Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fourteen patients with clinical Stage I hepatocellular carcinoma (T1N0M0) were studied. All patients were asymptomatic, and their conditions were detected by alpha-fetoprotein (AFP) serosurvey and/or ultrasonography (US) either in the natural population in the early years of the study or in the high-risk population in the later years of the study. Cirrhosis was present in all patients. Radical resection was performed in all patients. There were no operative deaths or hospital deaths in this series. The 5-year survival rate after resection was 100%. There were seven long-term survivors in this series (14.2 years (alive), 11.3 years (alive), 8.8 years (alive), 8.8 years, 7.9 years, 7.6 years (alive), and 7.2 years after resection). The authors discuss aspects concerning early diagnosis, treatment, and prognosis of hepatocellular carcinoma (HCC).
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PMID:Solitary minute hepatocellular carcinoma. A study of 14 patients. 170 61

Cirrhosis is the usual end-result of chronic active autoimmune hepatitis. Different immunological abnormalities divide chronic active hepatitis into 3 subgroups: type I with anti-smooth muscle antibody; type II with anti-liver/kidney microsome antibody type 1 (anti-LKM1 antibody) and type III with an antibody directed against a soluble hepatic antigen. Three quarters of the patients are young women. The liver disease is often diagnosed at the stage of chronic active hepatitis, during evaluation of the subject's general condition or during investigations for an episode of jaundice; it is seldom diagnosed at the stage of constituted or decompensated cirrhosis. Fulminant forms are rare. Extrahepatic autoimmune manifestations are frequently encountered. Treatment relies on immunosuppressants, in practice corticosteroids. Corticosteroid therapy significantly prolongs the patient's life, but it does not prevent the passage to cirrhosis. In the long term these patients are exposed to all the complications of cirrhosis, notably the occurrence of hepatocellular carcinoma.
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PMID:[Cirrhosis secondary to chronic autoimmune hepatitis]. 206 15

Antibodies against hepatitis C virus (anti-HCV) were detected in 60.8% of 78 patients with hepatocellular carcinoma (HCC). Cirrhosis, present in most of the patients, as well as alcohol abuse, age, sex, and alpha-fetoprotein were equally distributed in the anti-HCV-positive and -negative groups. HBsAg positivity was significatively higher in negative anti-HCV group. By contrast, hepatitis B virus (HBV) antibodies were detected more frequently in positive anti-HCV patients than in the negative anti-HCV group. These data must be considered with caution because of the small number of HBsAg-positive patients. It is concluded that the high prevalence of anti-HCV in patients with HCC may suggest an etiological role of the hepatitis C virus, although in relationship to age, alcohol abuse and cirrhosis, the similarity in the two groups questions this hypothesis.
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PMID:Serum antibodies to hepatitis C virus in Italian patients with hepatocellular carcinoma. 216 May 17

Hepatocellular carcinoma (HCC), the most frequent malignant tumour of the liver, is the commonest cancer occurring in males in the world. The annual incidence of the disease worldwide is estimated to be one million cases. There are variations in its geographical distribution. It tops the list of malignancies amongst males in sub-saharan Africa; it is the second most common cancer in Southeast Asia, including Hong Kong, and ranks third amongst males in China. It is relatively rare in America, Europe North Africa, and the Middle East. During the last 15 years, epidemiologic and laboratory investigations have established a strong and specific association between chronic hepatitis B virus (HBV) infection and HCC. Hepatic cirrhosis is another major aetiologic factor incriminated. In areas with a low incidence of HCC, cirrhosis due to alcohol may be a relatively more important predisposing factor. Chronic non-A, non-B hepatitis (NANBH) infection has now been incriminated as a cause of HCC, especially in Japan. Other environmental factors, particularly chemical carcinogens such as Aflatoxin, smoking, genetic predisposition and sex hormones may also act to promote hepatocarcinogenesis. The exact mechanisms of neoplastic transformation, however, are still far from understood. The following factors are discussed in detail: 1. HBV infection 2. Cirrhosis 3. NANBH infection 4. Aflatoxin B1 5. Cigarette smoking 6. Alcohol A number of less important associated diseases are also listed in Table I. At the end of this paper, a tentative scheme for hepatocarcinogenesis has been proposed and the methods for prevention is discussed in light of the risk factors considered.
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PMID:Hepatocarcinogenesis. 216 75

Hepadnaviruses share properties of virion structure, genome structure and replication, epidemiologic behavior, and pathogenic effects, including an association with hepatocellular carcinoma (HCC). Epidemiologic evidence implicating hepadnavirus infection in HCC includes the observation that the geographic distributions of HBV infection and HCC are similar, that the incidence of HCC is much higher in hepadnavirus infected than uninfected hosts, and that viral DNA sequences are integrated in the cellular DNA of most (e.g., 80-90%) but not all hepadnavirus-associated HCC. Cirrhosis further increases the risk of HCC in HBV infected humans. The precise role of hepadnaviruses in development of most HCC is unclear, although the finding of viral integrations within or near protooncogenes in a few cases suggests the possibility that these integrations may play a direct role in these HCC. However, in the great majority of HCC associated with HBV infections, viral integrations are in different cellular DNA sites in different HCC, integrations are not within domains of known protooncogenes, and integrations are not found in some 10-15% hepadnavirus-associated HCC, suggesting that persisting viral sequences are not directly involved in the development of these HCC as viral sequences are for tumors caused by viruses with oncogenes or viruses that act by a "promoter-insertion" mechanism. It is possible, however, that oncogenic mutations could arise via other mutagenic mechanism that may operate in chronic hepatitis B and/or cirrhosis and which do not involve persisting viral integrations. For example, liver regeneration, which is a feature of the cirrhosis associated with chronic HBV infection (and sometimes with chronic hepatitis B) involves proliferation of many cells with HBV integrations, and such integrations have been shown to be unstable and may lead to mutations through post-integration rearrangements of cellular sequences at sites of viral integrations. Viral sequences appear to be lost or deleted at some such sites of rearranged cell DNA. Chronic HBV infection shares pathologic features of liver cell injury and reactive inflammation, liver regeneration, and in man sometimes cirrhosis with other important risk factors for HCC including chronic alcoholic liver disease, chronic non-A, non-B hepatitis, hemochromatosis, and crypogenic cirrhosis, suggesting that this common pathologic process may be carcinogenic by a mechanism that does not depend specifically on the factor which initiates liver cell injury. The pathogenetic role of chronic hepadnavirus infection in such a process would be in causing liver cell injury with reactive inflammation and hepatocyte proliferation (regeneration).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hepadnaviruses in cirrhotic liver and hepatocellular carcinoma. 216 15

Two hundred seventy-one patients with various forms of alcoholic liver disease were followed up for an average of 87.9 months. The survival was the lowest for alcoholic cirrhosis (average 10-year survival: 23.8%). Prognosis was grave especially in cirrhotic patients who continued drinking, owing mainly to the increased death due to gastrointestinal bleeding. The development of hepatocellular carcinoma (HCC) was observed during the first six years only in cirrhosis. The average 5-year probability rate of developing HCC for cirrhosis was 16.3%. The rate was significantly higher for the cirrhotic patients who abstained than for those who continued drinking. Serial biopsies were performed on 66 non-cirrhotic patients who continued drinking. The mean duration of histological follow-up 46.0 months. Cirrhosis developed eventually in 30.3% of the cases. In conclusion, the present study indicates that continued drinking causes progressive liver damage and a poor prognosis. Our data also suggest that abstinence is associated with an increased risk of HCC in cirrhosis. Thus, it is important to recover from alcoholism before cirrhosis develops.
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PMID:[Long-term follow-up study of alcoholic liver disease]. 217 75

Forty-two patients with nonalcoholic steatohepatitis were followed for a median of 4.5 yr (range = 1.5 to 21.5 yr). Except for two patients with lipodystrophy, all were obese; 35 of 42 were women, 26 of 32 were hyperlipidemic and 15 were hyperglycemic. Upper abdominal pain was the most common reason for presentation. Initial liver biopsy specimens showed the presence of macrovesicular fatty infiltration, lobular (acinar) inflammation, apoptosis, Mallory bodies (in four cases) and fibrosis (in 18 cases). Cirrhosis was present at initial diagnosis in one subject and in another two subjects liver biopsy showed marked fibrosis with disturbed architecture. Serial liver biopsy specimens revealed minimal or no apparent progression of the disorder in most of the patients, in keeping with their benign clinical course. However, one patient showed progression from fibrosis to cirrhosis during the 5-yr observation period, and in the patients with extensive fibrosis the liver disease evolved from one of active inflammation to one of inactive cirrhosis without fat or inflammation. The patient with cirrhosis later died of hepatocellular carcinoma. The severity or type of hepatic change did not correlate with the degree of obesity, hyperlipidemia or hyperglycemia. However, in individual patients, poorly controlled diabetes and rapid weight loss preceded the onset of steatohepatitis. We conclude that nonalcoholic steatohepatitis is a cause of hepatic inflammation histologically resembling that of alcohol-induced liver disease but usually slowly progressive and of low-grade severity. However, the disorder may ultimately result in cirrhosis. Nonalcoholic steatohepatitis should be distinguished from alcoholic steatohepatitis and recognized as a further cause of "cryptogenic cirrhosis."
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PMID:The natural history of nonalcoholic steatohepatitis: a follow-up study of forty-two patients for up to 21 years. 1503 Sep 72

The value of ultrasonography and serum alpha foetoprotein assay in the detection of hepatocellular carcinoma was evaluated in a retrospective study of 217 patients, (135 men and 82 women; mean age 58 years) who had been hospitalized for 18 months. Cirrhosis was of alcoholic origin in 76 per cent of the cases and complicated by ascites in 54 per cent. Twenty-four patients (11 per cent) had hepatocellular carcinoma diagnosed at ultrasonography in 20 cases. The carcinoma was diffuse in 7 cases, focal in 13 cases and less than 3 cm in diameter in 3 cases. A second ultrasonography diagnosed hepatocellular carcinoma in 4 cases. In 25/217 patients (11.5 per cent) the focal lesion seen at sonography was obviously not a carcinoma. Among the 207 patients who had a serum alpha foetoprotein assay, the result was normal in 167 (81 per cent) and 4 of these had a carcinoma. Among the 40 patients with an abnormal level of alpha foetoprotein, 19 had a carcinoma. This study confirms the good sensitivity of ultrasonography in the detection of hepatocellular carcinoma, but it also shows its low specificity, especially in cases with focal lesions. Ultrasonography and serum alpha foetoprotein assay should be used to detect hepatocellular carcinomas in cirrhotic patients who may benefit from surgical treatment. In the other patients, ultrasonically-guided biopsy should provide a firm diagnosis of carcinoma before undertaking other treatments, such as chemoembolization.
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PMID:[Is the focal echographic lesion of the liver in patients with cirrhosis always correlated with hepatocellular carcinoma? 217 cases]. 246 Aug 50

Hepatocellular carcinoma and cirrhosis frequently coexist. In populations with a low incidence of hepatocellular carcinoma, the tumor often arises as a complication of long-standing symptomatic cirrhosis, which may be micronodular or macronodular and which is usually alcoholic in origin, and cirrhosis per se is the major etiologic association of the tumor. The relation between these two pathologic conditions in populations with a high incidence of hepatocellular carcinoma has not hitherto been analyzed. In this study the association was examined in 463 southern African black men with hepatocellular carcinoma. Cirrhosis, almost always macronodular and rarely showing features of alcholic toxicity, was present in 63.1% of the patients. No differences were found in the age structure, clinical features, hepatic function, serum alpha-fetoprotein concentrations, or hepatitis B virus status between patients with hepatocellular carcinoma with and without cirrhosis. Patients with cirrhosis survived slightly longer, but the difference was not biologically significant. It is concluded that the relation between hepatocellular carcinoma and cirrhosis in southern African blacks differs substantially from that in low incidence regions of the tumor.
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PMID:Hepatocellular carcinoma with and without cirrhosis. A comparison in southern African blacks. 247 Jun 34

In a consecutive series of 35 cases of HCC, 21 (60%) had a habitual alcoholic intake of greater than 80 g/die and 26 (74.2%) were positive for at least one HBV serum marker. At tissue level, HBsAg was positive in non-tumoral tissue in 8 cases (22.9%) and HBcAg in 6 cases (17.1%) in non-neoplastic tissue and in 3 cases (8.6%) in neoplastic tissue with focal type positivity. The positivity of HBsAg presented at cytoplasmatic level and that of HBcAg almost exclusively at nuclear level. The comparatively low expression of HBV antigens at tissue level can be explained by the integration of viral DNA in the host genome which probably took place in many of these cases. Cirrhosis was associated with HCC in 23 cases (65.7%). In 9 (25.7%) cirrhosis was macronodular, in 4 (11.4%) micronodular and in 10 (28.6%) it was mixed. 18 cases (51.4%) presented an association of significant alcoholic consumption and positivity of at least one HBV marker. In 19 cases (54.3%), cirrhosis was associated with positivity of at least one HBV marker. Finally, in 14 cases (40%) there was an association of cirrhosis, alcohol and positivity of at least one HBV marker. These results suggest a multifactorial aetiology of HCC in our geographic area, identifying the factors in question in cirrhosis of the liver, independently of its aetiology (through the hyperplastic-regenerative process that characterises it) in HBV and in alcohol (with direct and independent pathogenetic mechanisms known only in part, or mediated by cirrhosis of which HBV and alcohol represent the two main aetiological agents). In cases in which more than one of the aetiological factors considered was observed, it is legitimate to admit a cocarcinogenic perhaps synergistic hypothesis of this cancer.
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PMID:[Hepatocellular carcinoma. Significance of the association with cirrhosis, alcohol consumption and the hepatitis B virus (serum markers and tissue antigens)]. 253 6


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