目的探讨硬化型肝癌与肝内肿块型胆管癌的影像特征、病理特征及鉴别诊断情况。方法选取96例硬化型肝癌患者及194例肝内肿块型胆管癌患者,均进行CT、MRI检查,分析影像学检查中的强化特征。对手术切除的肿瘤组织进行苏木精-伊红(HE)染色...目的探讨硬化型肝癌与肝内肿块型胆管癌的影像特征、病理特征及鉴别诊断情况。方法选取96例硬化型肝癌患者及194例肝内肿块型胆管癌患者,均进行CT、MRI检查,分析影像学检查中的强化特征。对手术切除的肿瘤组织进行苏木精-伊红(HE)染色观察细胞形态,并采用Elivision二步法免疫组化检测肿瘤组织中人磷脂酰肌醇蛋白聚糖3(GPC3)、肝细胞抗原(Hep Par 1)、细胞角蛋白(CK)19、CK17表达情况。绘制受试者工作特征(ROC)曲线,计算曲线下面积(AUC),评估免疫组化相关指标对硬化型肝癌与肝内肿块型胆管癌的鉴别诊断价值。结果硬化型肝癌患者的年龄、淋巴结转移率均低于肝内肿块型胆管癌患者,病毒性肝炎、病灶靠近肝脏边缘患者比例均高于肝内肿块型胆管癌患者,差异均有统计学意义(P﹤0.05)。硬化型肝癌与肝内肿块型胆管癌患者动态增强扫描影像典型强化率分别为60.42%、61.86%,二者非典型强化表现存在部分重合,但肝内肿块型胆管癌的非典型强化方式更为复杂,特征性更明显。免疫组化染色显示,硬化型肝癌患者肿瘤组织中GPC3、Hep Par 1阳性表达率均明显高于肝内肿块型胆管癌患者,CK19阳性表达率明显低于肝内肿块型胆管癌患者,差异均有统计学意义(P﹤0.01)。GPC3+Hep Par 1+CK19联合检测诊断硬化型肝癌的AUC为0.942(95%CI:0.900~0.977),高于各指标单独检测。结论硬化型肝癌与肝内肿块型胆管癌动态增强均为典型强化时,难以进行鉴别诊断;当为非典型强化时,肝内肿块型胆管癌表现更为复杂,部分具有特征性,而硬化型肝癌表现较为单一,可进行鉴别诊断;GPC3、Hep Par 1、CK19联合检测可提高鉴别诊断价值。展开更多
A 69-year-old man was admitted to our hospital in October 2003,for further examination of two liver tumors.He was diagnosed with hepatocellular carcinoma(HCC) arising from decompensated hepatitis B virus(HBV)-related ...A 69-year-old man was admitted to our hospital in October 2003,for further examination of two liver tumors.He was diagnosed with hepatocellular carcinoma(HCC) arising from decompensated hepatitis B virus(HBV)-related cirrhosis.Long-term lamivudine administration improved liver function dramatically despite repeated treatment for HCC.His Child-Pugh score was 9 points at start of lamivudine treatment,improving to 5 points after 1 year.His indocyanine green at 15 min after injection test score was 48%before lamivudine treat-ment,improving to 22%after 2 years and to 5%after 4 years.Radiofrequency ablation controlled the HCC foci and maintained his liver function.In April 2009,abdominal computed tomography revealed a tumor thrombus in the right portal vein.Since his indocyanine green test results had improved to less than 10%,we performed a right hepatectomy,which was successful.To our knowledge,there have been no documented reports of patients undergoing successful right hepatectomy for HCC arising from decompensated cirrhosis.The findings observed in our patient indicate the importance of nucleoside analogs for treating HBV-related HCC.展开更多
About 30% of patients with cirrhosis have diabetes mellitus(DM).Nowadays,it is a matter for debate whether type 2 DM in the absence of obesity and hypertriglyceridemia may be a risk factor for chronic liver disease.DM...About 30% of patients with cirrhosis have diabetes mellitus(DM).Nowadays,it is a matter for debate whether type 2 DM in the absence of obesity and hypertriglyceridemia may be a risk factor for chronic liver disease.DM,which develops as a complication of cirrhosis,is known as "hepatogenous diabetes".Insulin resistance in muscular and adipose tissues and hyperinsulinemia seem to be the pathophysiologic bases of diabetes in liver disease.An impaired response of the islet β-cells of the pancreas and hepatic insulin resistance are also contributory factors.Non-alcoholic fatty liver disease,alcoholic cirrhosis,chronic hepatitis C(CHC) and hemochromatosis are more frequently associated with DM.Insulin resistance increases the failure of the response to treatment in patients with CHC and enhances progression of fibrosis.DM in cirrhotic patients may be subclinical.Hepatogenous diabetes is clinically different from that of type 2 DM,since it is less frequently associated with microangiopathy and patients more frequently suffer complications of cirrhosis.DM increases the mortality of cirrhotic patients.Treatment of the diabetes is complex due to liver damage and hepatotoxicity of oral hypoglycemic drugs.This manuscript will review evidence that exists in relation to:type 2 DM alone or as part of the metabolic syndrome in the development of liver disease;factors involved in the genesis of hepatogenous diabetes;the impact of DM on the clinical outcome of liver disease;the management of DM in cirrhotic patients and the role of DM as a risk factor for the occurrence and exacerbation of hepatocellular carcinoma.展开更多
AIM To investigate the associations of different types of pre-S deletions with hepatitis B virus(HBV) genotypes.METHODS The sequences of the pre-S region, basal core promoter(BCP) mutation, and precore(PC) mutation we...AIM To investigate the associations of different types of pre-S deletions with hepatitis B virus(HBV) genotypes.METHODS The sequences of the pre-S region, basal core promoter(BCP) mutation, and precore(PC) mutation were examined through direct DNA sequencing or clonal analysis and sequencing in 273 HBV carriers, namely 55 asymptomatic carriers, 55 carriers with chronic hepatitis(CH), 55 with liver cirrhosis(LC), 53 with liver cirrhotic hepatocellular carcinoma(LC-HCC), and 55 with noncirrhotic HCC. A total of 126 HBV carriers(46.2%) harbored pre-S deletions. The DNA sequences of pre-S deletion mutants from 43 age-matched genotype B(HBV/B)-infected carriers and 43 agematched genotype C(HBV/C)-infected carriers were further examined, aligned, and compared.RESULTS No significant difference was observed in the mean age distribution(P = 0.464), male sex(P = 0.805), viral load(P = 0.635), or BCP mutation(P = 0.117) between the HBV/B and HBV/C groups. However, the rate of PC mutation was significantly higher in the HBV/B-infected carriers than in the HBV/C-infected carriers(P = 0.003). Both genotypes exhibited a high rate of deletion in the C-terminal half of the pre-S1 region and N-terminus of the pre-S2 region(86.0% and 79.1% in the HBV/B group; 69.8% and 72.1% in the HBV/C group, respectively). Epitope mapping showed that deletion in several epitope sites was frequent i n both genotypes, particularly p S1-BT and p S2-B2. Conversely, the rate of p S2-B1 deletion was significantly higher in the HBV/B group(72.1% vs 37.2%, P = 0.002), and the rate of pS 2-T deletion was significantly higher in the HBV/C group(48.8% vs 25.6%, P = 0.044). Functional mapping showed that the rate of deletion in three functional sites(the nucleocapsid binding site, start codon of M, and site for viral secretion) located in the N-terminus of the pre-S2 region was significantly higher in the HBV/B group(P < 0.05). One type of N-terminus pre-S1 deletion mutant with deletion of the start codon of the L protein was frequently observed in the HBV/C group(20.9% vs 9.3%, P = 0.228), particularly in the LC patients(42.9% vs 12.5%). Different patterns of pre-S deletions were also found between the HBV/B and HBV/C groups according to different clinical outcomes. In CH patients, deletion in the site for polymerized human serum albumin was more frequent in the HBV/B group(88.9% vs 36.4%, P = 0.028). In the LC-HCC patients, the rate of deletion in the pre-S2 region was significantly higher in the HBV/B group than in the HBV/C group(P < 0.05).CONCLUSION HBV/B- and HBV/C-infected carriers exhibit different patterns of pre-S deletion, which may be associated with the progression of liver diseases.展开更多
文摘目的探讨硬化型肝癌与肝内肿块型胆管癌的影像特征、病理特征及鉴别诊断情况。方法选取96例硬化型肝癌患者及194例肝内肿块型胆管癌患者,均进行CT、MRI检查,分析影像学检查中的强化特征。对手术切除的肿瘤组织进行苏木精-伊红(HE)染色观察细胞形态,并采用Elivision二步法免疫组化检测肿瘤组织中人磷脂酰肌醇蛋白聚糖3(GPC3)、肝细胞抗原(Hep Par 1)、细胞角蛋白(CK)19、CK17表达情况。绘制受试者工作特征(ROC)曲线,计算曲线下面积(AUC),评估免疫组化相关指标对硬化型肝癌与肝内肿块型胆管癌的鉴别诊断价值。结果硬化型肝癌患者的年龄、淋巴结转移率均低于肝内肿块型胆管癌患者,病毒性肝炎、病灶靠近肝脏边缘患者比例均高于肝内肿块型胆管癌患者,差异均有统计学意义(P﹤0.05)。硬化型肝癌与肝内肿块型胆管癌患者动态增强扫描影像典型强化率分别为60.42%、61.86%,二者非典型强化表现存在部分重合,但肝内肿块型胆管癌的非典型强化方式更为复杂,特征性更明显。免疫组化染色显示,硬化型肝癌患者肿瘤组织中GPC3、Hep Par 1阳性表达率均明显高于肝内肿块型胆管癌患者,CK19阳性表达率明显低于肝内肿块型胆管癌患者,差异均有统计学意义(P﹤0.01)。GPC3+Hep Par 1+CK19联合检测诊断硬化型肝癌的AUC为0.942(95%CI:0.900~0.977),高于各指标单独检测。结论硬化型肝癌与肝内肿块型胆管癌动态增强均为典型强化时,难以进行鉴别诊断;当为非典型强化时,肝内肿块型胆管癌表现更为复杂,部分具有特征性,而硬化型肝癌表现较为单一,可进行鉴别诊断;GPC3、Hep Par 1、CK19联合检测可提高鉴别诊断价值。
文摘A 69-year-old man was admitted to our hospital in October 2003,for further examination of two liver tumors.He was diagnosed with hepatocellular carcinoma(HCC) arising from decompensated hepatitis B virus(HBV)-related cirrhosis.Long-term lamivudine administration improved liver function dramatically despite repeated treatment for HCC.His Child-Pugh score was 9 points at start of lamivudine treatment,improving to 5 points after 1 year.His indocyanine green at 15 min after injection test score was 48%before lamivudine treat-ment,improving to 22%after 2 years and to 5%after 4 years.Radiofrequency ablation controlled the HCC foci and maintained his liver function.In April 2009,abdominal computed tomography revealed a tumor thrombus in the right portal vein.Since his indocyanine green test results had improved to less than 10%,we performed a right hepatectomy,which was successful.To our knowledge,there have been no documented reports of patients undergoing successful right hepatectomy for HCC arising from decompensated cirrhosis.The findings observed in our patient indicate the importance of nucleoside analogs for treating HBV-related HCC.
文摘About 30% of patients with cirrhosis have diabetes mellitus(DM).Nowadays,it is a matter for debate whether type 2 DM in the absence of obesity and hypertriglyceridemia may be a risk factor for chronic liver disease.DM,which develops as a complication of cirrhosis,is known as "hepatogenous diabetes".Insulin resistance in muscular and adipose tissues and hyperinsulinemia seem to be the pathophysiologic bases of diabetes in liver disease.An impaired response of the islet β-cells of the pancreas and hepatic insulin resistance are also contributory factors.Non-alcoholic fatty liver disease,alcoholic cirrhosis,chronic hepatitis C(CHC) and hemochromatosis are more frequently associated with DM.Insulin resistance increases the failure of the response to treatment in patients with CHC and enhances progression of fibrosis.DM in cirrhotic patients may be subclinical.Hepatogenous diabetes is clinically different from that of type 2 DM,since it is less frequently associated with microangiopathy and patients more frequently suffer complications of cirrhosis.DM increases the mortality of cirrhotic patients.Treatment of the diabetes is complex due to liver damage and hepatotoxicity of oral hypoglycemic drugs.This manuscript will review evidence that exists in relation to:type 2 DM alone or as part of the metabolic syndrome in the development of liver disease;factors involved in the genesis of hepatogenous diabetes;the impact of DM on the clinical outcome of liver disease;the management of DM in cirrhotic patients and the role of DM as a risk factor for the occurrence and exacerbation of hepatocellular carcinoma.
基金Supported by the National Science Council,Taiwan,No.NSC 96-2320-B-030-004-MY3
文摘AIM To investigate the associations of different types of pre-S deletions with hepatitis B virus(HBV) genotypes.METHODS The sequences of the pre-S region, basal core promoter(BCP) mutation, and precore(PC) mutation were examined through direct DNA sequencing or clonal analysis and sequencing in 273 HBV carriers, namely 55 asymptomatic carriers, 55 carriers with chronic hepatitis(CH), 55 with liver cirrhosis(LC), 53 with liver cirrhotic hepatocellular carcinoma(LC-HCC), and 55 with noncirrhotic HCC. A total of 126 HBV carriers(46.2%) harbored pre-S deletions. The DNA sequences of pre-S deletion mutants from 43 age-matched genotype B(HBV/B)-infected carriers and 43 agematched genotype C(HBV/C)-infected carriers were further examined, aligned, and compared.RESULTS No significant difference was observed in the mean age distribution(P = 0.464), male sex(P = 0.805), viral load(P = 0.635), or BCP mutation(P = 0.117) between the HBV/B and HBV/C groups. However, the rate of PC mutation was significantly higher in the HBV/B-infected carriers than in the HBV/C-infected carriers(P = 0.003). Both genotypes exhibited a high rate of deletion in the C-terminal half of the pre-S1 region and N-terminus of the pre-S2 region(86.0% and 79.1% in the HBV/B group; 69.8% and 72.1% in the HBV/C group, respectively). Epitope mapping showed that deletion in several epitope sites was frequent i n both genotypes, particularly p S1-BT and p S2-B2. Conversely, the rate of p S2-B1 deletion was significantly higher in the HBV/B group(72.1% vs 37.2%, P = 0.002), and the rate of pS 2-T deletion was significantly higher in the HBV/C group(48.8% vs 25.6%, P = 0.044). Functional mapping showed that the rate of deletion in three functional sites(the nucleocapsid binding site, start codon of M, and site for viral secretion) located in the N-terminus of the pre-S2 region was significantly higher in the HBV/B group(P < 0.05). One type of N-terminus pre-S1 deletion mutant with deletion of the start codon of the L protein was frequently observed in the HBV/C group(20.9% vs 9.3%, P = 0.228), particularly in the LC patients(42.9% vs 12.5%). Different patterns of pre-S deletions were also found between the HBV/B and HBV/C groups according to different clinical outcomes. In CH patients, deletion in the site for polymerized human serum albumin was more frequent in the HBV/B group(88.9% vs 36.4%, P = 0.028). In the LC-HCC patients, the rate of deletion in the pre-S2 region was significantly higher in the HBV/B group than in the HBV/C group(P < 0.05).CONCLUSION HBV/B- and HBV/C-infected carriers exhibit different patterns of pre-S deletion, which may be associated with the progression of liver diseases.
