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)

In well defined liver diseases in 69 alcoholics and in 71 patients without history of alcoholism the enzymatic findings were compared. Also a group of 43 alcoholics with praedelirium or delirium tremens were examined. In steatosis due to alcohol, the average of GGTP (145 U/l) attains values two times higher than in comparable cases of non-alcoholic origin (73 U/l). In cirrhotics with alcoholism, the average GGTP levels (477 U/l) exceed those obtained in patients with cirrhosis of other origin (110 U/l), four times more. Similar or higher GGTP values were found only in primary biliary cirrhosis. After a period of at least 3 months of abstinence, GGTP values had decreased (to 68 U/l) in the average). The highest values of GGTP were found in acute alcoholic hepatitis and in chronic alcoholics with praedelirium or delirium tremens. GGTP accords diagnostic hints in comparison with other enzymes, as shown by a quotient of GGTP-GPT. GGTP is very helpful for differentiation and long time observation of alcoholic liver disease, especially with regards controlling abstinence of alcohol.
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PMID:[Gamma-glutamyl-transpeptidase in alcoholic liver diseases]. 1 29

Serum alpha-fetoprotein levels were measured by radioimmunoassay in 473 patients with biopsy-proved noneoplastic hepatic disorders; 22% had values greater than 40 ng/ml, whereas only 1 of 350 patients with nonhepatic benign diseases had a value greater than this. Levels exceeded 40 ng/ml in more than 30% of patients with various types of hepatitis, and in 0% to 15% with inactive postnecrotic cirrhosis, primary biliary cirrhosis, biliary tract obstruction, and alcoholic liver disease. Values greater than 500 mg/ml were observed solely in viral subacute hepatic necrois. Only one patient had a level exceeding 3,000 ng/ml, the concentration at which alpha-fetoprotein is detectable by agar-gel diffusion. Of 75 patients with hepatoma, serum alpha-fetoprotein levels exceeded 40 ng/ml in 69%, and exceeded 3,000 ng/ml in 48%. These studies indicate that serum alpha-fetoprotein levels are elevated in several nonneoplastic hepatic disorders when a sensitive assay is used; this phenomenon may reflect hepatic regeneration.
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PMID:alpha-fetoprotein in noneoplastic hepatic disorders. 4 62

Serum-25-hydroxy-vitamin-D (25 OHD) concentration has been measured in 106 patients with untreated parenchymal and cholestatic liver disease. Low mean values were found in groups of patients with alcoholic hepatitis and cirrhosis, non-cirrhotic active chronic hepatitis, lupoid and cryptogenic cirrhosis, symptomatic primary biliary cirrhosis, and acute and chronic biliary disease. In a group of patients with presymptomatic biliary cirrhosis the mean value was not significantly different from normal. It is concluded that in the presence of significant parenchymal or cholestatic liver disease serum-25-OHD concentrations are usually low. The mechanisms for the reduction remain to be clarified, but low serum-25-OHD values may play a contributory role in the aetiology of osteomalacia in chronic liver disease.
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PMID:Serum-25-hydroxy-vitamin-D in untreated parenchymal and cholestatic liver disease. 6 May 15

A new method, radio-crossed immunoelectrophoresis, demonstrates alpha-fetoprotein (AFP) in sera with a sensitivity of 1 mug/1. By this method AFP with alpha mobility was not found in sera from healthy individuals, patients with chronic active hepatitis and cirrhosis, primary biliary cirrhosis, secondary liver cancer and cystic fibrosis. In some of the sera, AFP was elevated when measured by conventional radioimmunoassay method and the sera contained an AFP-like substance with gamma mobility when analyzed by radio-crossed immunoelectrophoresis. The nature of this gamma substance is still obscure and needs further investigation.
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PMID:Alpha-fetoprotein-like activity in sera from patients with malignant and non-malignant disease and healthy individuals. 6 Oct 78

Liver specimens from 103 patients with various hepatic diseases and from 297 consecutive liver biopsies examined routinely were stained with orcein after oxidation of the tissue sections with potassium permanganate. Orcein-positive dark brown cytoplasmic material could be demonstrated in 27 cases with long-standing cholestasis. These patients had either primary biliary cirrhosis, the cholestatic liver disease of ulcerative colitis or chronic active hepatitis, advanced alcoholic cirrhosis or secondary biliary cirrhosis due to extrahepatic biliary obstruction. Orcein-positive material could not be demonstrated in congenital disorders of bilirubin metabolism or in hemochromatosis. Similarly, it could not be found in acute, toxic, alcoholic or chronic persistent hepatitis.
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PMID:The occurrence of orcein-positive hepatocellular material in various liver diseases. 6 38

CH50 and the concentrations of C3, C4, C1 INH and factor B have been measured in sera from 34 control subjects and 178 patients with various hepatobiliary diseases, including primary biliary cirrhosis (PBC), chronic active hepatitis (CAH), cryptogenic cirrhosis (CC), alcoholic liver disease (ALD), Wilson's disease (WD), large duct biliary obstruction (LDBO) and viral hepatitis (VH). CH50 was decreased in CAH and CC. C3 was increased in PBC, LDBO and VH and decreased in CAH and CC. C4 was decreased in PBC, CAH, ALD and WD. C1 INH was increased in PBC, CAH, ALD, LDBO and VH. Factor B was increased in LDBO and VH and decreased in CC. In none of the patient groups was the mean C4 level increased or the mean C1 INH level decreased. All 5 indices of serum complement were lower in ascitic than nonascitic patients. Data on serum complement were similar in HBsAg positive and negative VH. Discriminant analysis facilitated separation of all the patient groups on the basis of complement data, except PBC and VA. Analysis of data using a within-group correlation matrix revealed a significant negative correlation between C4, the most discriminating variable of serum complement in CAH, and gamma-globulin concentration in CAH. The possible contribution of factors such as activation of complement, impaired hepatic synthesis of complement components, an acute phase response and cholestasis to altered serum complement profiles in different hepatobiliary diseases is discussed.
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PMID:Profiles of serum complement in patients with hepatobiliary diseases. 8 74

A double-antibody immunoprecipitation method was developed for detecting antibody to liver-specific membrane lipoprotein (anti-LSP) in sera of patients with various liver diseases and primary nonhepatic autoimmune diseases. Liver-specific membrane lipoprotein prepared from normal rat livers was labeled with 125I (chloramine-T) and monospecific antibody raised in rabbits. Cross-reactivity and absorption studies demonstrated that the assay used was highly specific. The frequency and titer of anti-LSP were similar for HBsAg-positive and -negative patients with both acute and chronic liver diseases. Patients with chronic active hepatitis had the highest frequenzy (25 of 44 cases, 57%) when compared with those with chronic persistent hepatitis (5 of 23 cases, 22%) and nonalcoholic cirrhosis (8 of 21 cases, 38%). Of the anti-LSP positive cases, the mean titer in patients with chronic active hepatitis tended to be the highest. In patients recovered from acute viral hepatitis, anti-LSP was transiently positive (7 of 20 cases, 35%) in the acute phase. In those who progressed to chronic hepatitis, a late rise as well as an early rise occurred in 6 of 10 patients before the diagnosis was made. Two of 6 patients with primary biliary cirrhosis had anti-LSP, but none of 41 patients with other nonviral liver diseases and none of 60 patients with primary nonhepatic autoimmune diseases. These data indicate that an autoimmune reaction directed against LSP can be initiated during the acute phase of viral hepatitis and it may persist in chronic hepatitis in both HBsAg-positive and -negative cases.
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PMID:Occurrence and significance of antibody to liver-specific membrane lipoprotein by double-antibody immunoprecipitation method in sera of patients with acute and chronic liver diseases. 10 59

It has been described that mitochondrial antibodies can be detected in the serum of primary biliary cirrhosis patients (over 90%) and that these antibodies are directed specifically against a component of the mitochondrial inner membrane. In the present study whole mitochondria isolated from rat liver were exposed to mitochondrial antibodies from patients with primary biliary cirrhosis, and to antibodies induced experimentally in rabbits to mitochondrial antigens of rat liver. This was an attempt to study the action of these antibodies and complement on mitochondrial functions. By studying respiratory control and oxidative phosphorylation of mitochondria, no significant, nor specific effect on mitochondrial membranes functions could be detected, after the incubation of suspensions of mitochdondria with normal or immune gamma-globulin (neither from rabbits nor from human) nor with the addition of complement. Furthermore, the respiration of fragmental mitochondria using succinate and NADH substrates was unaffected by the antibodies and complement. Similarly, mitochondrial APT-ase activity and swelling and contraction were not affected by antibody. Experiments are in progress to study the hypothesis of a lymphocyte dependent antibody mediated cytotoxicity in this system. In order to demonstrate that this autoimmune phenomenon might be associated with cellular immunity to a mitochondrial component, we have in a previous report demonstrated impairment of mitochondrial respiratory control by lymphocytes from rabbits sensitized in vivo with mitochondrial antigens. Subsequently we have recently shown evidence of sensitization. In-vivo of lymphocytes from patients with primary biliary cirrhosis as demonstrated by an injurious effect on rat liver mitochondria by lymphocytes from patients with this disease. Further studies are necessary to clarify the involvement of this phenomena in the possible mechanisms responsible for the pathogenesis of the lesions.
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PMID:Primary biliary cirrhosis. Study of the action of mitochondrial antibody plus complement on mitochondrial membrane functions. 13 54

A histopathological study was carried out on 27 patients with chronic inflammatory liver disease and clinical and/or biochemical evidence of cholestasis who had either mitochondrial antibodies against mitochondrial antigen fractions of 1.19 density ("PBC antigen"; 14 cases) or of 1.13 density ("CAH-PBC mixed-type antigen"; 13 cases). For comparison, the liver biopsies of 17 patients with chronic-aggressive hepatitis (CAH) and antinuclear and/or anti-smooth muscle antibodies but without cholestasis and mitochondrial antibodies, were evaluated. The 14 patients with mitochondrial antibodies against the PBC antigen showed the typical histological features of primary biliary cirrhosis (PBC). The 13 patients with mitochondrial antibodies against the CAH-PBC mixed-type antigen had heterogenous liver alterations. In 11 cases highly active CAH and/or active postnecrotic cirrhosis (AC) were found both with augmented ductular proliferation. Some of these cases showed distinct criteria of PBC as early bile duct lesions or absence of regular bile ducts. The liver histology of one case corresponded to classical PBC; another case to chronic persistent hepatitis. The CAH-patients without cholestasis and mitochondrial antibodies only occasionally showed bile duct proliferation. In conclusion, a high correlation was found between mitochondrial antibodies against the CAH-PBC mixed-type antigen and highly active CAH or early AC with augmented ductular proliferation. This represents an overlapping of CAH and PBC. In contrast, the cases with antibodies reacting to the PBC antigen showed the slowly progressive liver changes of typical PBC.
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PMID:Histopathological features in mixed types of chronic aggressive hepatitis and primary biliary cirrhosis. Correlations of liver histology with mitochondrial antibodies of different specificity. 13 50

Extrahepatic and intrahepatic biliary obstruction of different etiology were studied in 62 patients, who were investigated for the presence of lipoprotein X (Lp-X). It was found present in 19 of 20 cholestasis by lithiasis, in all three primary biliary cirrhosis patients, in 2 of 4 cirrhosis, in 5 of 13 hepatitis, in all three benign recurrent intrahepatic cholestasis and in 1 of 2 recurrent juandice of pregnancy. It was found in a Dubin Johnson. Lp-X disappeared in 4 patients within two weeks after relief of the obstruction. It was found in patients with cholestatic hepatitis during the first week of jaundice. It was found in the first 48 hours in three patients with cholestasis by lithiasis. Lp-X does not help in differential diagnosis between extrahepatic and intrahepatic biliary obstruction, but the time of its appearance could contribute to it in some cases. A word of caution is raised in indicating surgery in a cholestatic patient without the presence of Lp-X.
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PMID:LP-X in cholestasis. 17 23


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