者临床资料,采用Logistic回归分析法行单因素和多因素分析。结果 单因素Logistic回归分析显示,年龄、肝癌家族史、饮酒史、血小板计数、HBsAg阳性、血清HBV DNA和肝硬化等7个因素具有显著性意义,多因素Logistic回归分析显示,年龄(P=0.001,OR=1.077)、肝癌家族史(P=0.008,OR=4.351)、血小板计数异常(P=0.004,OR=9.071)、HBsAg阳性(P＜0.001,OR=16.418)、HBV DNA(P=0.004,OR=6.345)和肝硬化(P＜0.001,OR=9.315)为HCC发生的独立危险因素。结论 了解HCC发生的危险因素有助于预防,及时抗病毒和预防肝硬化的发生可能非常有意义。     

失代偿期乙型肝炎肝硬化患者尿液视黄醇结合蛋白水平及其临床意义探讨*

目的 探讨检测尿液视黄醇结合蛋白(RBP)水平诊断失代偿期乙型肝炎肝硬化患者并发急性肾损伤(AKI)的价值。方法 2015年5月～2018年5月我院救治的112例失代偿期乙型肝炎肝硬化患者和同期健康体检者35例,采用酶联免疫吸附法检测受试者尿液RBP水平,应用ROC曲线并计算曲线下面积(AUC)分析尿RBP诊断失代偿期肝硬化患者并发AKI的价值。结果 失代偿期肝硬化患者尿液RBP水平为(2.2±1.0)mg/L,显著高于对照组【(0.3±0.1)mg/L,P＜0.05】;28例重度腹水患者尿RBP、尿微量白蛋白(mAlb)和估算的肾小球滤过率(eGFR)水平分别为(3.2±0.6)mg/L、(24.9±7.7)mg/L和(58.3±13.9)mL/min/1.73 m²,其中尿RBP和尿mAlb水平均显著高于31例轻度腹水组或53例中度腹水组,而eGFR水平显著低于轻度腹水和中度腹水患者,差异有统计学意义(P＜0.05);重度腹水患者sCr水平与中度腹水组比较,差异无统计学意义【(92.8±14.0)μmol/L 对(89.8±14.4)μmol/L,P＞0.05】,但显著高于轻度腹水组【(80.4±11.9)μmol/L,P＜0.05】;单因素分析结果显示,43例继发AKI组与69例未继发AKI组在血小板计数和上消化道出血发生率方面比较,差异无统计学意义(P＞0.05),而在mAlb、eGFR、RBP、血钠、TBIL、白细胞计数、PTA、NH^3＋、肝性脑病和自发性腹膜炎方面比较,差异有统计学意义(P＜0.05);尿RBP诊断失代偿期肝硬化患者继发AKI的AUC为0.856(95%CI:0.777～0.915),对应的最佳截断点为2.6 mg/L,其诊断的敏感度和特异度分别为81.4%和84.1%。结论 尿RBP能反映失代偿期肝硬化病情的严重程度,甚至可作为继发AKI的标志物。     

血清降钙素原和C-反应蛋白水平预测肝硬化患者发生自发性细菌性腹膜炎的价值分析

目的 评估血清C-反应蛋白(CRP)和降钙素原(PCT)预测失代偿期肝硬化患者发生自发性细菌性腹膜炎(SBP)的临床价值。 方法 2014年12月～2018年6月我院住院的失代偿期肝硬化患者148例,检测血清CRP和PCT及腹水多形核细胞(PMN)计数,采用二分类Logistic回归分析和受试者工作特性曲线(ROC)下面积(AUC)分析指标诊断SBP的效能。 结果 在148例失代偿期肝硬化患者中,诊断SBP 90例,非感染性腹水患者58例;SBP患者Child-Pugh评分为(11.5±1.4),显著高于肝硬化患者,腹水PMN计数为 280.0(61.5,582.0)×10⁶/L,显著高于肝硬化患者,外周血WBC计数为(7.5±3.2)×10⁹/L,显著高于肝硬化患者,血清PCT为[3.91(1.32,9.61)ng/ml,显著高于肝硬化患者, 血清CRP为(32.0±21.7)mg/L,显著高于肝硬化患者; Logistic回归分析结果显示腹水PMN计数、血清PCT和CRP水平是失代偿期肝硬化患者发生SBP的独立危险因素(P均<0.05);腹水PMN计数、血清PCT和CRP诊断SBP敏感性分别为75.6%、73.3%和72.2%,特异性分别为68.9%、75.6%和88.9%,而以血清PCT=0.45ng/ml和CRP=12.68 mg/L为同时必须达到的标准,结果联合检测诊断SBP的敏感性为66.7%,特异性为90.0%。结论 检测腹水PMN计数及血清PCT和CRP水平有助于早期诊断失代偿期肝硬化患者并发SBP,对早期治疗有很大的益处。     

Chronic hepatitis B: a long-term retrospective cohort study of disease progression in Shanghai, China

BACKGROUND AND AIMS: The present study aimed to describe the disease progression of chronic hepatitis B patients without or with compensated cirrhosis at baseline, to estimate the risk of progression to decompensated cirrhosis, hepatocellular carcinoma and death, and to determine prognostic factors of disease progression in patients in Shanghai, China. METHODS: Stored medical records from 322 biopsy-confirmed chronic hepatitis B cases diagnosed between 1981 and 1993 were selected, and the status of patients was tracked in 1999-2000. Among consenting patients, ultrasound examination and laboratory tests were conducted. Person-year incidence rates, Kaplan-Meier analysis, log-rank tests, and Cox regression analysis were conducted. RESULTS: Among chronic hepatitis B patients without compensated cirrhosis, the incidence rates of decompensated cirrhosis, hepatocellular carcinoma, and death were 6.3, 2.8, and 7.6 per 1000 person-years, respectively, while for patients with compensated cirrhosis, the rates were 35.6, 8.2, and 35.2 per 1000 person-years, respectively. The 15-year survival rate was 88% for patients without compensated cirrhosis, compared with 56% for patients with compensated cirrhosis (P < 0.001). Cox regression analysis demonstrated that increased alpha-fetoprotein (AFP) (P < 0.01), gamma-globulin (P < 0.05), and high-level severity of hepatic fibrosis (P < 0.01) at baseline were risk factors of decompensated cirrhosis. Factors associated with a high risk of death included elevated AFP at baseline (P < 0.01), severity of hepatic fibrosis (P < 0.003), and sustained positivity for hepatitis B surface antigen (P < 0.004). CONCLUSION: Increased AFP and severity of hepatic fibrosis at baseline were associated with higher risk of decompensated cirrhosis and death. These data provide rare empirical estimates of the negative long-term outcomes for patients with chronic hepatitis B in Shanghai, China.     

恩替卡韦联合复方甘草酸苷治疗乙型肝炎肝硬化患者疗效及对肠道菌群的影响*

目的 观察恩替卡韦联合复方甘草酸苷治疗乙型肝炎肝硬化患者的疗效及对肠道菌群的影响。方法 2013年1月～2020年12月我院诊治的乙型肝炎肝硬化患者73例,采用随机数字表法将其分为对照组40例和观察组33例,分别给予恩替卡韦或恩替卡韦联合复方甘草酸苷治疗48周。采用ELISA法检测血清肿瘤坏死因子α(TNF-α)、白介素-6(IL-6)和IL-10水平,使用法国生物梅里埃公司的ATB半自动微生物鉴定系统进行细菌鉴定,使用美国GE公司 LOGIQ E9或PHILIPS EPIQ7型彩色多普勒超声诊断仪检测门静脉内径(DPV)、脾静脉内径(DSV)和脾脏厚度(SPT)。结果 在治疗48周末,观察组血清丙氨酸氨基转移酶(ALT)水平为(43.7±7.6)U/L,显著低于对照组【55.9±6.5)U/L,P<0.05】,而血清白蛋白、总胆红素和凝血酶原时间分别为(35.3±4.5)g/L、(15.2±3.6)μmol/L和(13.3±0.8)s,与对照组【分别为(34.5±4.2)g/L、17.6±2.9)μmol/L和(13.9±0.7)s】比,差异无显著意义(P>0.05);观察组血清HBV DNA水平为(1.3±0.3)lg copies/ml,与对照组的(1.4±0.4)lg copies/ml比,无显著性差异(P>0.05);观察组粪便拟杆菌和双歧杆菌数分别为(7.9±0.8)lg GFU/g和(9.3±1.5)lg GFU/g,显著高于对照组【分别为(5.5±0.6)lg GFU/g和(7.6±1.0)lg GFU/g,P<0.05】,而大肠杆菌、肠球菌和乳酸杆菌数量分别为(7.3±0.9)lg GFU/g、(7.0±1.2)lg GFU/g和(9.8±0.6)lg GFU/g,与对照组【分别为(7.9±0.7)lg GFU/g、(7.3±1.3)lg GFU/g和(9.5±0.5)lg GFU/g】比,差异无显著意义(P>0.05);观察组血清TNF-α和IL-6水平分别为(39.6±6.5)ng/L和(33.5±5.9)ng/L,显著低于对照组【分别为(48.7±7.6)ng/L和(40.6±4.3)ng/L,P<0.05】,而两组血清IL-10水平无显著性差异【(20.3±4.1)ng/L对(23.7±4.2)ng/L,P>0.05】;观察组DPV、DSV和SPT分别为(12.9±0.9)mm、(9.2±1.3)mm和(42.5±5.1)mm,与对照组【分别为(13.1±1.0)mm、(9.7±1.4)mm和(43.8±4.9)mm】比,差异无显著性意义(P>0.05)。结论 应用恩替卡韦联合复方甘草酸苷治疗乙型肝炎肝硬化患者能帮助改善肝功能,或可促进肠道菌群的恢复,值得进一步观察。     

Lamivudine treatment for decompensated cirrhosis resulting from chronic hepatitis B

The prognosis of decompensated cirrhosis resulting from chronic hepatitis B is poor, and the benefits of treatment with interferon are outweighed by serious side effects and by the risk of fatal exacerbation of disease activity. Lamivudine rapidly reduces hepatitis B virus (HBV)-DNA in serum to undetectable levels. We have treated 35 patients with chronic hepatitis B and decompensated cirrhosis with lamivudine 100 mg or 150 mg orally once daily. Pretreatment, all were positive for HBV-DNA in serum. Ten had Child-Pugh class B and 25 had Child-Pugh class C liver disease. Seven patients underwent liver transplantation within 6 months of treatment initiation, 5 patients died within 6 months, and 23 patients were treated for at least 6 months (mean = 19 months). In a majority of these 23 cases, there was a slow but marked improvement in liver function, which was most apparent after 9 months of treatment, with a decrease in serum bilirubin from 67 +/- 13 to 30 +/- 4 micromol/L (P <.05, baseline vs. 9 months), an increase in serum albumin from 27 +/- 1 to 34 +/- 1g/L (P <.05), and a decrease in Child-Pugh score from 10.3 +/- 0.4 to 7.5 +/- 0.5 (P <.05). Three patients developed resistance to lamivudine because of a mutation in the YMDD motif, but liver function did not deteriorate. We conclude that inhibition of viral replication with lamivudine results in a significant improvement of liver function in patients with decompensated HBV cirrhosis, but the long-term benefits remain uncertain.     

Risk factors for hepatocellular carcinoma in patients with liver cirrhosis.

OBJECTIVE: Although cirrhosis is known to predispose toward hepatocellular carcinoma (HCC), there is no agreement on the factors that can influence the risk for HCC in patients with cirrhosis. This study was designed to identify differences in cirrhosis-related risk factors for developing HCC in relation to epidemiological characteristics, stage of the disease and etiology. METHODS: 512 patients from southwestern Spain with Child-Pugh stage A or B cirrhosis were examined periodically by ultrasonography, and alpha-fetoprotein (AFP) concentration was measured. RESULTS: The average length of follow-up was 37 months. A total of 52 cases of HCC were detected, which represented a risk of 17% after 5 years of follow-up. The Cox model showed that the risk of HCC increased by 8% per year of increasing age. Male sex (relative risk: 3.4), hepatitis C virus infection (relative risk: 4.6), hepatitis B virus infection (relative risk: 2.9) and AFP levels higher than 15 ng/ml (relative risk: 2.5) were also shown to be risk factors. Among alcoholic patients, only age (risk increased by 15% per year), and hepatitis C virus infection (relative risk: 5.4) were risk factors for HCC. However, in patients infected by hepatitis C virus, the main risk factors were age (relative risk increased by 8% per year), male sex (relative risk: 3.9), co-infection with hepatitis B virus (relative risk: 4.9), and increased AFP (relative risk: 2.8). Of the patients with HCC, 71% were infected with hepatitis C virus. Alcoholism, Child-Pugh stage and duration of cirrhosis did not increase the risk of the appearance of HCC. CONCLUSIONS: The risk of HCC increased to 17% after 5 years of follow-up in patients with Child-Pugh stage A or B cirrhosis. Hepatitis C virus infection was the main risk factor in patients with cirrhosis. Other risk factors were age, male sex, hepatitis B virus infection and altered AFP level.     

恩替卡韦治疗失代偿期乙型肝炎肝硬化48周疗效观察

目的 观察恩替卡韦治疗失代偿期乙型肝炎肝硬化48周的疗效。方法 96例失代偿期乙型肝炎肝硬化患者被随机分为治疗组48例和对照组48例,其中治疗组给予恩替卡韦治疗48周。观察治疗前、治疗后24周和48周时的病毒学、生化学指标的变化情况。结果 患者在接受恩替卡韦治疗后24周和48周时血清HBV DNA水平小于1000 copies／ml比率分别为73．9％（34／46）和85．7％（36／42）,与对照组比较差别有显著性意义（P值分别等于0．009和0．004）;血清丙氨酸氨基转移酶复常率分别为84．8％（39146）和88．0％（37／42）,高于对照组的52．5％（21140）和44．1％（15／34）,差别有显著性意义（P值均为0．000）;Child-Pugh计分分别为8．42±2．78和8．92±2．76,较治疗前明显下降,也比对照组的10．75±3．14和11．41±2．69明显降低（P值分别为0．018和0．044）。结论 恩替卡韦治疗乙型肝炎肝硬化患者能有效地抑制病毒复制,降低HBV DNA水平,同时可以改善肝功能及Child-Pugh计分等指标。     

恩替卡韦治疗乙型肝炎失代偿期肝硬化的近期疗效观察

目的：观察恩替卡韦治疗乙型肝炎肝硬化失代偿期患者24周时的疗效。方法：乙型肝炎肝硬化失代偿期患者36例,采用恩替卡韦0.5mg/d,与32例对照组单纯支持对症治疗比较,观察24周时两组患者肝功能、Child-Pugh分级以及血清HBV DNA自基线下降的水平。结果：治疗24周时治疗组患者肝功能、Child-Pugh分级以及血清HBV DNA自基线下降的水平与对照组比较差异有显著性意义。结论：恩替卡韦能改善乙型肝炎肝硬化失代偿期患者肝功能,并能取得良好的抗病毒效果,提高生存率。     

Prevalence of hepatitis C infection and risk factors in hospitalized diabetic patients: results of a cross-sectional study

OBJECTIVES: Although there may exist a nosocomial risk of hepatitis C virus (HCV) infection in patients with type 1 or type 2 diabetes, this risk has not been fully investigated thus far and its magnitude is unknown. The aim of this multicenter cross-sectional study was to evaluate the prevalence of, and risk factors for, hepatitis C infection in consecutive hospitalized patients with diabetes and to assess the nosocomial risk and magnitude of HCV infection in these patients. PATIENTS AND METHODS: Consecutive hospitalized patients with diabetes seen in 11 French hepatogastroenterology and diabetology departments were studied. The prevalence of anti-HCV antibodies was compared with that observed in healthy blood donors and individuals seen during routine medical checkup. Diabetic patients with anti-HCV antibodies were compared with patients without anti-HCV antibodies for assessment of risk factors. RESULTS: In total 1561 patients were studied. Independent risk factors for HCV infection were assessed through multivariate analysis. Thirty-three patients (2.11%) had anti-HCV antibodies and 21 (63.70%) had HCV identified risk factors. The prevalence of HCV infection was higher in patients with diabetes than in blood donors (0.08%) or healthy controls (0.20%) (P<0.001). Multivariate analysis identified four independent risk factors for HCV infection: blood transfusion before 1991 [odds ratio (OR)=2.88, P=0.033], intravenous drug use (OR=21.37, P=0.012), treatment in a hepatogastroenterology center (OR=4.17, P=0.002) and a high number (>2) of previous admissions since the onset of diabetes (OR=2.52, P=0.039). CONCLUSION: A nosocomial source of HCV infection in hospitalized diabetic patients is suggested by the increased risk of HCV infection associated with the number of hospitalizations. This may account for at least 36% of cases of HCV infection.