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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This work details the histologic findings in 84 liver biopsy specimens from 28 patients with progressive familial intrahepatic cholestasis (PFIC), who met the clinical criteria of early onset of chronic unremitting cholestasis, exclusion of any known metabolic or anatomic etiology, and low serum gamma-glutamyl transpeptidase (GGTP) values. Hepato-canalicular cholestasis and disruption of the liver cell plate arrangement were early, uniform findings, and giant cell transformation was found in 56% of initial biopsies. Duct loss was a prominent finding; 70% of patients had ductal paucity, and many had abnormal bile duct epithelium, suggesting degeneration. Fibrosis was seen in the samples from 16 patients, including bridging fibrosis in specimens obtained from six patients during the first 2 years of life. Proliferating ductules at the margins of portal tracts increased as fibrosis progressed and were especially prominent in end-stage histology. Cirrhosis developed in nine of these patients and had a characteristic histologic pattern, consisting of biliary cirrhosis with diffuse stellate lobular fibrosis associated with severe cholestasis and pseudoacinar transformation. Mallory hyalin and hepatocellular carcinoma were observed in materials from some patients with advanced cirrhosis. The constellation of histologic findings in PFIC forms a recognizable pattern, and the liver histology appears to have a predictable progression.
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PMID:Histologic pathology of the liver in progressive familial intrahepatic cholestasis. 801 59

The western HCC registry comprised data from 322 patients who underwent hepatic resection for HCC over a 50-year period. The majority of patients had lesions > 4 cm and were symptomatic at presentation. Lesions were mostly unicentric. Cirrhosis was not a prevalent problem, unlike the East. In the most recent decade, 1980-1989, we noted a significant decrease in operative mortality from 19% to 10% overall, and 15% to 4% in the noncirrhotic group. We identified four variables that resulted in poorer postresectional outcome: cirrhosis, regional nodal disease, multicentric disease, and tumor-free resectional margin < 1 cm. Although these factors are associated with a poorer outcome after resection, whether they should serve as contraindications to surgery should be determined by individual surgeons, taking into account the patient's overall status, concomitant risk factors, and treatment objectives.
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PMID:Hepatoma registry of the Western world. Repeat Hepatic Resection Registry. 803 52

Cirrhosis is a risk factor for hepatocellular carcinoma. O6-methylguanine is a promutagenic and potentially carcinogenic DNA lesion produced by environmental alkylating agents. If it is not repaired, DNA replication can lead to a G-to-A transition mutation, which is a known mechanism of oncogene activation. We have found that the activity of the repairing methyltransferase enzyme is significantly lower in cirrhotic tissue than in non-cirrhotic diseased liver or in normal liver. This finding suggests a mechanism for cirrhosis being a risk factor for cancer of the liver: increased cellular proliferation together with persistence of O6-methylguanine might lead to malignant transformation of liver cells through mutation and oncogene activation.
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PMID:Deficient repair of DNA lesion O6-methylguanine in cirrhosis. 809

The most common etiogenic disease of portal hypertension that we experience is liver cirrhosis, which accounts for 84% of all cases. In patients with portal hypertension, congestion by portal blood due to cirrhosis causes a rise in portal pressure and development of collateral circulation between the portal system and the postcaval system is observed. Esophageal varices are associated with higher mortality than any other symptom of portal hypertension and are an important consideration in treatment. When emergency endoscopic examination and diagnosis show esophageal variceal bleeding, the varices must be constricted directly using a Sengstaken-Brakemor tube. If hemostasis is maintained, medical and surgical procedures can be performed after the recovery of body strength. Endoscopic Injection Sclerotherapy (EIS) has recently been widely carried out to prevent variceal bleeding and its application is increasing. However, treatment with EIS alone is not sufficient in terms of long-term efficacy, and surgical treatment is effective, especially in patients with gastric varices or splenomegaly. For Child A and B groups, both with good liver function, non-shunting operation, especially, the SUGIURA procedure, shows a marked effectiveness on varices. For group Child C, EIS is selected. The newly-developed Transjuglar Intrahepatic Portasystemic Shunt (TIPS), is being used, recently. For hepatic insufficiency, liver transplantation is expected to be one of the method for future treatment. Cirrhosis is also commonly accompanied by hepatoma, and this must be taken into consideration in treatment.
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PMID:[Etiology and management of esophageal varices]. 811 15

Of 176 hepatic transplants performed from 1986 to December 1992, 27 patients had small hepatocellular carcinoma (< or = 5 centimeters) complicating cirrhosis of the liver. All patients were asymptomatic for the hepatic malignancy and the diagnosis was established in each instance preoperatively by means of serial sonographic scans and alpha-fetoprotein levels. Cirrhosis was classified as Child's A in eight instances, as Child's B in 16 and Child C's in three. The cause was alcoholic in three patients, posthepatitic in 21 patients (eight hepatitis B virus [HBV] positive and 13 hepatitis C virus [HCV] positive) and undetermined in three. The in-hospital mortality rate was 11 percent (three of 27). Additionally, five patients died at different intervals after transplantation: only two died of neoplastic recurrence at 12 and 32 months, respectively (7.4 percent rate). Actuarial survival rates were 82 percent at one year and 71 percent at three years, with a mean follow-up period of 32 months (range six to 78 months). Morbidity related to the procedure was a relevant problem: 21 percent of the patients had prompt resumption of normal life while 37 percent required repeated hospitalization and 42 percent required strict control on an outpatient basis. The most frequent problem was HBV or HCV reinfection of the grafted liver, which occurred in 42 percent. Based on this experience, transplantation of the liver has shown an excellent oncologic accuracy for small hepatocellular carcinoma in cirrhosis of the liver, thus representing the most rational surgical procedure for patients with Child's B and Child's C cirrhosis classification. The relevant mortality and morbidity rates, strictly related to this procedure, suggest other options as more appropriate in those with Child A cirrhosis at this time.
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PMID:The role of transplantation in small hepatocellular carcinoma complicating cirrhosis of the liver. 814 37

In order to identify the prognostic factors of the resection of hepatocellular carcinoma, the results of 153 resections performed between January 1984 and December 1988 in 18 French centers were analysed. Cirrhosis was present in 76% of the patients. Among the postoperative complications (61%), the most frequent were ascites (35.3%) and liver failure (19%). Operative mortality was 20%. One-, 3- and 5-year survival rates were 52.7, 30.1, and 17.9%, respectively. The survival rate was significantly higher in patients with a curative resection, Pugh's class A or with a tumor less than 3 centimeters in diameter. After curative resection, actuarial survival rates without recurrence were 65, 24.4, and 16.7% after, 1, 3, and 4 years respectively. In this case, the survival rate was significantly related to the number of resected nodules and the size of the tumor but not to the presence of a capsule surrounding the tumor.
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PMID:[Resection of hepatocellular carcinomas. Analysis of prognostic factors of a multicenter series of 153 patients]. 839 76

Although essential for life, iron in excessive amounts may be toxic. The liver is particularly subject to the toxic effects of iron, since it is the major site of iron storage. Several inherited and acquired human disorders may result in hepatic iron overload, the most common of which are genetic hemochromatosis (GH) and transfusional iron overload. GH is an inherited disorder of iron metabolism, and in patients with GH excess iron absorbed from the gut is transported through the portal vein to the liver. The mechanisms by which excess iron exerts its cytotoxic effects include enhanced formation of free radicals and peroxidation of organelle membrane lipids. Lipid peroxidation can lead to structural and functional alterations in lysosomes, mitochondria and the endoplasmic reticulum. With massive iron overload, such iron-induced alterations may cause cell death, also known as sideronecrosis. At this stage, fibrogenesis is initiated and, if the excess iron is not removed, the increased deposition of collagen progresses to cirrhosis. However, the mechanisms underlying iron-induced fibrosis remain unclear. Transformation of fat-storing cells to collagen-producing myofibroblasts has been proposed to be induced either by iron; by lipid peroxides or other cellular factors released from iron-loaded, damaged hepatocytes; or by profibrogenic factors produced by activated Kupffer cells. In addition, iron may enhance the cytotoxic and, possibly, fibrogenic effects of other liver cell-damaging agents, such as alcohol or hepatotrophic viruses. Once cirrhosis is manifest, patients with GH demonstrate a 200-fold increase in the risk for development of hepatocellular carcinoma. In vitro, iron has been shown to possess mutagenic properties, but the results from in vivo models in which the genotoxic effects of iron overload have been studied are variable. Similarly, although iron has mitostimulatory effects on hepatocytes in vivo and preneoplastic cells in vitro, its role in tumor promotion and/or progression still remains unclear. Cirrhosis itself is of central importance in the carcinogenic process, but whether or not iron acts as an additional risk factor in this process, alone or by enhancing the tumorigenic properties of other hepatocarcinogens, has yet to be established.
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PMID:Iron as a hepatotoxin. 852 7

Most haemophiliacs treated with non-virally-inactivated clotting factor concentrates have been infected with hepatitis C virus (HCV). We have studied the natural history of chronic HCV infection by following all 138 HCV-positive patients from our centre for periods of up to 28 years. As well as the clinical and biochemical characteristics, we studied 116 liver samples from 63 patients obtained at elective biopsy (n = 103) or autopsy (n = 13). 36 (26%) of the patients were HIV positive, and three were chronic carriers of hepatitis B. Evidence of previous exposure to hepatitis A and B was found in 37.2% and 48.1% respectively. Raised transaminase levels were found in 82.6% of patients. 11 of 15 patients with normal transaminases tested by PCR for HCV RNA were positive, indicating that most patients, even in this group, have chronic hepatitis C infection. Cirrhosis was diagnosed by liver histology in 19 patients, and nine patients developed liver failure. The incidence of cirrhosis rose rapidly 15 years after HCV infection to 15.6 per 1000 person-years. Multivariate analysis showed that HIV status, length of time since HCV infection and age at HCV infection were independently associated with both the development of cirrhosis and liver failure. Two patients developed hepatocellular carcinoma: one of these was exposed only to a single batch of FVIII concentrate 11 years earlier. Chronic hepatitis C is increasingly recognized as a major cause for morbidity and mortality in haemophiliacs, especially those who are HIV positive and who were infected at an older age.
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PMID:The natural history of chronic hepatitis C in haemophiliacs. 907 37

Evidence of a tumorigenic potential of the hepatitis C virus (HCV) has so far come mainly from epidemiological data. Longitudinal studies have shown that 16 of 62 anti-HCV antibody (ab)-positive Japanese patients developed hepatocellular carcinoma (HCC) within 5 yr. HCC-related deaths were significantly (p = 0.01) higher in Swedish anti-HCV ab-positive patients than in anti-HCV ab-negative controls (18 vs. 4%). The relative frequency of anti-HCV ab in HCC patients has been reported to be as high as 72% in Spain, 49-62% in Italy and 58% in France. It ranges between 9 and 36% in the USA and is about 26% in Germany. In HBV-endemic areas like South East Asia and Equatorial Africa, HCV-related HCCs play a minor role. The relative risk of developing HCC was elevated (up to 69.1-fold) for anti-HCV ab-positive patients as compared to anti-HCV ab-negative controls in almost all geographic areas studied to date. There is some evidence for an increased risk of developing HCC when hepatitis B virus (HBV) coinfection is present. Cirrhosis is likely to represent an additional risk factor for the development of HCC in anti-HCV ab-positive patients. Blood transfusions are the source of infection in barely one third of anti-HCV ab-positive HCC patients. There seems to be no significant difference in age or gender between anti-HCV ab-positive and ab-negative HCC patients. The additional impact of alcohol consumption and of the HCV genotype is presently under investigation. On the molecular level, HCV replication intermediates have been detected in HCC tissue and point mutations within the p53 gene have been demonstrated. However, the pathomechanism leading to HCV-mediated cell transformation remains unsolved.
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PMID:Hepatitis C virus infection as a major risk factor for hepatocellular carcinoma. 883 91

In endemic areas infection with hepatitis B virus is a common cause of chronic liver disease in childhood. High levels of viral replication and mild ALT abnormalities are the rule in children infected perinatally and many of them are likely to maintain viral replication through their youth. Conversely about 90% of children infected later in life clear HBeAg and achieve sustained remission of liver disease before reaching adulthood. The eventual outcome of infection and disease in these patients remains unpredictable as reactivation of liver damage and viral replication may occur after several years of sustained remission. Cirrhosis is a rare and early complication of chronic HBV infection in children, and a risk factor for hepatocellular carcinoma. IFN therapy can accelerate HBV DNA clearance, improving the spontaneous anti-HBe seroconversion rate in Caucasian children by two to three times. Hepatitis delta is the most severe form of chronic viral hepatitis in childhood. Cirrhosis can be diagnosed in up to 26% of patients at presentation, and few cases respond to IFN therapy. Hepatitis C is relatively rare in children. Before the discovery of HCV, blood transfusions were the most common source of infection. Hepatitis C is usually a mild, asymptomatic disease in otherwise healthy children, but has a poor propensity to spontaneous remission over the years. For this reason, and based on the experience in adults, IFN treatment is now being evaluated.
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PMID:Chronic viral hepatitis in childhood. 886 29


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