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)

Geographic area, age and sex influence the epidemiology of hepatoma. Aetiological factors are aflatoxins, sex hormones, thorotrast, alpha 1-antitrypsin deficiency, immunosuppression, vinylchloride, parasites, cirrhosis of the liver, and the hepatitis-B virus. Early diagnosis of the tumour is possible using alpha 1-fetoprotein estimations and modern morphological methods, particularly scintiscanning. Tumour resection is therapeutically desirable, while selective chemotherapy remains palliative and liver transplantation failed to prolong survival.
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PMID:[Primary liver cell carcinoma, aetiology and clinical picture (author's transl)]. 9 Dec 71

The immunocellular response to fetal antigens was studied in ten patients with hepatocarcinomas. Homogenized extracts of human fetal liver and purified human alpha-fetoprotein were used as antigen substances. The control group included 15 patients with cirrhosis of the liver. The level of circulating T lymphocytes (E-rosettes) was also registered. Patients with hepatocarcinoma showed a definite response to both antigens, determined by the degree of inhibition of leukocyte migration. The migration indices were as follows: x = 0.65 +/- 0.16 for homogenized fetal liver antigen, and x = 0.79 +/- 0.13 for alpha-fetoprotein antigen. These values were 0.93 +/- 0.13 and 0.95 +/- 0.15 respectively in the cirrhotic patients. The differences in the migration indices for the two groups were statistically significant with both antigens (p less than 0.0005 and p less than 0.005). The decrease of the number of T lymphocytes in patients with hepatomas was also significant (p less than 0.005). The determination with homogenized fetal antigen was more sensitive than with alpha-fetoprotein (p less than 0.01). A significant relationship between the severity of the tumor and the immunocellular response could also be seen (r = 0.84; p less than 0.001). Response tended to diminish as the tumor progressed. The disappearance of immunocellular response seemed to depend at least in part on the decreasing number of T lymphocytes, since there was a significant inverse correlation between the two parameters (r = -0.75; p less than 0.01).
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PMID:[Immunocellular response to fetal antigens in patients with hepatoma (author's transl)]. 9 78

The frequency of Hepatitis Bs antigen and antibody was determined in healthy subjects and patients with acute and chronic liver disease. The frequency of HBs Ag in healthy subjects was 2.9% and HBs Ab 35%. The high prevalence of antibody in normal individuals suggests a constant non-parenteral sub-clinical exposure to hepatitis virus. Thirty-three per cent patients with acute viral hepatitis, 20% with cirrhosis and 10% with hepatocellular carcinoma were HBs Ag positive, while HBs Ab was detected in 22% cases of acute viral hepatitis and 37% with other liver disorders. This pattern of prevalence of HBs Ab suggests that hepatitis B virus may be an important etiological agent in acute and chronic liver disease in Pakistan.
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PMID:Prevalence of hepatitis B surface antigen and antibody in healthy subjects and patients with liver disease. 9 84

Enzyme deviations in injured livers were studied by analyzing isozyme patterns of phosphorylase using a newly developed electrophoretic method, which separates six molecular species of this enzyme, i.e. M,FM,F,L,L', and FL'. In hepatic injuries caused by CCl4 and galactosamine intoxications of rats, F appeared in early stages and L' (and FL') in later stages of the injuries with a concurrent decrease or loss of L, which is a sole isozyme component of adult liver. In injured livers of patients with hepatitis and cirrhosis of the liver, increases in FL' activity were also found. Appearance of F was found only in hepatocellular carcinoma. The results obtained with phosphorylase isozyme analysis support the idea that an undifferentiated gene expression takes place in the injured livers of non-malignant hepatic disorders.
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PMID:Studies of liver phosphorylase in hepatic injuries II. Alteration in isozyme pattern. 15 93

The activities of glutamic-oxaloacetic transaminase (GOT), glutamic-pyruvic transaminase (GPT) and glutamate dehydrogenase (GLD) were determined in liver biopsy specimens and sera of patients with various liver diseases. Mitochondrial and cytosol isozymes of GOT were also separated for their assay. The activity ratio of GOT/GPT in serum was found to reflect the ratio in liver cytosol. The increased ratio in advanced or severe liver diseases, such as liver cirrhosis, was due to the greater decrease in liver cytosol GPT activity, this being pronounced in primary hepatoma. The activity of GLD decreased similarly but less markedly. The relatively greater decrease in GPT compared with GOT in advanced liver diseases was not mainly due to leakage of the enzyme from the liver, but to a specific mechanism associated with hepatic injury or its progression. Other pathological conditions of the liver such as those in obstructive jaundice and alcoholic liver injury also appeared to result in reduced liver GPT activity, which was reflected in the serum as an increased GOT/GPT ratio.
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PMID:The mechanism of release of hepatic enzymes in various liver diseases. II. Altered activity ratios of GOT to GPT in serum and liver of patients with liver diseases. 16 Jan 82

It is well known that incidence of chronic obstructive lung disease in adult patients with alpha 1-antitrypsin deficiency (ATD) is high. Adult carriers of this genetic trait with cirrhosis of the liver, and also with fibrosis of the liver and hepatoma, have been reported. A causal relationship between ATD and liver lesions has been suspected. In most cases liver disease has been recognized at post morten, - in a few cases, however, intra vitam, when severe symptoms of the liver disease had become apparent. The case of a 59 year-old patient is reported with PIZZ-homozygous ATD, moderate pulmonary emphysema and with marked portal fibrosis and focal transition in cirrhosis of the liver without any sequelae. The clinical course has been rather benign so far.
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PMID:[Alpha 1-antitrypsin deficiency, liver cirrhosis and pulmonary emphysema (author's transl)]. 16 Apr 81

A patient with hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease), treated with ethinyl estradiol, multiple blood transfusions, and iron-dextran, developed hepatocellular carcinoma and acquired hepatocerebral degeneration. In addition to the carcinoma, the liver contained extensive arteriovenous maliformations, telangiectasis, and changes of Osler atypical cirrhosis. The carcinoma possibly had its genesis in the presence of an ocongenic serum hepatitis virus, or the cirrhosis, or both.
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PMID:Hereditary hemorrhagic telangiectasia. A case with hepatocellular carcinoma and acquired hepatocerebral degeneration. 16 31

Alpha-fetoprotein (AFP) is an alpha1-glycoprotein (M.W. about 65000) appearing in the fetal serum of most mammals including man during the early stages of pregnancy; 4 weeks after birth it disappears altogether or exists at very low concentrations as in the normal adult. AFP is formed in the yolk sac, the fetal liver and the gastro-intestinal tract. One of its physiological functions in fetal life is supposed to be the protection of the fetus from maternal oestrogens (oestrophilic property). The clinical significance of AFP is based on the regular and increasing production in primary liver cell carcinoma, less frequently in teratogenetic tumors where it serves as a control of therapy and course of the disease. Less frequent, minor and temporary increases in the AFP serum level occur in several primary tumors with secondary liver involvement, and in inflammatory gastro-intestinal diseases, e.g. of the liver (hepatitis, cirrhosis). AFP has an increasing importance in gynecology (gestational age, fetal distress syndrom, malformations, hydatidiform mole/chorion carcinoma). The physico-chemical properties of AFP are widely known. Both fetal and tumor AFP appear to be immunologically and biochemically identical, as are that of tissue and biological fluids. The differences observed (variants, microheterogeneity) depend mainly on the different content of sialic acid. An antigenetic relationship exists, between the AFP of most species. The immunodiffusion (Ouchterlony) is the most frequently used but relatively insensitive test (1-5 mug/ml) in finding AFP, whereas the radioimmunoassay is the most sensitive one (up to 0,25 ng/ml) and permits the determination of normal serum levels in adults (below 20 ng/ml). The serum concentration in healthy pregnant women lies up to 500 ng/ml, in patients with hepatitis, liver cirrhosis and other liver diseases mostly under 3 mug/ml, whereas in those with primary liver cell carcinoma levels up to and above 600 mg-percent have been found.
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PMID:[Carcinofetal antigens. I. alpha-fetoprotein (author's transl)]. 16 80

Most of the knowledge of post-hepatitic cirrhosis comes from studies performed in the last five years on the hepatitis B antigen-related variety. The position of other types of hepatitis (particularly type A) as an aetiological factor in cirrhosis remains conjectural. In general, the post-hepatitic cirrhosis develops insidiously after a mild or unrecognised acute episode of hepatitis. General progress is slow. Early deaths are due to liver failure. Later, primary hepatocellular carcinoma assumes increasing importance. Needle biopsy of the liver is usually necessary to confirm the diagnosis of cirrhosis and to estimate the degree of activity. Sampling errors when such a small specimen of liver is obtained must be taken into account, when formulating a diagnosis and prognosis. Prednisolone therapy is usually given if the patient is symptomatic, biochemical tests are abnormal and the liver biopsy confirms active chronic hepatitis with or without cirrhosis. The evidence of benefit is not so strong as for other forms of active hepatitis and cirrhosis such as the lupoid type. The management of the cirrhosis is otherwise along orthodox lines.
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PMID:Viral hepatitis and cirrhosis. 16 21

Significant liver disease including fatty metamorphosis, alcoholic hepatitis, cirrhosis, and hepatoma occur in two thirds of subjects who consume alcoholic beverages in sufficient quantities to interfere with work and social responsibilities; this is of major importance in the rapidly escalating morbidity and mortality from alcoholism. Chronic alcoholics should be routinely evaluated for the presence of altered liver function and structure. Clearance of indocyanine green using dichromatic ear densitometry and computer and analysis provides a simple and sensitive method for mass screening of such patients. Clinical studies of lymphocyte reactivity to purified alcoholic hyaline may be valuable in recognizing alcoholic hepatitis, the precursor of cirrhosis. Ethanol toxicity, malnutrition and constitutional factors contribute to the development of hepatic fibrosis and cirrhosis in alcoholics. Ethanol and/or acetaldehyde and the supernatant from lymphocytes stimulated by alcoholic hyaline cause a significant increase in the incorporation of proline into collagen of the damaged liver. Abstinence and correction of nutrient deficits are the cornerstones of treatment for alcoholic liver disease; a daily meal and dietary supplements should be provided for those with liver injury who continue to imbibe. Alcoholics with progressive liver disease despite supportive therapy may be aided by pharmacologic agents which suppress immunologic response and reduce fibrogenesis.
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PMID:Liver disease of the alcoholic. 16 41


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