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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In Asia, Africa and other tropical areas primary hepatic carcinoma (PHC) is associated with liver cirrhosis of the post-necrotic (macronodular) type. Chronic viral hepatitis is likely to be the cause of this cirrhosis in many patients from regions where chronic infection with the hepatitis B virus (HBV) is common. More than 95% of patients with hepatoma (in Mali and Senegal) have evidence of infection with HBV, a much higher frequency than in controls. Thirty-nine of 62 PHC patients had hepatitis B surface antigen (HBSAg) (controls: 8 of 98) and 56 of 63 (controls: 26 of 100) had antibody against hepatitis B core antigen (anti-HBC). In earlier studies we demonstrated a maternal effect of HBSAg. If the mother has the antigen and the father does not, the children are much more likely to also have HBSAg than if the father has the antigen and the mother does not (93/161 = 57.8% when mother is positive vs. 28/135 = 20.7% when father is positive; p = 0.6 X 10(-10)). Studies in Greece and in the Solomon Islands show that presence of HBSAg in parents affects the sex ratio of the offspring of the mating. This implies that the presence of the agent in a parent can affect the fetus early in life. Parental studies in the African hepatoma patients showed that there is a very high frequency of HBSAg in mothers (71.6%) while the frequency in fathers (18.5%) is significantly less. This suggests that the development of hepatoma in offspring is related to infection in parents. We described a vaccine several years ago which may be useful in preventing infection with hepatitis B. Strategies are discussed which might be effective in preventing the development of carriers with, it is hoped, a consequent decrease in the frequency of HBV carriers, chronic hepatitis and primary hepatic carcinoma. The strategy would employ methods for decreasing the frequency of the agent in the environment by the application of public health methods including the vaccination of appropriate newborns and other members of the population.
Leber Magen Darm 1976 Dec
PMID:[The relation of infection with the hepatitis B-agent to primary hepatic carcinoma (author's transl)]. 19 Apr 99

A case report is given of a 49 year old white male patient, who had suffered for several years from liver cirrhosis and who finally died from hepatoma. Although a hepatoma was suspected in this case it was not demonstrated intra vitam, though at autopsy it was found to have invaded the lower vena cava, continuing into the right atrium. Problems of early diagnosis of hepatoma are discussed in context with this case.
Leber Magen Darm 1976 Dec
PMID:[Multiple nodular densities on chest X-ray in liver cirrhosis--a diagnostic problem? (author's transl)]. 19 May 1

The onset of spontaneous hemolytic jaundice in a young subject should lead to the search for Wilson's disease when clinical examination reveals cirrhosis. This hemolysis may evolve in the form of severe jaundice to a stage where the cirrhosis remains usually latent or well tolerated. The intervention of a toxic, allergic of infective factor liable to produce a hepatic lesion which frees a dose of copper sufficient to trigger off hemolysis, is discussed. The mechanism of the latter, that of the coagulation disorders observed, liver cell failure and widespread intravascular coagulation, are analysed in this paper and compared with data in the literature. The dramatic character of the case indicates that it is necessary to treat as a routine with penicillamine all homozygous forms of Wilson's disease.
Sem Hop 1976 Dec 09
PMID:[Severe hemolytic jaundice and Wilson's disease]. 19 22

In 9 years in Kenya, 34 examples of primary liver cancer wer diagnosed in patients in the first two decades of life. This represents 4.7% of all liver cancers during this period. The larger proportion (29) were hepatocellular carcinoma. In the second decade, there was a notable association with macronodular cirrhosis. Analogy with experimental work suggests that cells in mitotic cycle may be more vulnerable to the effect of environmental carcinogens. Five examples of hepatoblastoma were identified at ages from 2 months to 14 years; none showed the features of "mixed" tumours. The ratio of hepatoblastoma to hepatocellular carcinoma was the reverse of that found in other large series of juvenile hepatic tumours. The histopathological features of these tumours are described and problems of their classification are discussed.
Br J Cancer 1977 Dec
PMID:Primary cancer of the liver in Kenyan children. 20 98

A retrospective examination in South-west Scotland of formalin-fixed paraffin-embedded liver tissue by an immunoperoxidase technique revealed hepatitis B surface antigen (HBsAg) in eight out of 81 cases (10%) of primary hepatocellular carcinoma (PHC) and in four out of 82 cases (5%) of cirrhosis. No positive staining was found in 112 controls without overt liver disease matched for age and sex. Unlike most previous studies showing an association between HBsAg and PHC, the present investigation was carried out in an area where HBs antigenaemia is infrequent and PHC is an uncommon tumour. While possibly hepatitis infection is an important cause of PHC, the association between HBsAg and PHC could be due merely to activation by the tumour of latent virus B in a previously infected person.
J Clin Pathol 1977 Dec
PMID:Incidence in South-west Scotland of hepatitis B surface antigen in the liver of patients with hepatocellular carcinoma. 20 8

Telangiectasia-associated hepatic fibrosis (TAHF) in a 68-year-old woman with hereditary haemorrhagic telangiectasia (HHT) is described. The patient died of oat-cell carcinoma of the lung. In addition to the structural alterations which have been described previously in HHT, the liver exhibited focal midlobular hepatocytic necrosis and tumour metastases. The possibility that treatment of HHT was causally related to some of the hepatic abnormalities found in our patient and the differentiation of TAHF from true cirrhosis are discussed.
J Clin Pathol 1977 Dec
PMID:'Pseudocirrhosis' in hereditary haemorrhagic telangiectasia. 20 9

The concentration of serum immunoreactive prolyl hydroxylase (SIRPH) was measured in thirty patients with chronic active hepatitis, thirteen with primary biliary cirrhosis, four with alcoholic or idiopathic cirrhosis, and four with acute hepatitis; the values were compared with those in twenty-three control subjects. Increases in SIRPH were found in all the groups with liver diseases, individual values being highest in primary biliary cirrhosis in which about two-thirds of patients had values more than two standard deviations above the mean value in the control subjects. No correlation was found between SIRPH and other tests of liver function or some routine laboratory tests. SIRPH may reflect some hitherto unknown of unmeasured process in the diseased hepatic cells.
Eur J Clin Invest 1977 Dec
PMID:Serum immunoreactive prolyl hydroxylase in liver disease. 20 93

Glucagon was tested for its effect on plasma adenosine 3',5'-cyclic monophosphate (cyclic AMP), insulin, and glucose in healthy subjects and in patients with advanced cirrhosis of the liver. In the normal subjects, intravenous infusion of glucagon caused a significant increase in plasma cyclic AMP, glucose, and insulin. In advanced cirrhotics, plasma cyclic AMP, glucose, and insulin did not increase. Adenylate cyclase concentration was measured in liver tissue from end stage cirrhotic patients and from brain-dead organ donors whose cardiovascular function was maintained in a stable state. Basal and total adenylate cyclase concentration were not different in the two groups. Adenylate cyclase from the livers of advanced cirrhotics was, however, significantly less responsive to glucagon stimulation than was that from donor livers. Hepatocytes in advanced cirrhosis have abnormal metabolic behavior characterized by abnormal adenylate cyclase-cyclic AMP response to hormonal stimulation.
Gastroenterology 1978 Dec
PMID:Cyclic AMP metabolism and adenylate cyclase concentration in patients with advanced hepatic cirrhosis. 21 45

Three hundred and eighty-five patients mostly with chronic liver diseases and 729 apparently healthy adults were studied for hepatitis B surface antigen (HBsAg) with reversed passive hemagglutination and antibody (anti-HBs) with passive hemagglutination. In healthy adults around 15% was HBsAg positive and in 45% was anti-HBs positive, estimating hepatitis B virus (HBV) infection in nearly two thirds of the population. The infection already occurred before adulthood. The prevalences of HBsAg were invariably over 80% in chronic hepatitis, cirrhosis and hepatocellular carcinoma (hepatoma) indicating an intimate relationship to HBV. On the contrary, the positive rates of anti-HBs in these diseases were far lower than those in healthy people and patients with other diseases, this is similar to the situation in chronic HBsAg carriers. The prevalence of HBsAg in hepatoma patients was unusually high, being 82.7% in contrast to 11.9% in patients with other malignancies. Not only hepatoma patients with cirrhosis but also those without cirrhosis were found to have high prevalence of HBsAg. The fact indicates an even more intimate relationship between hepatoma and HBV.
Acta Hepatogastroenterol (Stuttg) 1978 Dec
PMID:Hepatitis B virus infection and chronic liver disease in Taiwan. 21 87

The presence of hepatitis B surface (HBsAg) and core (HBcAg) antigens was investigated by immunofluorescence in specimens of liver tissue obtained at necrospy in 107 patients with primary hepatic carcinoma. HBsAg was detected in the cytoplasm of liver cells in 16 cases, and in eight of them the antigen was also found in malignant cells. HBcAg, which was present in the nuclei of liver cells in eight cases, was detected in the nuclei of tumour cells in six of these and also in two other cases showing HBsAg, but not HBcAg, in the nonneoplastic tissue. Although most of the primary hepatic carcinomas studied were associated with cirrhotic changes in the non-neoplastic tissue, HBsAg and HBcAg were also detected in the absence of underlying cirrhosis. Hepatitis B virus markers were demonstrated in non-neoplastic tissue, mainly in patients with a well-differentiated carcinoma, and only in these cases were they found also in the neoplastic tissue. These results show that hepatitis B virus antigens, including HBcAg, can be detected in the neoplastic cells of well-differentiated carcinoma of the liver. Although these cells could have been infected after the malignant transformation, a direct oncogenic role of the virus cannot be excluded.
J Clin Pathol 1978 Dec
PMID:Hepatitis B virus antigens in primary hepatic carcinoma: immunofluorescent techniques on fixed liver tissue. 21 38


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