sVAP-1在慢性乙型肝炎患者血清中的表达水平及临床意义

目的探讨慢性乙型肝炎患者血清可溶性血管黏附蛋白-1(sVAP-1)的表达水平及临床意义。方法选择2018年1月至2019年1月沧州市人民医院收治的96例慢性乙型肝炎患者作为研究对象,将患者分为乙型肝炎病毒(HBV) DNA阳性组60例和HBV DNA阴性组36例,另选择50名同期健康体检者作为正常对照组。对比各组血清sVAP-1的表达水平,分析血清sVAP-1的表达水平与HBV DNA及肝脏炎性反应的关系。结果血清sVAP-1在慢性乙型肝炎组中的表达水平显著高于对照组,在慢性乙型肝炎HBV DNA阳性组中的表达水平显著高于HBV DNA阴性组,差异均有统计学意义(P均0.05)。HBV DNA阳性组中丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、总胆红素(TBil)水平显著高于HBV DNA阴性组,白蛋白(Alb)水平显著低于HBV DNA阴性组(P0.05)。sVAP-1水平与HBV DNA、ALT、AST、TBil水平呈正相关(P0.05),与Alb水平呈负相关(P0.05)。结论 sVAP-1在慢性乙型肝炎患者血清中的表达水平升高,且其与HBV DNA水平及肝脏炎性损伤有关。     

乙型肝炎后肝硬化患者血浆降钙素原与肝组织HBcAg表达的关系

目的　探讨乙型肝炎后肝硬化患者血浆降钙素原 (PCT)与肝组织HBcAg表达的关系。方法　应用免疫发光法测定 5 2例乙型肝炎后肝硬化患者血浆PCT水平 ,免疫组化S P法检测肝组织HBcAg的表达 ,并与肝组织病理结果比较。 结果　随肝组织损伤程度加重 ,血浆PCT水平及肝组织HBcAg的表达程度逐渐增加。HBcAg表达阳性组血浆PCT水平显著高于HBcAg表达阴性组。浆型表达组显著高于核型表达组 (P值均 <0 .0 1)。结论　乙型肝炎后肝硬化患者血浆PCT水平变化与肝组织HBcAg的表达程度及分布类型密切相关 ,它们在致肝组织病变持续加重过程中均具有重要作用     

HBsAg水平在慢性HBV感染者疾病进展中的动态监测价值

目的探讨HBsAg水平在慢性HBV感染者疾病进展监测中的临床价值。方法收集2011年5月-2015年12月在安徽医科大学第二附属医院门诊及住院时未进行抗病毒治疗的1107例不同临床阶段的慢性HBV感染者的临床资料,并根据疾病状态分为HBeAg阳性慢性乙型肝炎组(HBeAg阳性CHB组,n=356)、HBeAg阴性慢性乙型肝炎组(HBeAg阴性CHB组,n=264)、乙型肝炎肝硬化代偿期组(LC-C组,n=116)、乙型肝炎肝硬化失代偿期组(LC-D组,n=201)、原发性肝癌组(PLC组,n=170),比较不同临床阶段患者之间HBsAg表达水平的差异及HBsAg水平与临床特征的相关性。计量资料多组间比较采用方差分析,进一步两两比较采用LSD-t检验;两组间比较采用t检验。计数资料组间比较采用χ2检验。相关性分析采用Pearson检验。结果HBeAg阳性CHB组、HBeAg阴性CHB组、LC-C组、LC-D组、PLC组之间患者血清HBsAg、HBV DNA水平比较,差异均有统计学意义(F值分别为100.45、86.26,P值均0.001)。502例HBeAg阳性患者的HBsAg、HBV DNA水平均高于605例HBeAg阴性患者(t值分别为16.67、16.22,P值均0.001)。HBeAg阳性值均CHB、LC-C、LC-D和PLC 4组间HBsAg和HBV DNA水平差异均有统计学意义(F值分别为42.92、27.38,P值均0.001);HBeAg阴性的CHB、LC-C、LC-D和PLC 4组间的HBsAg和HBV DNA水平差异亦均有统计学意义(F值分别为6.04、4.10,P值均0.05)。不同HBsAg水平(1000 IU/ml、1000~20 000 IU/ml、20 000 IU/ml)患者间HBV DNA水平差异有统计学意义(F=189.51,P0.001)。HBeAg阳性CHB组、HBeAg阴性CHB组、LC-C组、LC-D组患者血清HBsAg水平与HBV DNA水平均呈正相关(r值分别为0.554、0.501、0.320、0.432,P值均0.001)。结论 HBsAg定量水平随疾病进展而逐步降低,且HBsAg与HBV DNA水平密切相关,动态监测HBsAg变化有助于发现HBV感染后疾病进展情况。     

HBeAg阴性慢性乙型肝炎的临床特点

20 0 1年 1月～ 2 0 0 1年 6月 ,我院收治慢性乙型肝炎患者3 5 1例。本文重点分析 HBe Ag阴性慢乙肝患者的临床特点 ,并与 HBe Ag阳性患者进行比较。资料分析 :本组 3 5 1例慢乙肝均符合 2 0 0 0年 (西安 )全国传染病与寄生虫病会议修订的诊断标准。入选标准 :1明确诊断为慢性乙型肝炎 ;2第一次入院 ;3 HBs Ag与 HBV DNA皆阳性 ;4排除其它原因导致的肝损害及肝硬化 ;5未用抗病毒药物及免疫调节剂。其中 HBe Ag阳性 2 5 6例 ,阴性 95例(占 2 7.0 6% )。两组临床资料比较见表 1。HBe Ag阴性慢乙肝患者第一次住院的年龄明显高于 HBe …     

慢性乙型肝炎患者幽门螺杆菌感染的调查分析

目的探讨慢性乙型肝炎患者幽门螺杆菌(H.pylori)的感染情况及其临床意义。方法将167例慢性乙型肝炎患者分为肝炎组、肝硬化组、肝癌组,研究H.pylori感染状况与76例健康对照者的关系,并进一步分析H.pylori感染与肝功能、临床并发症的关系。结果慢性乙型肝炎患者H.pylori感染率为64.1%,明显高于健康对照组34.2%(P<0.01)。其中肝硬化组71.8%和肝癌组75.0%又高于肝炎组51.5%(P<0.05)。H.pylori阳性患者肝性脑病、上消化道出血及ALT水平高于H.pylori阴性患者(P<0.05),H.pylori阳性和H.pylori阴性患者的腹水并发症及TBIL差异无统计学意义(P>0.05)。结论慢性乙型肝炎患者H.pylori感染率显著增加,且H.pylori感染可能加重肝病病程。     

31例HBsAg阴性慢性乙型肝炎患者的临床及病理分析

目的了解HBsAg阴性慢性乙型肝炎(隐匿性乙型肝炎)患者的发病情况、临床和病理特点以及可能的发病机制。方法对31例反复肝功能异常、HBsAg阴性HBV感染患者进行临床、肝组织病理及免疫组化分析;采用荧光定量PCR方法对血清HBVDNA进行定量分析,以免疫组化法检测肝组织内HbsAg和HBcAg的表达,按慢性肝炎病理诊断标准进行分级(G)及分期(S)。结果31例HBsAg阴性慢性乙型肝炎患者中,18例肝组织病理和免疫组化检测证实为慢性乙型肝炎,其中7例诊断为肝炎后肝硬化;18例肝组织学检查HBsAg阳性2例,HBcAg阳性16例;病理分级、分期G4S4有7例,G1-3、S2-3有11例。结论HBsAg阴性HBV感染仍是我国原因不明肝病的主要原因之一,低水平HBV感染可导致慢性肝炎,甚至肝硬化或肝癌。     

血管内皮生长因子在胃癌中表达及其预后意义

目的研究血管内皮生长因子(VEGF)在胃癌组织中表达的临床意义.方法应用抗 VEGF 多克隆抗体的免疫组织化学方法,观察 VEGF 在胃癌组织中的表达,分析 VEGF 表达与不同监床病理因素及预后之间关系.结果 128例胃癌 VEGF 阳性表达率为64.1%;Ⅲ、Ⅳ期病人 VEGF 阳性表达率明显高于Ⅰ期患者(P<0.05);VEGF 阳性表达率与肿瘤的生长方式、浸润深度及淋巴线转移关系之间有显著统计学意义,肿瘤呈浸润型生长(71.8%)或浸及浆膜者(73.5%)明显大于膨胀型生长(52.0%)或无浆膜浸润者(53.3%)(P<0.025),淋巴结转移阳性肿瘤(75.0%)明显大于无淋巴结转移者(50.0%)(P<0.05);此外,在86例术后随访患者中,VEGF 阳性表达肿瘤患者的术后5年生存率明显低于 VEGF 阴性表达肿瘤患者(P<0.05).     

血管内皮细胞生长因子与乙型肝炎病变的关系

目的研究血管内皮细胞生长因子（vascularendothelialgrowthfactor,VEGF）与乙型肝炎(乙肝)分级(G)和分期(S)的关系。方法250例乙肝患者肝活检标本用VEGF单克隆抗体进行免疫组织化学(S-P法)染色。结果VEGF在肝组织表达有胞浆型、膜窦型及窦内皮细胞型;VEGF主要由肝细胞分泌,其次在肝窦内皮细胞、贮脂细胞、成肌纤维细胞及单核细胞也示阳性。无明显病变的血管内皮细胞及肝细胞VEGF染色阴性。提示随分级增高VEGF表达增强,其间差异有极显著意义（χ     

重型乙型病毒性肝炎肝内ICAM-1 mRNA表达

目的探讨细胞间粘附分子-1(ICAM-1)mRNA在重型乙型肝炎肝内的表达水平及其意义。方法用原位杂交技术检测11例正常人,5例慢性无症状HBsAg携带者(AsC)、15例慢性乙型肝炎和30例重型乙型肝炎患者肝内ICAM-1 mRNA原位表达。结果正常人和AsC肝细胞无ICAM-1 mRNA表达;重型乙型肝炎患者肝细胞ICAM-1 mRNA表达明显增强,其表达水平显著高于慢性乙型肝炎。结论ICAM-1在重型乙型肝炎肝坏死中起重要作用。     

乙肝患者体内HBV复制与肝损伤的相关性探讨

目的 探讨乙型肝炎(乙肝)患者体内病毒复制与肝损伤的关系.方法 取400份住院乙肝患者血清,测定HBV-DNA水平、乙肝病毒血清标志物(HBV-M)及肝功指标ALT及AST.分析各指标间的相关性.结果 HBeAg 阳性患者HBV-DNA水平明显高于HBeAg 阴性患者,P＜0.05;二者的HBV-DNA水平与ALT及AST均无显著差异;大三阳与小三阳患者HBV-DNA水平与ALT及AST亦均无显著性差异.结论 乙肝患者 HBV-DNA水平与肝损伤程度无明显相关性.     

Risk stratification for hepatitis B virus related hepatocellular carcinoma

Hepatitis B virus (HBV) infection is the major cause of chronic hepatitis, cirrhosis, and hepatocellular carcinoma (HCC) worldwide, especially in the Asia–Pacific region. Several hepatitis B viral factors predictive of clinical outcomes in HBV carriers have been identified. The Risk Evaluation of Viral Load Elevation and Associated Liver Disease/Cancer‐HBV (REVEAL‐HBV) study from Taiwan illustrated the strong association between HBV‐DNA level at study entry and risk of HCC over time. In this community‐based cohort study, male gender, older age, high serum alanine aminotransferase level, positive hepatitis B e antigen, higher HBV‐DNA level, HBV genotype C infection, and core promoter mutation are independently associated with a higher risk of HCC. Another large hospital‐based Elucidation of Risk Factors for Disease Control or Advancement in Taiwanese Hepatitis B Carriers cohort of Taiwanese patients further validated the findings of REVEAL‐HBV. The risk of HCC started to increase when HBV‐DNA level was higher than 2000 IU/mL. Both HBV‐DNA and HBsAg levels were shown to be associated with HCC development. While HBV‐DNA level had better predictive accuracy than HBsAg level, when investigating the overall cohort in patients with HBV‐DNA level < 2000 IU/mL, HBsAg level ≥ 1000 IU/mL was identified as a new independent risk factor for HCC. With the results from REVEAL‐HBV, a risk calculation for predicting HCC in non‐cirrhotic patients has been developed and validated by independent cohorts (Risk Estimation for Hepatocellular Carcinoma in Chronic Hepatitis B).Taken together, ample evidence indicates that HBsAg level can complement HBV‐DNA level in predicting HCC development, especially in HBV carriers with low viral load. In conclusion, HBV treatment guidelines should include the risk stratification of HCC to individualize the management of HBV carriers with different levels of HCC risk.     

Hepatitis B virus genotypes and clinical manifestation among hepatitis B carriers in Thailand

BACKGROUND: Hepatitis B virus (HBV) genotypes have distinct geographic distributions. The aim of the present study was to evaluate the distribution of HBV genotypes and their clinical relevance in Thailand. METHODS: Hepatitis B virus genotypes among 107 hepatitis B carriers residing in Thailand were evaluated using serologic and genetic methods. They were clinically classified into asymptomatic carriers with normal serum alanine transaminase (ALT) levels and patients with chronic liver disease, such as those with chronic hepatitis (CH), liver cirrhosis (LC) and hepatocellular carcinoma (HCC). RESULTS: Hepatitis B virus genotype distribution among the 107 patients was 25.2% for genotype B, 72.0% for genotype C and 2.8% for genotype D. The serum ALT levels, HBV-DNA and hepatitis B e antigen positivity were significantly higher in carriers infected with genotype C HBV than in those infected with genotype B (P < 0.05). The proportion of genotype B HBV was higher in asymptomatic carriers than in patients with CH and those who developed liver disease, such as LC and HCC (45.5, 16.9 and 25.0%, respectively; P < 0.05). In contrast, the proportion of genotype C HBV was higher in patients who developed liver disease and CH than in asymptomatic carriers (68.7, 83.0 and 50.0%, respectively; P < 0.05). Phylogenetic analysis based on entire genome sequences revealed three HBV isolates, which were classified into a subgroup of genotype C in isolates from South-East Asian countries. CONCLUSIONS: Genotypes B and C are the predominant types among hepatitis B carriers residing in Thailand and those genotypes influence the clinical manifestation in carriers with chronic hepatitis B infection.     

Basal core promoter T1762/A1764 and precore A1896 gene mutations in hepatitis B surface antigen-positive hepatocellular carcinoma: a comparison with chronic carriers.

BACKGROUND: Chronic hepatitis B virus (HBV) infection is associated with hepatocellular carcinoma (HCC), and specific viral factors have been identified that may increase the risk for HCC development. However, the differences in these viral factors in chronic carriers who seldom develop HCC compared with HCC patients have not been adequately evaluated. METHODS: From 1989 to 2005, 101 hepatitis B surface antigen-positive patients presented to our clinic with HCC. Baseline basal core promoter (BCP) T1762/A1764 mutants, precore (PC) A1896 mutants, HBV genotypes and HBV DNA in HCC patients were compared with 67 chronic carriers who had been followed for a mean of 112.1+/-77.7 standard deviation months. RESULTS: At baseline, HCC patients had lower levels of serum albumin, but higher values of alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, bilirubin and alpha-foetoprotein than those of chronic carriers (P<0.001 for all comparisons). The presence of genotype C, higher frequencies of PC A1896 mutants, BCP T1762/A1764 mutants and higher circulating levels of HBV DNA were more frequently detected in HCC patients than that in chronic carriers (P<0.001 for all observations). Logistic regression analysis revealed that BCP T1762/A1764 mutants [odds ratio (OR) 11.14, 95% confidence interval (CI) 3.05-40.72; P<0.001] and PC A1896 mutants (OR 3.75, 95% CI 1.14-12.34; P<0.05) were significantly associated with HCC development. CONCLUSION: Our results indicate that the presence of BCP and PC mutations significantly increases the risk for HCC in chronic hepatitis B patients. These mutations were less often detected in chronic carriers who seldom develop HCC.     

Comparison of recurrence after hepatic resection in patients with hepatitis B vs. hepatitis C-related small hepatocellular carcinoma in hepatitis B virus endemic area.

PURPOSE: Hepatitis B virus (HBV) and hepatitis C virus (HCV) infection are two important factors in the development of hepatocellular carcinoma (HCC). The carcinogenic mechanism of HBV and HCV is considered to be different. It is interesting to compare the recurrence after hepatic resection in patients with small HCC who were infected with HBV or HCV. METHODS: From 1991 to 1995, 145 patients who were positive for hepatitis B surface antigen (HBsAg) or antibody to HCV (anti-HCV) and diagnosed as small HCC (< or =3 cm) in three medical centers in Taiwan were evaluated in this study. All patients underwent hepatic resection. Among them, 83 (57.2%) were infected by HBV, 51 (35.2%) were infected by HCV, and 11 (7.6%) had dual HBV and HCV infection. RESULTS: Anti-HCV+ HCCs were associated with older age, lower serum albumin, higher alanine transaminase (ALT) level and multi-nodular tumors during diagnosis. During the follow-up, 92 (63.4%) patients developed tumor recurrence. Anti-HCV + HCC had a higher cumulated recurrence rate than HBsAg+ HCC (72.4% vs 53.6 % at 5 year, P = 0.032). In multivariate analysis, the presence of vascular invasion and lower serum albumin levels (<3.9 g/dl) were the determinants for tumor recurrence. CONCLUSIONS: HCV infection, as compared with HBV infection, had a higher cumulated recurrence after hepatic resection in patients with small HCC. Low serum albumin level was significantly associated with recurrence among these patients.     

慢性乙肝病毒感染者血清血管内皮生长因子的研究

目的:检测慢性乙型肝炎病毒感染患者血清中血管内皮生长因子(VEGF)的水平,探讨其临床意义.方法:采用双抗体夹心ELISA法对50例肝细胞癌、40例乙型肝炎肝硬化、36例乙型肝炎肝纤维化、40例慢性乙型肝炎患者血清中VEGF进行检测,并以43例健康者作为对照.同时采用全自动生化分析仪检测所有人员的肝功能常规指标.结果:慢性乙型肝炎、肝纤维化、肝硬化、肝细胞癌组患者血清VEGF浓度明显高于正常对照组(P＜0.01,P＜0.05,P＜0.05,P＜0.05),同时四组患者之间比较,差异均有统计学意义(P＜0.05).四组患者血清VEGF水平与肝功能指标AST、ALT无相关性,与GGT成正相关(r=0.337,P＜0.05).结论:VEGF与慢性乙型肝炎病毒感染者病情密切相关,可作为病情发展动态监测的指标.VEGF与GGT联合检测,可显著提高肝细胞癌的检出率.     

Influence of hepatitis C virus infection on circulating levels of sICAM-1 and VEGF in patients with hepatitis C and hepatocellular carcinoma (HCC) and their role in enhancing detection of HCC

Infection with hepatitis C virus (HCV) is characterized by inflammatory liver damage and a long viral persistence associated with an increased risk of developing hepatocellular carcinoma (HCC). Intercellular adhesion molecule-1 (ICAM-1) plays a key role during liver inflammation and also expressed in HCC. Its cellular expression is associated with the release of soluble form (sICAM-1) in the peripheral blood. The process of angiogenesis plays a critical role in liver damage-associated HCV infection and in tumor growth and metastasis. Vascular Endothelial Growth Factor (VEGF) is an important angiogenic factor regulating tumor angiogenesis. This study aimed at investigating the influence of HCV infection on serum profile of sICAM-1 and VEGF in patients with hepatitis C and HCC and their diagnostic value as useful markers reflecting progressive liver damage and development of HCC. Serum levels of sICAM-1 and VEGF were determined in the serum of fifteen HCV infected patients, fifteen HCV-positive patients with superimposed HCC as well as ten healthy control subjects by enzyme linked immunosorbent assay. HCV RNA copy numbers were analyzed by Real-time polymerase chain reaction using TaqMan probe technology. Alpha-fetoprotein levels and serum aminotransferases activities were also measured. The group of patients with hepatitis C and superimposed HCC had significantly higher sICAM-1 and VEGF values than HCV infected patients (1178.113 +/- 631.87 vs. 313.67 +/- 82.72 & 320.88 +/- 117.99 vs. 132.45 +/- 91.56, p < 0.001 respectively). In comparison to healthy subjects, HCV infected patients showed dramatically elevated serum levels of VEGF (132.45 +/- 91.56 vs. 7.76 +/- 7.41, p < 0.001). On the other hand, sICAM-1 levels were elevated in patients with HCV as compared with healthy controls, but this did not reach statistical significance (313.67 +/- 82.72 vs. 230.3 +/- 47.4, p > 0.05). A highly significant correlation was found between VEGF and sICAM-1 levels in all patients (r = 0.731, p < 0.001) also between VEGF, sICAM-1 and AFP (r = 0.473, p < 0.001, r = 0.690, p < 0.001, respectively) as well as between sICAM-1 and AST activities (r = 0.367, p < 0.05). A weak correlation was found between the level of viremia and VEGF, sICAM-1 levels, yet this did not reach statistical significance (r = 0.312, p = 0.09 & r = 0.228, p > 0.05 respectively). The sensitivity of HCC detection using AFP alone was 93.3%. It yielded 100% detection sensitivity when combined with sICAM-1 and/or VEGF with diagnostic accuracy reaching 96.67%. In conclusion, HCV infection and the development of HCC on top greatly affect the serum profile of VEGF and sICAM-1. VEGF as it stimulates endothelial cell growth, it could modulate the expression of sICAM-1 and both could be considered as convenient markers of progressive liver damage, endothelial activation and therefore could improve detection and management of HCC.     

血清可溶性IL-2受体测定在急慢性肝脏疾病中的意义

目的 探讨急慢性肝病可溶性白介素2受体的改变,为诊断病情演变和预后判定寻找可靠的依据。 方法 健康对照(n=30)研究,采用夹心酶联免疫吸附法测定173例各型肝病患者血清IL-2受体(sIL-2R)水平,包括急性病毒性肝炎80例,慢性乙型肝炎21例,肝炎后肝硬化35例和原发性肝癌37例,并对测定结果进行分析。 结果 各组患者血清sIL-2R均明显高于对照组(P<0.01),其中急性病毒性肝炎黄疸期血清sIL-2R明显高于恢复期(P<0.01),各型急性肝炎之间血清sIL-2R无显著差异(P>0.05);急性肝炎组明显高于慢性肝炎组(P<0.01);慢性乙型肝炎ALT异常组血清sIL-2R明显高于ALT正常组(P<0.01);Child's C级肝炎后肝硬化者明显高于CHild'B,A级者(P<0.01);原发性肝癌者血清sIL-2R水平与肿瘤体积大小有关(P<0.05)。 结论 急慢性肝病患者血清sIL-2R水平均明显增高,其水平的高低在一定程度上反映了机体免疫功能状态和肝细胞损伤的程度。     

Quantitative HBV DNA and AST are strong predictors for survival after HCC detection in chronic HBV patients

Hepatitis B virus infection (HBV) is an important co-factor in the development of hepatocellular carcinoma (HCC). We studied whether quantitative HBV DNA at time of HCC detection influences survival of HCC patients. All diagnosed HCC cases between 2000 and 2008 at our university-based reference centre were analysed to determine the influence of hepatitis B viral load on overall survival. Clinical and virological findings were evaluated in univariate and multivariate analyses, survival rates were assessed for HCC patients with a high viral load (HBV DNA ≥10(5) copies/ml) and low viral load (HBV DNA <10(5) copies/ml). HCC was diagnosed in 597 patients, including 98 patients with HBV. The group of 37 patients (38%) who had a high viral load contained more HBeAg-positive patients, had lower serum albumin levels and higher serum aspartate aminotransferase (AST ) and alanine aminotransferase (ALT ) levels. The one- and five-year survival rates of HCC patients with a high viral load were 58% and 11% and for HCC patients with a low viral load 70% and 35%, respectively. In multivariate analysis a higher AST level and higher viral load were significantly associated with shorter overall survival (HR=2.30; p=0.018, HR=1.22; p=0.015, respectively). HBeAg positivity, low albumin level or high AST or ALT levels in HCC patients are associated with a higher HBV DNA . HBV DNA level at detection is associated with overall survival of HCC patients. These findings support the concept that after HCC detection adequate suppression of HBV DNA by nucleoside analogue therapy may improve survival.     

Serum alpha-fetoprotein levels in patients with advanced hepatitis C: results from the HALT-C Trial

BACKGROUND/AIMS: Alpha-fetoprotein (AFP) has been useful in the diagnosis of hepatocellular carcinoma (HCC) but lacks specificity. We assessed serum AFP among patients with chronic hepatitis C and advanced fibrosis to establish predictors of AFP elevations and changes with antiviral therapy. METHODS: Serum AFP was measured at baseline and on therapy in patients in the Hepatitis C Antiviral Long-Term Treatment against Cirrhosis (HALT-C). AFP levels were correlated with patient demographic and clinical features. RESULTS: Baseline AFP was > or = 20 ng/mL in 191 of 1145 patients (16.6%). Mean AFP values were significantly higher in patients with cirrhosis than in those with bridging fibrosis (22.5 vs. 11.4 ng/mL, P < 0.0001). Factors independently associated with raised serum AFP in patients with cirrhosis were female gender, black race, decreased platelet count, increased serum AST/ALT ratio, serum ferritin, and Mallory bodies in liver biopsies. Serum AFP levels decreased significantly during therapy with pegylated interferon alpha-2a and ribavirin. HCC was identified in six subjects, only three of whom had AFP > 20 ng/mL. CONCLUSIONS: Among patients with advanced chronic hepatitis C, serum AFP values are frequently elevated, even in the absence of HCC. Factors associated with raised AFP include severity of liver disease, female gender and black race. Serum AFP levels decline during antiviral therapy.