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)

Percutaneous liver biopsies obtained from patients with a history of chronic alcoholism and normal liver, fatty liver, alcoholic hepatitis, or active cirrhosis were incubated with tritiated proline to determine the pattern of collagen biosynthesis in these conditions. Incorporation of labeled proline and hydroxyproline into salt-soluble and insoluble fractions of collagen was evaluated by radiochemical analysis and tissue localization documented by autoradiography. Biopsy specimens of alcoholic hepatitis and cirrhosis exhibit a significant increase in the amount of radioactive proline and hydroxyproline in salt-soluble and insoluble collagen. Marked accumulation of radioactivity occurred over bile ducts, fibroblasts, and collagen fibers in the portal area and over hepatocytes, fibroblasts, and collagen fibers in the centrilobular area. Fatty liver is associated with an increase in uptake of proline and hydroxyproline in the salt-soluble fraction of collagem; silver grains appear in the periphery of fat-laden cells and in areas of focal inflammation. Digestion by collagenase indicates that labeling over fibroblasts and collagen reflects active synthesis, whereas, entry of proline into the cell protein pool is responsible for accumulation of radioactivity in other sites. In vitro ethanol causes a significant increase in the incorporation of proline and hydroxyproline into collagen in biopsy specimens of alcoholic hepatitis or active cirrhosis, but has no effect on collagen synthesis by normal or fatty liver.
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PMID:Collagen biosynthesis in liver disease of the alcoholic. 117 Feb 67

Oestrone (E1), oestradiol (E2), testosterone (T), androstenedione (A) and cortisol (F) as well as LH and the percentage of binding of E1, E2, T and F in plasma were measured and compared in normal young and old male subjects and in male patients with fatty liver, chronic hepatitis and cirrhosis of the liver. The alterations seen were most marked in the cirrhotic patients, but were partially also found in patients with fatty liver and in normal old subjects: a definite increase in E1, a smaller increase in E2, a decrease in T and a rise in LH. F remained unchanged. The ratios of E2/T and E1/T were higher in cirrhotic patients than in healthy young subjects. As the percentage of bound T in plasma rose, the oestrogen/androgen imbalance was greater in patients with liver disease and in old subjects than the ratio of total hormone plasma concentration indicates. The biological relevance of the extremely high E1 plasma concentrations in patients with cirrhosis of the liver is not known. It is suggested that the combination of elevated E1 and E2 and reduced T, which is strongly bound by increased sexual hormone binding globulin (SHBG) may be responsible for gynaecomastia and hypogonadism in chronic liver diseases. As similar alterations of steroid plasma concentrations and their binding to plasma proteins are found both in patients with liver disease and in old men, these changes may be caused by the same mechanism: namely an altered liver function.
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PMID:Steroid hormones and their binding in plasma of male patients with fatty liver, chronic hepatitis and liver cirrhosis. 117 87

Malnutrition is common among alcoholics because alcohol displaces protein-, vitamin-, and mineral-containing foods in the diet, and chronic alcohol consumption results in maldigestion and malabsorption of essential nutrients. In addition, alcohol exerts direct toxic effects on both the liver and gut, resulting in structural alterations in the intestine and the development of fatty liver, alcoholic hepatitis, and cirrhosis. Liver injury is preceded by an adaptive phase characterized by accelerated metabolism of drugs (including ethanol), and hyperlipemia, secondary to hypertrophy and hyperactivity of the smooth endoplasmic reticulum. Side effects include enhanced hepatotoxicity of CCI4 and possibly energy wastage. Alcoholics should not be led to beleive that correction or prevention of nutritional deficiency will prevent liver damage in the face of continued alcohol abuse.
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PMID:Alcohol and malnutrition in the pathogenesis of liver disease.. 117 54

On the basis of examinations of altogether 197 patients the results of the changes of GOT and GPT were compared with the old and new colour tests of the AWD Dresden in normal histology, virus hepatitis, fatty liver, liver cirrhosis and posthepatic occlusion. Though the new colour test reveals a higher sensitivity, the differential diagnosis between selected liver diseases, especially virus hepatitis and posthepatic occlusion syndrome have become more difficult. The cause for this is the less significant separability between the individual regions of reference.
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PMID:[Information value of 2 color tests in the determination of alanine and aspartate-aminotransferases in liver and biliary tract diseases]. 118 10

The jejuno-ileal bypass for weight reduction can hardly be considered a non-specific treatment: 3-4% of the patients develop chronic hepatic damage, 1-2% suffer hepatic failure due to massive fatty liver, rapidly progressing liver cirrhosis or hepatic fibrosis. Fatty liver is an invariable sequel of this operation. Once the above-mentioned symptoms set in or an incipient cirrhosis or fibrosis is diagnosed, immediate restoration of normal passage is required. The intestinal bypass syndrome observed in the patient (fem.) (viz. table 1) does not wholly coincide with the enteral bile acid loss syndrome occurring in extensive ileum resection (56) where usually there is no evidence of fatty liver, icterus, cholestasis or encephalopathy. Animal experiments seem to confirm that the blind loop in the broadest sense of the term is responsible for the sometimes fatal hepatic damage. Possibly we are confronted here with a pattern of hepatic damage due to toxic nutritive effects similar to cirrhosis as a sequel of low-protein and low-calorie intake or to the phenomenon observed in animal experiments. The cholestasis confirmed by biopsy and chemical methods is a manifestation of these hepatic disorders. The clinical aspects resemble the Reye syndrome that we know in pediatrics. Patients have to be carefully selected and informed about possible postoperative damage; a continuous clinical follow-up with biopsy of the hepatic tissue is also indicated.
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PMID:[Liver damage following intestinal by-pass surgery for weight reduction]. 122 12

A model has been developed for the administration to rats and baboons of ethanol as part of a nutritionally adequate liquid diet. With this regimen, ethanol intake was much higher than with conventional procedures. All animals gained or maintained their body weight, and liver morphology was normal in the controls. Isocaloric substitution of carbohydrate by ethanol (36% of total calories in rats and 50% in baboons) resulted in the production of fatty liver in all animals, while the baboons also developed alcoholic hepatitis and cirrhosis with increased activities of serum glutamic oxaloacetic transaminase. Inebriation and manifestation of dependence upon withdrawal of the diet were observed in baboons and quantitated in the rat. Chemical alterations produced by ethanol at the fatty liver stage were characterized by hyperlipemia, striking triglyceride accumulation in the liver and enhanced activities of microsomal drug metabolizing enzymes, including the microsomal ethanol oxidizing system (MEOS). Ultrastructural changes of the mitochondria and the endoplasmic reticulum were already present at the fatty liver stage and persisted throughout the hepatitis and cirrhosis. The lesions were similar to those observed in alcoholics (including the inflammation and the central sclerosis), and differed strikingly from the alterations produced by other models of liver injury. In showing that all aspects of liver injury observed in alcoholics can be reproduced in animals by the feeding of pure ethanol with an adequate diet, this study incriminates ethanol itself as a cause for the hepatic complications. This new experimental model is proposed as a tool for the study of the pathogenesis and treatment of alcoholic liver injury and dependence.
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PMID:Alcoholic liver injury: experimental models in rats and baboons. 123 25

The activities of serum cholinesterases were determined in parallel with acetyl-, butyryl- and propionyl-thiocholiniodide in healthy persons and patients with acute and chronic hepatitis, cirrhosis of the liver, fatty liver, cholestasis, intoxication and malignant tumors. The following normal values were obtained: See Article. The correlations between the various methods, especially between butyryl- and propionylthiocholiniodide are statistically significant. Compared to healthy persons, the activity of serum-cholinesterases, determined with the three substrates, decreased significantly in patients with acute and chronic hepatitis, cirrhosis of the liver, intoxication and malignant tumors. A change of specificity of serum-cholinesterases towards acetyl-, butyryl- and propionylthiocholiniodide in normal persons and patients with endogenous or exogenous coma of the liver was not observed. In all cases a parallel decrease of activity in sera was determined.
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PMID:[Comparative methods for the determination of the activity of serumcholinesterases (acylcholin-acyl-hydrolase E.C. 3.1.1.8) and their diagnostical value (author's transl)]. 124 30

The levels of C3, cholinesterase, albumin and prothrombin were determined in 46 patients (27 males and 19 females) - 26 with cirrhosis of the liver, 9 with acute hepatitis, 6 with chronic aggressive hepatitis, 1 with chronic persistent hepatitis and 4 with fatty liver. In all patients and, particularly in those with cirrhotic liver, it was shown that the normal or pathological level of serum C 3 is related both qualitatively and quantitatively to the normal or pathological levels of cholinesterase, albumin, and prothrombin. The percentage in which the levels of these four parameters were pathological was considerably higher in the cases with hepatic coma than in the cases without hepatic coma. The determination of the range of confidence for the 4 parameters showed that, in the patients with hepatic coma, cholinesterase reacted most sensitively to liver damage (0.5 - 0.94) followed by C3 and prothrombin (0.33 - 0.81). Also in the cases without hepatic coma, cholinesterase was the most sensitive indicator (0.05 - 0.29), followed by prothrombin (0.03 - 0.24), albumin and C3 (0.00-0.16).
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PMID:Serum levels of C3 and cholinesterase in various diseases of the liver. 125 98

Increased concentrations of neopterin have been found in conditions causing a stimulation of cellular immunity, including various malignancies. In liver diseases, serum or urinary neopterin levels have been studied in acute viral hepatitis, chronic hepatitis, fatty liver and liver cirrhosis. In the present study neopterin serum levels have been measured in 16 patients with hepatocellular carcinoma (HCC), in 32 patients with liver cirrhosis, and in 28 healthy subjects as controls. Mean values of serum neopterin were significantly increased (p < 0.01) in patients with HCC (15.89 +/- 6.34 nmol/l) when compared with those of normal subjects (4.74 +/- 2.13 nmol/l), but no difference was observed between patients with HCC (associated or not with liver cirrhosis) and patients with liver cirrhosis. Neopterin concentrations are not affected by liver cirrhosis aetiology, nor by its clinical severity, and are not correlated to the values of serum alpha-fetoprotein, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, gamma-glutamyl-transferase, and gamma-globulin. The results show that there is a consistent overlap of values in patients with HCC and liver cirrhosis; macrophage activation seems to be a feature of chronic liver diseases, irrespective of HCC development.
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PMID:Serum neopterin levels in patients with hepatocellular carcinoma. 128 21

Hepatitis B virus (HBV) markers were studied with Sorin RIA kits in serum samples from 390 patients suffering from histologically confirmed chronic liver disease. On the basis of negative HBsAg, anti-HBs, anti-HBc tests, HBV infection was excluded in 235 of the cases. The diagnosis was fatty liver and/or alcoholic hepatitis in 52%, while chronic active hepatitis and/or liver cirrhosis only in 21.7%. Part or present HBV infection was proven in 155. In 53% of these cases the diagnosis was chronic active hepatitis and/or liver cirrhosis, whereas fatty liver and alcoholic hepatitis occurred in 27.7%. Detailed HBV marker analysis was performed in 76 patients. Previous infection without replication (positive anti-HBs and/or anti-HBc and/or anti-HBe) was proven in 48 cases, 12 patients had active HBV infection (positive HBsAg, HBe, IgM anti-HBc), while in 16 cases HBV integration (positive HBsAg, anti-HBc, anti-HBe) was proven. HBsAg-IgM complex seropositivity was shown in every case with active HBV replication. Because of therapeutic, prognostic and epidemiologic reasons, the significance of detailed HBV serology in chronic liver diseases is stressed.
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PMID:The significance of detailed hepatitis B virus serology in chronic liver diseases. 129 81


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