Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary liver cancer, particularly HCC, is increasing in certain countries, notably Japan. Although hepatitis B virus has been etiologically linked to hepatocarcinogenesis and integration of its DNA into hepatocyte chromosomal DNA has been emphasized, other etiologic factors seem to have an interplay with virus infection. Histopathology of HCC has geographic variations. An expanding encapsulated HCC is most common in Japan, whereas it is nearly nonexistent in the West; such regional differences can only be explained by differences in the major etiologic factors. Early detection of HCC is now possible with ultrasound examination combined with AFP measurement, and this strategy has been executed with success in the Far East where HCC is endemic among cirrhotics. The speed of tumor growth can be measured with accuracy by ultrasound examination. Preneoplastic or early lesions of HCC in a cirrhotic liver seem to be adenomatous hyperplastic nodules or foci, and the conventional histological criteria for malignant liver cells do not seem applicable to such lesions. Although advanced cirrhosis is a real deterrent for hepatic surgery, hepatic resection affords a better survival compared with any nonsurgical therapeutic modality. Transcatheter arterial embolization is one of the current preferences of the hepatologist for inoperable patients. Lastly, a new staging scheme has been proposed for the assessment of prognosis and for comparison of efficacy of various therapeutic modalities.
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PMID:Primary liver cancer. Quadrennial review lecture. 301 22

Cure of primary liver tumours remains possible only by surgery and early diagnosis will therefore continue to be important; the value of regular screening of cirrhotic patients for development of HCC by ultrasound scanning and estimation of AFP is now established. Prognosis of irresectable HCC depends largely on the general condition of the patient at the time of diagnosis and is better in the absence of cirrhosis. Radiotherapy has little role in the management of patients with HCC, but benefit with acceptable morbidity may be obtained from parenteral chemotherapy, with doxorubicin or its derivatives used as single agents, or with a combination of 5-FU and methyl-CCNU. There may be advantage from regional therapy given via the hepatic artery and early results from the combination of embolization with arterial doxorubicin are encouraging. The use of radiolabelled antibodies to tumour-related determinants of hormonal manipulation show promise. Worthwhile results from the non-surgical management of peripheral (intrahepatic) cholangiocarcinoma and primary hepatic sarcoma remain scarce. Isolated hepatic metastases from colorectal primaries may be resectable; for those that are not, results from regional chemotherapy with 5-FU or FUDR are encouraging, but cost and high morbidity currently limit more general application.
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PMID:Chemotherapy and radiotherapy of malignant hepatic tumours. 303 57

Recent reports have demonstrated the possibility of using ultrasound to detect hepatocellular carcinomas under 3 cm (small HCC). Our aim was to assess the incidence of small HCC in an Italian ultrasonographic series. Among 17,133 scans of unselected patients, we detected 85 HCC, 9 of which were under 3 cm. All patients had cirrhosis and 6 were HBsAg positive. An echo-guided biopsy was performed in all cases, and the diagnosis was always correct. We conclude that echographic follow-up is warranted in Italy for cases at risk for HCC such as HBsAg+ cirrhotics and patients with chronic aggressive HBsAg+ hepatitis older than 35, in agreement with the reports of Far Eastern authors.
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PMID:Small hepatocellular carcinoma: an Italian experience. 303 16

The attempt to divide the large group of chronic HBsAg carriers into "healthy" vs. those with chronic hepatitis of various intensities is sometimes difficult. The major problems are overlap in clinical manifestations, hepatic test results and histologic as well as virologic features. Nevertheless, this separation is not only conceptually important, but may also be useful in patient management, particularly because of the risk of transition to cirrhosis and HCC. Although at least 75% of patients with HCC associated with HBV have cirrhosis, the time point at which the cirrhosis developed is not established, particularly since the vast majority of chronic HBsAg carriers fall into the "healthy" category. Important unanswered questions are, therefore: how often do "healthy" carriers develop cirrhosis and/or HCC, including the time relations between the two? Does the transformation to HCC result from one or several identifiable acute events in the "healthy" carrier (or in mild CPH) or is it a gradual process of progressing chronic hepatitis B in which intercurrent exacerbations may still play a role? Do the quantitative observations as to the relation between persistent HBV infections and HCC in the East apply to Western countries? Our hypothesis concerning pathogenesis is based on pathologic, molecular, clinical and epidemiologic observations and concepts, and is supported by studies of hepadna virus-infected animals. This thesis proposes that integration of HBV DNA into host chromosomes in acute or chronic hepatitis or during the "healthy" carrier state corresponds to an initiation event similar to that described in chemical carcinogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relation of the hepatitis B virus carrier state to hepatocellular carcinoma. 303 25

A long-term follow-up study of liver cirrhosis (LC) was performed in 582 patients diagnosed by peritoneoscopy and liver biopsy in the 26 years from 1958 to 1984. The etiology of LC consisted of hepatitis B virus (HBV) in 21%, alcoholic in 39% and cryptogenic in 39%. Fifty-nine percent of patients had died. Causes of death were hepatocellular carcinoma (HCC 44%), liver failure (30%), rupture of esophageal varices (14%), gastrointestinal bleeding (4%) and non-liver-related causes (8%). HCC accounted for increasing percentages (68%) since 1980. In all groups classified by the etiology, the causes of death had the same order in incidence. The age of onset of LC increased by 10 years from 42 to 52 years old and the age of death by 15 years from 43 to 58 in the 26-year period. The cumulative survival rate improved over the period. The 50% survival year was 7.9 in total patients, and 7.0, 8.5 and 10.0 in the three periods 1958-64, 1965-74 and 1975-84, respectively. It was 9.5, 6.3 and 9.8 in HBV, alcoholic and cryptogenic, respectively. LC patients survived 40-44% of the life expectancy of the general population in Japan in all age groups. Cox's multiregression life-table method selected three important prognostic factors from 7 parameters: a poor prognosis with a history of heavy alcohol consumption and old age at onset, and a better prognosis with recent onset.
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PMID:Follow-up study of 582 liver cirrhosis patients for 26 years in Japan. 343 93

In Taiwan the prevalence of anti-Delta was low among asymptomatic HBsAg carriers, patients with HCC and acute type B hepatitis, intermediate in HBsAg carriers on hemodialysis, patients with chronic type B hepatitis and liver cirrhosis, particularly HBeAg negative ones, and very high in intravenous drug abusers. It is important to prevent the spread of HDV infection in this hyperendemic area of HBV.
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PMID:Hepatitis delta virus infection in Taiwan. 362 18

The precise nature of the relationship between cirrhosis and HCC remains to be elucidated. However, it seems likely that no single explanation will cover the various forms the association takes in different parts of the world. In the high HCC incidence regions of sub- Saharan Africa and the Far East, an etiology common to the two disorders, HBV and possibly other hepatitis viruses, seems to account for the majority of cases. The role of aflatoxin in these areas is uncertain because it appears not to cause cirrhosis in man. In populations in which HCC is uncommon, alcoholic cirrhosis is the most frequent association of HCC. There is no convincing evidence to support a shared etiology in this situation because alcohol has not thus far been proved to be directly oncogenic for the liver. Possibly, cirrhosis renders the hepatocytes more susceptible to environmental carcinogenic factors. The same explanation may apply to hemochromatosis. There is at present little evidence for the postulate that HCC is an inevitable consequence of the hyperplasia of cirrhosis.
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PMID:Relationship between hepatocellular carcinoma and cirrhosis. 608 59

During the past 20 years, trends have been observed in primary hepatocellular carcinoma in Thailand. There is a definite increase in the association between HCC and cirrhosis of liver from 16.6% in 1958 to 50.78% in 1968 and 73.93% in 1978 series. The increase in percentage is associated with increase in mean age group from 44.61 +/- 9.77 in 1958, to 48.84 +/- 12.35 (p < 0.01) in 1978. This reflects the important role which hepatitis B plays in the etiology of HCC-associated with cirrhosis in Thailand. Also, the aggregation of people in the city of Bangkok may cause an increase in the hepatitis B carrier.
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PMID:Carcinoma of the liver in Thailand, trends in two decades. 625 11

The aflatoxin B1 content of liver tissue was measured in patients who died from chronic liver disease [hepatocellular carcinoma (HCG) (5), schistosomal liver fibrosis (1), chronic aggressive hepatitis (1)] and compared with fifteen controls who died of motor traffic accidents (10), drowning (1), malnutrition (1), idiopathic cardiomegaly (1) and lung infection (2). Significant levels of aflatoxin B1 were found in hepatocellular carcinoma patients who were also hepatitis B surface antigen (HBsAg) negative. Histology showed HCC arising in macronodular cirrhosis.
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PMID:Aflatoxin B1 in hepatocellular carcinoma. 625 85

The prevalence of serum hepatitis B virus markers was studied in three groups of age- and sex-matched patients: a. 31 patients with liver cirrhosis and hepatocellular carcinoma (c-HCC); b. 31 patients with chronic liver disease (CLD) and c. 62 hospitalized control subjects. The overall exposure rate to the hepatitis B virus was 90% in c-HCC, 80% in CLD and 58% in control subjects. The prevalence of hepatitis B surface antigen (HBsAg) was 29%, 13% and 1.6% in the three groups, respectively. The prevalence of hepatitis B surface antibody was significantly lower in c-HCC (9.6%) than CLD (42%) and control subjects (40%). The serological evidence of continuous viral replication (HBsAg positivity or isolated high titre hepatitis B core antibody positivity) was more common in c-HCC (39%) than CLD (12%) and control subjects (1.6%). The prevalence and patterns of aggregation of serum hepatitis B virus markers were similar in the 31 patients with c-HCC and in 11 patients with HCC without concomitant liver cirrhosis (n-HCC). In conclusion, the overall exposure rate to the hepatitis B virus is similar in c-HCC and CLD. However, serological evidence of continuous viral replication is more common in the former group. A defective clearance of the hepatitis B virus in hepatocellular carcinoma is a possible explanation of the phenomenon. The strength of the association between hepatitis B virus infection and hepatocellular carcinoma appears to be similar in c-HCC and n-HCC.
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PMID:Case-control study of hepatitis B virus infection in chronic liver disease and hepatocellular carcinoma. 632 29


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