Epidemiology of primary liver cancer in French Polynesia

Thirty-one cases of primary liver cancer recorded since 1980 to 1988 in French Polynesia are studied. Four risk factors are brought to the fore: male, more than 50 years old, birth in Austral archipelago and in this case AgHBs carriage. The relative risk for birth in Austral archipelago reach to 9.23. The relative risk for AgHBs carriers from this archipelago reach to 42.7. Costs of primary liver cancer and to immunization against hepatitis B virus are compared. Authors suggest to start an immunization program.     

原发性肝癌及非自身免疫性肝病自身抗体检测研究

采用线性免疫印迹法,对本院2012年至2014年非自身免疫性肝炎(non-autoimmune hepatitis,NAIH)(75例)、非自身免疫性肝硬化(non-autoimmune cirrhosis,NAIC)(118例)、原发性肝癌(primary liver cancer,PLC)(332例)患者进行临床常用的两大类15项自身抗体(4项抗肝抗原与11项抗可提取核抗原ENA抗体)进行检测,观察发生率并探索其在PLC中的临床意义。结果显示三组非自身免疫性肝病(non-autoimmune liver disease,NAILD)(肝炎、肝硬化、肝癌)中发生率较高的自身抗体为抗线粒体M2型(AMA-M2)(5.3%、10.2%、6.6%)、抗SSA(4.0%、8.5%、7.2%)、抗着丝粒相关蛋白B(CENP-B)(4.0%、5.9%、3.0%),但组间无显著差异(P0.05)。分层分析,HBsAg阴性的PLC组抗AMA-M2、抗SSA、抗CENP-B,抗SSB、抗SLA/LP阳性发生率与HBsAg阳性的PLC组存在显著差异(P0.05);甲胎蛋白(AFP)阴性(AFP20μg/L)PLC组中抗CENP-B抗体的发生率显著高于AFP阳性PLC组(P0.05);Spearman相关性分析表明PLC患者中,抗AMA-M2、抗CENP-B与AFP负相关;抗AMA-M2与前白蛋白、碱性磷酸酶及血红蛋白呈正相关;抗SSA、抗CENP-B与年龄呈正相关;抗SSA与白蛋白、血红蛋白呈正相关(P0.05)。多因素回归分析发现,联合抗AMA-M2,抗CENP-B,抗SSA抗体可作为PLC发生的独立危险因素(OR=2.187,P0.05,95%CI 1.133-4.222)。本研究证实自身免疫性疾病常用的15种自身抗体在NAIH、NAIC、PLC之间无显著差异。AFP阴性、HBsAg阴性组中的PLC患者自身抗体发生率相对较高。抗AMA-M2,抗CENP-B和抗SSA抗体联合检测,可作为PLC的高危因素,但相关机制有待进一步研究。     

Carcinoma-in-situ of testis in testicular feminization syndrome.

A light microscopical study of an excised testis from a 14 1/2-year-old girl with incomplete type of testicular feminization syndrome revealed a carcinoma-in-situ pattern in a part of the gonad. An identical histological pattern has repeatedly been demonstrated in infertile men who developed gross testicular germ cell tumours. It is suggested that germ cell carcinomas in patients with testicular feminization syndrome may be preceded by this characteristic intratubular germ cell abnormality.     

原发性肝癌患者的临床诊疗特点分析

目的了解南方某三甲医院原发性肝癌（PLC）住院患者的基本特征和治疗特点。方法回顾性分析某院2010年1月至2011年12月间2353例PLC住院患者的临床资料。结果患者平均年龄（52.48±11.65）岁,男性占88.7%,82.7%的患者伴乙型肝炎病毒（HBV）感染。89.1%（386/433）为肝细胞癌,6.0%（26/433）为胆管细胞癌,4.8%（21/433）为混合型。33.1%（778/2353）患者AFP〈20μg/L。巴塞罗那分期（BCLC）0～A期患者占27.0%,主要进行外科手术治疗（45.0%）,联合治疗占14.9%;B期患者占19.0%,主要进行肝动脉化疗栓塞术（TACE）（43.0%）,10.5%患者行联合治疗;C期患者占42.0%,主要是对症支持治疗（43.9%）和TACE治疗（40.0%）,7.7%患者为联合治疗;D期患者占12.0%,其中对症支持治疗79.9%、TACE治疗15.2%和联合治疗1.5%。结论 PLC人群以中年男性HBV感染者占绝大多数,且以中晚期患者为主。规范化治疗有待进一步提高,多学科协作治疗模式有待进一步发展。     

Combined hepatocellular-cholangiocarcinoma: a rare biphenotypic primary liver cancer

Combined hepatocellular carcinoma-cholangiocarcinoma (cHCC-CCA) is a fascinating and rare primary liver cancer. This biphenotypic neoplasm is characterized by the unequivocal presence of hepatocellular and cholangiocytic histomorphology. Here, we report a case of cHCC-CCA in a 64-year-old man with risk factors for HCC treated with segmentectomy.     

Risk of cirrhosis and primary liver cancer in alpha 1-antitrypsin deficiency

Previous reports have suggested an association between homozygous alpha 1-antitrypsin deficiency, cirrhosis, and primary liver cancer. To assess the risk of these complications we conducted a retrospective study based on 17 autopsied cases of alpha 1-antitrypsin deficiency identified during the period 1963 to 1982 in the city of Malm?, Sweden. During the study period, autopsies were performed in 38,250, or 68.2 percent, of all patients in the city who died. From the homozygote frequency in the population, 21 of these were expected to have alpha 1-antitrypsin deficiency. The disease had been diagnosed in 20, and autopsies had been performed in 17 (1 child and 16 adults). Each autopsied case was matched with four controls selected from the same autopsy register, and the Mantel-Haenszel odds ratio (ORmh) was calculated. The results indicated a strong relation between alpha 1-antitrypsin deficiency and cirrhosis (ORmh = 7.8; 95 percent confidence limits, 2.4 to 24.7) and primary liver cancer (ORmh = 20; 95 percent confidence limits, 3.5 to 114.3). When data were stratified according to sex, these associations were statistically significant only for male patients. We conclude that men with alpha 1-antitrypsin deficiency may be at higher risk for cirrhosis and primary liver cancer. The apparent male predominance suggests the additive effects of exogenous factors.     

Expression of sialyl-Tn, Tn and T antigens in primary liver cancer

Sialyl-Tn, Tn and T antigens are caused by aberrant or incomplete glycosylation of apomucins and are related to the aggressiveness of malignant neoplasms. Using 41 liver samples from patients with cholangiocarcinoma (including four with cirrhosis), 21 with combined hepatocellular-cholangiocellular carcinoma and 17 with hepatocellular carcinoma, the expression of sialyl-Tn, Tn and T antigens were characterized immunohistochemically and the correlation with apomucin profiles was evaluated. The prevalence of sialyl-Tn, Tn and T antigens expression was 89, 95 and 51% in cholangiocarcinoma without cirrhosis; 25, 75, and 0% in cholangiocarcinoma with cirrhosis; 29, 90, and 48% in combined hepatocellular-cholangiocellular carcinoma; and 0, 12 and 6% in hepatocellular carcinoma, respectively. Sialyl-Tn antigen was frequently expressed in cholangiocarcinoma without cirrhosis compared with cholangiocarcinoma with cirrhosis and combined hepatocellular-cholangiocellular carcinoma (P < 0.01). Although sialyl-Tn expression was associated with MUC1, MUC6 and MUC7 expression, the expression sites among them were not identical in the individual cases. These data suggest that the different expressions of sialyl-Tn antigen among cholangiocarcinoma without cirrhosis, cholangiocarcinoma with cirrhosis and combined hepatocellular-cholangiocellular carcinoma may reflect the biological features inherent to these tumors, such as the ability of invasion.     

'Neuroendocrine' differentiation in primary neoplasms of the liver.

Thirty primary liver neoplasms (16 hepatocellular, nine biliary, and five epithelioid haemangioendotheliomas) were studied for the expression of the general 'neuroendocrine' markers, neurone specific enolase (NSE) and protein gene product 9.5 (PGP 9.5). Grimelius silver staining for neurosecretory granules and immunostaining for S100 protein, HMB-45, vasoactive intestinal polypeptide (VIP), and calcitonin were also performed. Eleven of the 16 hepatocellular carcinomas stained positively for PGP 9.5, four for NSE, six for HMB-45, and two for S100 protein. Seven exhibited granular staining by the Grimelius method; eight showed immunostaining for VIP, and two for calcitonin. Three of the five haemangioendotheliomas demonstrated positive immunostaining for PGP 9.5, and two for NSE; of the nine biliary carcinomas, two showed staining for PGP 9.5 and NSE, and four contained cells staining with the Grimelius technique. Primary neoplasms of liver may show 'neuroendocrine' differentiation and this aspect of their phenotypic expression has to be considered before predicting the site of origin of a tumour in the liver.     

Mechanism of liver injury following ischemia.

To clarify whether ischemic liver injury is due to ischemia itself or reperfusion, histopathological and functional changes in the liver were examined before and after liver ischemia in rats with porto-systemic collateral channels. Effects of oxygen-derived free radical scavengers or an inhibitor of platelet aggregation on development of ischemic liver injury were also examined. Liver ischemia was produced by ligation of the portal vein and hepatic artery at liver hilum for 1 hr. The primary lesion of ischemic liver injury was cloudy swelling of liver cells in the periportal and midzonal regions; it developed during ischemia. The cloudy swelling of liver cells induced uneven distribution of sinusoidal blood flow after reperfusion, and consequently individual liver cell necrosis and focal hepatocellular necrosis in the midzonal regions developed later. Elevation of cytoplasmic enzyme activities in the serum after reperfusion was due to leakage across the damaged plasma membrane of liver cells. The treatment with superoxide dismutase, catalase, or heparin had not altered the liver injury that was attributed to ischemia, biochemically and histologically. These results suggest that ischemic liver injury is due to liver cell damage developed during ischemia, and that the ischemic liver injury is not alleviated or prevented by superoxide dismutase, catalase, or heparin.