拉米呋定联合苦参素治疗慢性乙型肝炎临床分析

[目的]观察拉米呋定联合苦参素治疗慢性乙型肝炎(CHB)的疗效及对慢性肝炎病毒P基因(YMDD)变异的影响。[方法]收集乙型肝炎病毒(HBV)HBeAg、HBV-DNA阳性的CHB患者106例,分为拉米呋定联合苦参素(Ⅰ)组、苦参素(Ⅱ)组、拉米呋定(Ⅲ)组。分别检测血清HBeAg、抗-HBe、HBV-DNA、肝脏生化指标和YM-DD变异。[结果]治疗12个月时,Ⅰ组HBeAg/抗-HBe转换率为44.4%,优于Ⅲ组(P<0.05),HBV-DNA阴性率及YMDD变异率较Ⅲ组低(P<0.05)。[结论]拉米呋定联合苦参素在一定程度上提高CHB疗效并可减少YM-DD变异。     

替比夫定治疗e抗原阴性的慢性乙型肝炎疗效观察

目的 探讨替比夫定治疗HBeAg阴性慢性乙型肝炎(CHB)的临床疗效.方法 52例未经抗病毒治疗的HBeAg阴性CHB患者随机分为观察组和对照组各26例,观察组口服替比夫定,600 mg/d;对照组口服拉米夫定,100 mg/d,均连续用药48周.观察两组治疗12、24和48周HBV-DNA转阴率、ALT复常率及酪氨酸一蛋氨酸一天冬氨酸一天冬氨酸(YMDD)变异情况.结果 观察组治疗12、48周时HBV-DNA阴转率及ALT复常率均明显高于对照组,P均＜0.05;观察组未检测到YMDD变异,对照组3例于治疗48周时检测到YMDD变异.结论 替比夫定治疗HBeAg阴性慢性乙型肝炎效果确切、耐药率低、安全性好,值得借鉴.     

拉米夫定治疗慢性乙型肝炎发生YMDD变异的研究

目的探讨拉米夫定治疗慢性乙型肝炎（CHB）发生YMDD变异的临床意义。方法分别用荧光定量PCR、ELISA检测72例用拉米夫定治疗的CHB患者治疗前（0个月）、治疗中（9、12、18个月）YMDD变异的情况、HBVDNA定量水平、两对半等指标。结果72例CHB患者中,拉米夫定治疗前未检查出YMDD变异,治疗9、12、18个月分别检出YMDD变异8例（11.1%）,17例（23.6%）,28例（38.9%）,随治疗时间的延长,YMDD变异率升高（P〈0.05）。另外用药前HBVDNA定量〉108copies/ml与HBVDNA定量〈108copies/ml相比YMDD变异率显著升高（P〈0.005）。HBeAg阳性组与HBeAg阴性组的患者在不同治疗时间YMDD变异率,差异无显著性（P〉0.05）。结论YMDD变异的发生随治疗时间的延长而增加。血清病毒载量可作为应用拉米夫定治疗YMDD变异产生的早期预测指标。     

拉米夫定治疗慢性乙型肝炎患者3年疗效观察

目的初步探讨LAM长期治疗HBeAg阳性和HBeAg阴性的两组慢性乙型肝炎(CHB)患者生化学、病毒学指标的变化及临床转归的差异。方法对63例诊断为CHB的患者均给予拉米夫定100mg,每日一次,进行3年的随访观察,动态检测患者的HBV血清标志物,HBV DNA,ALT、AFP、YMDD变异、B超等指标。结果拉米夫定治疗HBeAg阳性和HBeAg阴性的CHB患者3年时,HBeAg阳性组ALT复常率、HBV DNA阴转率、肝细胞癌发生率及HBsAg阴转率分别为64.7%、64.7%、0%、0%;HBeAg阴性组ALT复常率、HBV DNA阴转率、肝细胞癌发生率及HBsAg阴转率分别为70.4%、77.8%、0%、0%。两组间ALT复常率、HBV DNA阴转率、肝细胞癌发生率及HBsAg阴转率两组差异均无统计学意义(P0.05);HBeAg阳性组YMDD变异率(43.3%)显著高于HBeAg阴性组(18.2%),x2=4.720,P0.05;HBeAg阴性组肝硬化患者(37.0%)显著高于HBeAg阳性组(5.9%),x2=3.866,P0.05。结论拉米夫定治疗HBeAg阳性CHB患者较HBeAg阴性患者更容易发生YMDD变异,HBeAg阴性CHB患者较HBeAg阳性患者更易发生肝硬化。     

拉米夫定联合三甲益肝冲剂治疗慢性乙型肝炎对肝纤维化指标的影响

[目的]观察拉米夫定联合三甲益肝冲剂对慢性乙型肝炎(CHB)血清肝纤维化指标的影响.[方法]将106例CHB随机分为对照(30例)、拉米夫定(32例)、拉米夫定联合三甲益肝冲剂(44例)治疗组,疗程12个月.采用放射免疫法检测各组治疗前后血清透明质酸(HA)、层黏连蛋白(LN)、Ⅲ型前胶原(PCⅢ)、Ⅳ型胶原(Ⅳ-C)水平.[结果]拉米夫定及联合治疗组治疗后各项血清肝纤维化指标均明显下降,联合治疗组优于拉米夫定组.[结论]拉米夫定联合三甲益肝冲剂能显著降低CHB患者血清肝纤维化指标.     

单磷酸阿糖腺苷联合拉米夫定治疗慢性乙型肝炎2O例临床观察

将80例成年慢性乙型肝炎（CHB）患者随机分成Ⅰ、Ⅱ、Ⅲ、Ⅳ组各20例，分别予单磷酸阿糖腺苷（Ara-Amp）、拉米夫定（LAM）、Ara-Amp＋LAM及常规护肝药治疗。结果治疗后2a，Ⅲ组ALT复常率、HBeAg转阴率、HBV-DNA转阴率、血清转换率，显著高于Ⅳ组（P〈0．01），YMDD变异率显著低于Ⅱ组（P〈0.01）；HBeAg转阴率、血清转换率，高于Ⅰ、Ⅱ组（P〈0．05）。证实Ara-Amp联合LAM治疗CHB可以明显提高HBeAg转阴率及血清转换率，降低YMDD变异率，缩短疗程。     

拉米夫定治疗慢性乙型肝炎失败的相关因素分析

目的探讨拉米夫定治疗慢性乙型肝炎（CHB）失败的相关因素。方法回顾性分析224例拉米夫定治疗CHB患者的临床资料,根据其疗效分为失败组和成功组,比较两组年龄、性别、用药前ALT、HBV DNA水平、治疗24周后HBV DNA阴转、规则用药、HBeAg性质及HBV YMDD变异等因素。结果拉米夫定治疗失败96例,成功128例;与成功组比较,失败组治疗前ALT水平、治疗24周后HBV DNA阴转率、HBeAg阳性患者治疗中阴转和血清转换率低（P〈0.01）,治疗前HBV DNA水平和HBV YMDD变异率高,患者不规则用药（P〈0.01）,两组在年龄和性别间的差异无显著性意义（P〉0.05）。结论ALT、HBV DNA基线水平,治疗24周后HBV DNA阴转、用药规则,HBV YMDD变异及治疗后HBeAg性质改变均是影响拉米夫定治疗CHB疗效的相关因素。     

拉米夫定加肝络欣治疗慢性乙型肝炎疗效及对YMDD变异的影响

观察拉米夫定加肝络欣联合治疗慢性乙型肝炎的疗效及对慢性乙型肝炎病毒P基因(YMDD)变异的影响。收集乙型肝炎病毒(HBV)HBeAg、HBVDNA阳性的慢性乙型肝炎患者6 7例,分为拉米夫定加用肝络欣组(A组)、单用拉米夫定组(B组)。分别检测血清HBeAg、抗-HBe、HBVDNA ,肝脏生化指标和基因YMDD变异。在治疗5 6周时,拉米夫定联合肝络欣组HBeAg/抗-HBe转换率(39. 4 % ) ,优于拉米夫定组(P <0 .0 5 )。HBVDNA阳性率及YMDD变异率都比拉米夫定组低(P <0 . 0 5 )。拉米夫定联合肝络欣能在一定程度上提高治疗慢性乙型肝炎的疗效并可减少YMDD变异。     

阿德福韦治疗耐拉米夫定的慢性乙型肝炎164例疗效观察

将328例拉米夫定耐药的慢性乙型肝炎（CHB）患者随机分为观察组、对照组各164例,对照组继续使用拉米夫定并常规治疗,观察组停用拉米夫定前2个月加用阿德福韦10mg/d,疗程3个月。结果观察组肝功能、肝纤维化指标改善情况及HBeAg转阴率、HBeAg/抗-HBe转换率明显优于对照组,HBV-DNA持续保持阴性水平。证实阿德福韦治疗耐拉米夫定CHB效果确切。     

恩替卡韦联合医用臭氧治疗慢性乙型肝炎对病毒复制及肝纤维化的影响

[目的]探讨恩替卡韦(Entecavir,ETV)联合医用臭氧自血疗法(major autohaemotherapy,MAH)治疗慢性乙型肝炎(chronic hepatitis B,CHB)对病毒复制及肝纤维化的影响。[方法]选取2016年8月~2017年8月我院收治的CHB患者136例。随机分为对照组和观察组,每组各68例。对照组给予ETV口服。在此基础上,观察组加用MAH。两组均连续治疗3个月。分别于治疗前、治疗1个月、治疗3个月,采用聚合酶链反应(PCR)检测乙型肝炎病毒核酸(hepatitis B virus,HBV-DNA)定量,比较两组治疗后HBV-DNA定量下降情况。计算HBeAg血清转阴率和HBeAg血清转换率。采用酶联免疫法(ELISA)检测血清肝纤维化指标。[结果]治疗3个月,观察组HBV-DNA定量下降值,HBeAg血清转阴率和HBeAg血清转换率均高于对照组(P0.05)。且两组HBV-DNA定量下降值,HBeAg血清转阴率和HBeAg血清转换率均高于治疗1个月(P0.05)。治疗1个月和3个月,观察组血清透明质酸(LN)、层粘连蛋白(HA)、Ⅲ型前胶原肽(PⅢP))和Ⅳ型胶原(Ⅳ-C)均低于同期对照组(P0.05);治疗1个月,观察组血清LN、HA、PIIIP和Ⅳ-C均低于治疗前(P0.05);治疗3个月,两组血清LN、HA、PⅢP和Ⅳ-C均低于治疗前和治疗1个月(P0.05)。两组均未发生严重不良反应。[结论]ETV联合MAH治疗CHB,能更加持久有效地抑制HBV的复制,同时显著改善血清肝纤维化指标,且不良反应少。值得临床推广应用。     

Comparison of clinical manifestations and epidemiology between acute hepatitis A and acute hepatitis E in Taiwan

BACKGROUND AND AIMS: Acute hepatitis A (AHA) and acute hepatitis E (AHE) are endemic in developing countries. They share similar transmission routes and clinical manifestations. To compare the differences in epidemiology, clinical picture and prognosis between these two enterically transmitted forms of hepatitis, we enrolled 58 consecutive AHA or AHE patients (42 men and 16 women; age 16-74 years) from January 1990 to April 2001. RESULTS: In comparison to AHA, patients with AHE were older (56.2 +/- 15.4 vs 30.7 +/- 11.0 years, P < 0.0001), and more frequently had a history of travel within 3 months before onset of illness (68.8 vs 30.8%, P = 0.003). In laboratory data, AHE patients had lower serum levels of albumin (3.4 +/- 0.4 vs 3.8 +/- 0.4 g/dL, P = 0.016), alanine aminotransferase (1912 +/- 1587 vs 3023 +/- 1959 U/L, P = 0.015), and aspartate aminotransferase (1681 +/- 1444 vs 2374 +/- 2869 U/L, P = 0.24), but a higher serum bilirubin level (17.8 +/- 12.3 vs 8.7 +/- 5.0 mg/dL, P = 0.003) than AHA patients. Moreover, five (15.6%) patients with AHE compared with none with AHA died. This probably indicates that AHE had a worse outcome than AHA in our study. In analysis of epidemiological factors, older age of onset of illness was the only significant predicator of outcome. From an epidemiological survey, most AHE patients were imported while most AHA patients were not. However, native AHE and imported AHA did occur in Taiwan. CONCLUSION: Patients with AHE in Taiwan had older age of onset, more records of traveling history, and poorer clinical manifestations than those with AHA, and age seemed to be the most important factor to influence outcome.     

Viral hepatitis and the surgeon

BACKGROUND: Viral hepatitis is an infection of the liver caused by one or more of six known (HAV-HGV) hepatotropic viruses. It is a common problem among health care workers and their patients. Surgeons are at particular risk of both acquiring and transmitting some of these viruses from and to their patients. Unfortunately, specific immunoprophylaxis for viral hepatitis is presently limited to protecting against the spread of hepatitis A and B viral infections, leaving a high degree of vigilance and careful surgical technique as the only means available to prevent the transmission of other viruses relative to the surgeon. The purpose of this paper is to review the various forms of viral hepatitis including the nature of the virus, serologic testing, clinical features, epidemiology (with specific reference to those issues that arise in surgical practice), treatment and prevention.     

The medical impact of hepatitis D virus infection in Asia and Africa; time for a reappraisal

Although hepatitis D is believed to be an important medical problem in Africa and many areas of Asia, the geographical distribution and prevalence rates of infection with the hepatitis D virus (HDV) vary considerably, are often inconsistent and sometimes conflicting. Discrepancies may depend on methodological problems, primarily on different modalities of patients' recruitment; these are analysed in this mini‐review, in order to provide a uniform clinical approach when testing patients with chronic HDV disease.     

Detection of HBV core promoter and precore mutations helps distinguish flares of chronic hepatitis from acute hepatitis B

Background and Aim: Acute exacerbation of chronic hepatitis B has to be distinguished from acute hepatitis, because treatment strategies differ between them. Methods: Mutations in the core promoter and precore region of hepatitis B virus (HBV) were determined in 36 patients with acute exacerbation of chronic hepatitis B, in whom alanine aminotransferase (ALT) increased above 500 IU/L, as well as the 36 patients with acute hepatitis. Results: Mutations in the core promoter (A1762T/G1764A) and precore region (G1896A) were more frequent in patients with acute exacerbation of chronic hepatitis than acute hepatitis (81% vs 19%; P < 0.0001 and 58% vs 6%; P < 0.0001, respectively). Of the 19 patients with mutations in both the core promoter and precore region, 17 (89%) had acute exacerbation of chronic hepatitis. In contrast, among the 32 patients with the wild‐type for both the core promoter and precore region, 29 (89%) developed acute hepatitis. By multivariate analysis, the double mutation in the core promoter was predictive of acute exacerbation in chronic hepatitis with the highest odds ratio at 26.4. Conclusions: In patients with hepatitis B having ALT levels >500 IU/L, mutations in the core promoter and precore region are useful in distinguishing acute exacerbation of chronic from acute HBV infection. Detection of these mutations would be useful for commencing prompt antiviral treatments on patients with acute exacerbation of chronic hepatitis for a better prognosis.     

HBV感染者HCV的重叠感染关系研究

目的 研究HBV感染患者中HCV的重叠感染状况及其相互关系。 方法 采用ELISA法对767例HBV感染患者同步检测HBV和HCV血清标志物,对可疑HCV感染但抗HCV阴性和/或抗-HCV阳性患者血清,采用PCR法检测HCV-RNA。 结果 HCV重叠感染率为4.82％,且在各类乙肝患者中存在非常显著差异(P<0.01);HBV/HCV感染组重症肝炎的发生率显著高于非HCV感染组(P<0.01);HBV/HCV感染组HBsAg阳性率显著低于单纯HBV感染组(P<0.05);HBV/HCV感染组HCV-RNA阳性率显著低于单纯HCV感染组(P<0.05)。 结论 HCV重叠感染与乙肝患者的发病、病情加重及重症肝炎的发生相关;HCV可抑制或中止HBsAg携带状态,但这种作用远不如对病情的加重作用重要;同时HBV对HCV的复制亦存在抑制作用。     

316例慢性未定型肝炎临床与病理研究

探讨慢性未定型肝炎临床与病理特征，采用多种血清学及组织学方法研究316例慢性未定型肝炎。并以同期的慢性乙型肝炎及慢性丙型肝炎作为对照。慢性未定型肝炎具有以下临床及病理特征。1、青年男性发病居多，无输血及输血制品史，无季节性及家庭聚集性。2、起病隐袭，无明显急性过程，肝病症状及体征少而轻。3、血清ALT呈轻、中度升高，且反复波动，4、肝组织炎症改变较轻，退行变明显，不同程度脂肪变性较为突出，该型肝炎可能系一种或一种以上未知肝炎病毒感染所致。     

缺血性肝炎的生化和病理特点分析

目的探讨缺血性肝炎的生化和病理特点以及二者之间的关系,提高对该病的诊断水平。方法回顾性分析45例缺血性肝炎,并对9例缺血性肝炎患者行肝穿刺组织病理检查。结果缺血性肝炎患者ALT、AST、LDH明显升高,TBil、γ-GT、AKP多在正常范围内。随着肝脏缺血时间延长各项指标呈升高趋势,肝缺血时间6~12 h及〉12 h患者明显高于〈6 h患者,差异具有统计学意义。随着住院时间延长各项指标与入院当时相比明显下降,差异具有统计学意义。心脏源性缺血性肝炎与失血性低血容量性缺血性肝炎患者相比,LDH水平明显升高。不同病理分级患者生化变化差异无统计学意义。缺血性肝炎患者肝组织变化轻微,多为肝小叶中央轻-中度间质炎症。患者多死于原发病而非缺血性肝炎。结论缺血性肝炎患者生化变化明显,而组织变化轻微,显示出二者的不一致性。组织学的变化特点以及缺血性肝炎病因恰能更好的解释生化变化及其预后特点。从病理上,缺血性肝炎患者预后取决于原发病而非休克肝;积极治疗原发病,改善肝脏微循环是抢救成功的关键。     

Sequence variability of hepatitis C virus and its clinical relevance

SUMMARY. Chronic type C hepatitis is a potentially serious disease that can lead to cirrhosis and hepatocelluler carcinoma. This complex disease is caused by the hepatitis C virus (HCV), a positive sense, single-stranded RNA virus. HCV has been assigned to a separate genus within the Flaviviridae, and shares a close relationship to the pestiviruses. Nucleotide sequence variation has been observed in genomes amplified from serum of patients with HCV infection, and cloning of RNA amplified from patients infected with HCV has confirmed the heterogeneity of the agent responsible for post-transfusion and sporadic hepatitis C. The variability of HCV is structured in a way that immediately suggests a two tiered classification: this nomenclature comprises 'types' corresponding to the major branches in a phylogenetic tree of sequences from genomic or subgenomic regions of the genome, and 'subtypes', corresponding to the more closely related sequences within some of the major groups. This genotyping designation has provided an epidemiological tool for studying geographical differences in hepatitis C infection. Clearly discernible patterns of genotype distribution have been found in those countries that have been studied so far. In many European countries genotype distributions vary with the age of patients, reflecting rapid changes in genotype distribution with time within a single geographical area. Unfortunately we know very little about modes of transmission within different communities. There is considerable interest in the clinical significance of different HCV genotypes, and the intriguing question of whether these differences may affect the spectrum of the disease associated with hepatitis C. These data also have implications for diagnosis and treatment of acute and chronic hepatitis C. A uniform typing scheme and nomenclature will facilitate our understanding of the disease caused by this virus worldwide.     

Comparison of clinical, virologic and pathologic features in patients with acute hepatitis B and C

BACKGROUND AND AIMS: The clinical outcomes of adult-acquired acute infection of hepatitis C virus (HCV) and hepatitis B virus (HBV) are quite different. In order to compare the clinical, biochemical, virologic and pathologic pictures in these two groups of patients, we enrolled 22 adult patients with acute hepatitis C and 16 adult patients with acute hepatitis B, on whom liver biopsies were performed within 3 months of acute onset of the illness. RESULTS: The results showed that a significantly younger age, a higher ratio of the clinical symptoms of jaundice, nausea, vomiting, and poor appetite, a higher mean serum level of alanine transaminase, aspartate transaminase, and total bilirubin were present in patients with acute hepatitis B patients than in those with acute hepatitis C (P < 0.05). There was a significantly higher degree of periportal inflammation and total necro-inflammatory activity in the acute hepatitis B patients (P = 0.002 and 0.049, respectively). Fifteen (68.2%) of the 22 patients with acute hepatitis C had detectable serum HCV-RNA, but only two (14.3%) of the 14 tested patients with acute hepatitis B had detectable serum HBV-DNA, detected by using the branched DNA signal amplification assay. Eighteen (82%) of the 22 acute hepatitis C patients and none of the 16 acute hepatitis B patients progressed into a chronic hepatitis stage (P < 0.001). CONCLUSION: The manifestations of mild clinical symptoms, lower mean serum transaminases and bilirubin levels, a lesser degree of histological periportal necroinflammation, and more patients with a high circulatory viral load among the acute hepatitis C patients, may lead to more of that group developing chronicity than patients with acute hepatitis B.