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)

Possible mechanisms whereby alcohol abuse and alcohol-related diseases may promote the development of cancer are analyzed. The mechanisms discussed include: (a) contact-related local effects on the upper gastrointestinal tract; (b) the presence of low levels of carcinogens in alcoholic beverages; (c) induction of microsomal enzymes involved in carcinogen metabolism; (d) various types of cellular injury produced by ethanol and its metabolites and their relationship to cancer, particularly in the liver; (e) the nutritional disturbances frequently associated with alcohol abuse. The relationship between alcohol-induced cirrhosis and hepatocellular carcinoma is also discussed, and case histories of patients seen at the Bronx Veterans Administration Medical Center with hepatocellular carcinoma in the absence of cirrhosis are reviewed. Data are presented demonstrating the induction, by chronic ethanol consumption, of microsomal enzymes which convert procarcinogens to carcinogens. These data were derived from experiments in which the ability of microsomes isolated from liver, intestine, and lung tissues of ethanol-fed and control rats to activate several test carcinogens was examined in the Ames Salmonella-mutagenicity test. The hypothesis is presented that ethanol-mediated induction of enzyme systems which activate procarcinogens to carcinogens in various tissues contributes to the enhanced incidence of cancer in the alcoholic.
Cancer Res 1979 Jul
PMID:Alcohol-related diseases and carcinogenesis. 22 Nov 10

The association of chronic liver disease with long-standing arsenic ingestion is well documented, although the spectrum and incidence of liver disease due to arsenic remain uncertain. We report two patients with chronic liver disease and arsenical skin changes that followed previous chronic arsenic ingestion. One patient developed macronodular cirrhosis and the other non-cirrhotic portal hypertension with perisinusoidal fibrosis. The latter patient developed a primary liver cell cancer. There is only one previously reported case of malignant hepatoma in a non-cirrhotic liver complicating chronic arsenicism. Lack of awareness of this uncommon but well described cause of chronic liver disease may account for a small proportion of patients with "cryptogenic" liver disease. Previous arsenic administration should be considered as a cause of chronic liver disease, especially when typical skin changes or internal neoplasia develop.
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PMID:Liver disease associated with chronic arsenic ingestion. 22 36

Knowledge of the cellular changes that lead to hepatic neoplasia in humans is limited. Cirrhosis is a common antecedent or accompaniment of liver cell carcinoma and it seems that both its etiology and its time of duration are relevant risk factors. Many cellular changes have been observed in patients and among populations considered to be at risk. Of these, liver cell dysplasia is the most striking, and studies of its prevalence, natural history, and association with particular forms of cirrhosis suggest that it is a precancerous change. Bile duct carcinoma may follow infestation with liver flukes and duct epithelial hyperplasia is present before the development of cancer. Angiosarcoma from several causes is commonly preceded by a peculiar fibrosis, vascular changes, and Kupffer cell hyperplasia.
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PMID:Precancerous changes in the human liver. 22

Liver cell dysplasia was noted on histological examination of nontumorous liver from 24 of 50 (48%) black southern African males with hepatocellular carcinoma (HCC). Macronodular cirrhosis was present in 40 (80%). There was no statistically significant difference between the frequency of dysplasia in 50% of 40 cirrhotic and 40% of 10 noncirrhotic livers, or in 52.6% of 38 hepatitis B antigen (HBAg) positive and 33.3% of 12 HBAg negative HCC patients. HBAg positivity was present in 80% of 40 cirrhotic and in 60% of 10 noncirrhotic HCC patients. This lack of significant correlation between liver cell dysplasia, and both cirrhosis and HBAg positivity in HCC patients in contrast to findings in Uganda and the United States, suggests a different pathogenetic mechanism for dysplasia in southern Africa. Liver cell dysplasia in man appears to be analogous to preneoplastic experimentally-induced hyperplastic foci or areas.
Cancer 1979 Nov
PMID:Liver cell dysplasia: association with hepatocellular carcinoma, cirrhosis and hepatitis B antigen carrier status. 22 74

Family member of 13 patients with hepatitis B surface antigen (HBsAg) positive primary hepatocellular carcinoma (PHC) were tested for the presence of hepatitis B virus-associated antigens and antibodies. Of the 122 members examined, circulating HGsAg was detected in 47 (39%), antibody to HBsAg (anti-HBs) was found in 37 (30%), and antibody to hepatitis B core antigen (anti-HBc) alone was present in 13 (11%). The relatives with the highest frequency of HBsAg positivity were the offspring of the propositus, followed by the nieces and nephews and the grandchildren. Anti-HBs and anti-HBc were detected most often in the spouses and non-blood relatives. Evidence for past and present hepatitis B virus (HBV) infection was more frequently found in the Asian family members when compared to the non-Asians. The e antigen (HBeAg) was present in 38% of the HBsAg positive individuals, including four with PHC; antibody to HBcAg (anti-HBe) was rarely detected. These results indicate that clustering of HBV infection was commonly present in family members of patients with PHC. The HBsAg positive individuals may be major contributors to the endemic pool of the virus, and may themselves be potential cases of chronic active type B hepatitis, cirrhosis, and PHC.
Cancer 1979 Dec
PMID:Evidence for clustering of hepatitis B virus infection in families of patients with primary hepatocellular carcinoma. 22 43

The disappearance rates(K) of FT-207 from the blood in patients with primary hepatoma and advanced cirrhosis of the liver were significantly lower than those in control patients with cancer but normal liver function. Pretreatment with tocopheryl nicotinate and indomethacin increased the K values in the control subjects, but was without effect on the K values in patients with primary hepatoma.
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PMID:Decreased disappearance rate of 1-(2-tetrahydrofuryl)-5-fluorouracil (FT-207) from the blood and its unresponsiveness to tocophreyl nicotinate and indomethacin in patients with primary hepatocellular carcinoma. 22 96

Plasma and 24-h urinary adenosine 3':5'-monophosphate (cyclic AMP) and guanosine 3':5'-monophosphate (cyclic GMP) were measured by radioimmunoassay in 12 normal subjects, 33 patients with six types of non-neoplastic disease (cholelithiasis, peptic ulcer, coronary heart disease, hypertension, regional ileitis, and cirrhosis), and 34 patients with five types of disseminated neoplastic disease (acute myelocytic leukemia; Hodgkin's disease; and metastatic cancer of the lung, colon, and breast). In patients with non-neoplastic disease, cyclic nucleotide values in plasma and urine did not differ significantly (P greater than 0.05) from those in normal subjects. In patients with disseminated cancer, cyclic AMP values in plasma and urine likewise did not differ significantly from those in normal subjects. Plasma cyclic GMP, in contrast, was significantly elevated in all five types of cancer patients, and urinary cyclic GMP was significantly elevated (five times the normal mean) in patients with acute myelogenous leukemia and Hodgkin's disease.
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PMID:Plasma and urine cyclic guanosine 3':5'-monophosphate in disseminated cancer. 22 52

Plasma and 24-hour urinary cyclic AMP and cyclic GMP levels were determined by saturation analysis in specimens from normal subjects and from 101 patients with tumours of the gastrointestinal tract, breast, lung, bladder or prostate, or with cirrhosis of the liver. Relative to 46 control subjects, plasma cyclic GMP concentrations were significantly elevated in seven patients with gastric tumours, 20 patients with cancer of the breast, six patients with lung cancer, and 12 patients with cirrhosis of the liver. Urinary cyclic GMP/creatinine ratios were significantly increased in cirrhotic patients and in the lung and oesophageal cancer groups. In no cancer group were increases in plasma or urine cyclic GMP levels sufficiently consistent to be of value in the diagnosis of human malignant disease. Changes in extracellular fluid cyclic nucleotide levels in the cirrhotic group were very similar to those that have been reported for primary hepatoma patients.
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PMID:Plasma and urine cyclic nucleotide levels in malignant disease and cirrhosis of the liver. 23 Feb 5

The occurrence of liver cirrhosis and PHC cases were analyzed from the autopsy material of three hospitals. In the course of this work 13,369 autopsy reports were examined. In 339 cases liver cirrhosis was established, the frequency of association with PHC was 19.4% (66 cases). Out of 66 PHC cases 17 (25.6%) were associated with a secondary malignant tumor. This number is 10 times greater than that of other tumors of epithelial origin. It also exceeds the enlarged number of linked secondary tumors as shown in the case of certain lymphoproliferative diseases.
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PMID:Secondary malignant tumors accompanied by primary hepatocellular carcinoma. 23 Jun 84

The dockyards of Genoa are exposed to many known or suspect carcinogenic agents, namely, asbestos, silica, polycyclic aromatic hydrocarbons, and halogenated hydrocarbons; other possibly harmful substances are trace amounts of aromatic amines, welding smokes, paints, and lipid-removing solvents. A cohort study of causes of death of 2190 dockyard workers in Genoa was conducted between January 1, 1960 and December 31, 1975. Mortality rates were calculated for 20 different occupational categories, for which there exist different levels of exposure to noxious substances. Two control groups were selected: the general male population of Genoa and all male employees (462) of San Martino Hospital, Genoa for the same period of time. Causes of death that demonstrated significant excesses for both control groups were: cancer of the colon, excluding the rectum; cancer of the larynx; cancer of the lung, bronchus, and trachea; cancer of the kidney, urinary bladder, and other urinary organs; respiratory diseases; and cirrhosis of the liver. The data obtained from these 20 job categories revealed different types and levels of risk for various carcinogenic agents.
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PMID:Mortality among shipyard workers in Genoa, Italy. 23 Jul 74


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