Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum gamma-glutamyl transpeptidase (gamma-GT) level was estimated in 132 patients with different liver diseases (chronic persistent and chronic active hepatitis, postnecrotic cirrhosis, chronic alcholic hepatitis and alcoholic cirrhosis, cholestasis syndrome, fatty liver, Gilbert disease) and malignancies with and without liver involvement. The gamma-GT levels were compared with the values for serum bilirubin, transaminases (GOT, GPT) and alkaline phosphatase in the same patients. gamma-GT values were normal in chronic persistent hepatitis and increased in chronic active hepatitis. Very high activities were measured in chronic alcoholic cirrhosis in contrast to postnecrotic cirrhosis. gamma-GT proved to be more sensitive than alkaline phosphate as an index of cholestasis and liver involvement in malignancies. It is suggested that gamma-GT activity offers valuable aid in differential diagnostics of liver-diseases. gamma-GT being an inducible enzyme, its activity may be raised by enzyme inducing drugs also in subjects without liver disease.
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PMID:Serum gamma-glutamyl transpeptidase: its clinical significance. 2 44

Monooxygenase enzymes are involved in the biotransformation of drugs and of environmental carcinogens. The activity of 7-ethoxycoumarin 0-deethylase and associated NADPH-cytochrome c reductase was determined in 9000 g supernatant from bioptically obtained liver specimens from patients with various liver diseases in order to study in vitro drug metabolising capacity. Monooxygenase and reductase activity was significantly higher in the livers of 21 patients with alcoholic liver disease (fatty liver, alcoholic hepatitis, cirrhosis of the liver) than in 22 normal controls or in six patients with chronic active hepatitis. The raised activity of drug-metabolising enzymes obtained from alcoholics with liver damage differs from normal values found in five alcoholics without liver disease. Both groups were comparable in respect to the amount of alcohol consumed and duration of abuse. A strikingly low monooxygenase activity was observed in eight patients with cirrhosis of the liver and ascites, with, however, no apparent effect on reductase activity. The results show that alcoholic liver disease is associated with enhanced monooxygenase and reductase activity, but alcoholism, per se, is not. This rise of drug-metabolising enzyme activity could lead to selectively increased rates of biotransformation in patients with alcoholic liver damage.
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PMID:Monooxygenase enzyme activity in alcoholics with varying degrees of liver damage. 11 58

Liver protocallagen proline hydroxylase activity (PPH activity) was determined in patients with various liver diseases, CCl4-induced liver fibrosis rats and cholin deficiency (tcd) fatty liver rats. The following results were obtained: Liver PPH activity in patients with chronic hepatitis was higher than that in patients with acute hepatitis, while the activity in patients with liver cirrhosis was much higher than that in patients with chronic hepatitis. The activity was higher in patients with chronic active hepatitis than in those with chronic inactive hepatitis. Patients with active and progressive liver cirrhosis were found to have an especially high PPH activity, in whom the activity reflected well the degree of liver fibrosis. Even though fibrosis in persistent hepatitis was almost negligible or slight, the degree of liver PPH activity in persistent hepatitis was similar to that in liver cirrhosis. Liver PPH activities in CCl4-induced liver fibrosis rats and CD fatty liver rats elevated proportionally to the lapse of time. Whilst liver PPH activity in rats of CD fatty liver without fibrosis in 23 to 31 weeks after the start of the experiment was slightly lower than that in rats of CD fatty liver with fibrosis. But liver PPH activity of the former was considerably higher than that of control rats.
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PMID:Liver protocollagen proline hydroxylase in human liver diseases and experimental liver fibrosis. 19 57

A number of chronic hepatic lesions can result from adverse reactions to medicinal agents. Such lesions include a form of chronic active hepatitis; hepatic steatosis, phoepholipidosis and granulomatosis; several vascular lesions; two types of noncirrhotic portal hypertension; several types of cirrhosis and several neoplasms.
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PMID:Drug-induced chronic hepatic disease. 22 60

The large number of chemical agents administered for therapeutic or diagnostic purposes can produce various types of hepatic injury by several mechanism. Acute injury may be cytotoxic, cholestatic or mixed. Cytotoxic injury may consist of necrosis or steatosis. Cholestatic injury may be cholangiolitic (hepatocanalicular) or bland (canalicular). Chronic hepatic lesions caused by medicinal agents include chronic active hepatitis, steatosis, cirrhosis, fibrosis, hepatoportal sclerosis (non-cirrhotic portal hypertension), hepatic vein thrombosis, peliosis hepatis, adenoma, carcinoma, and angiosarcoma. There is a useful relationship between the type of hepatic injury and the chemical setting in which the drugs are employed. Some agents produce the liver damage because they are intrinsic (true, predictable) hepatotoxins. Other (non-predictable "hepatotoxins"), produce hepatic injury only in the rare and unusually susceptible individual (idiosyncratic injury). Hepatotoxic agents can be recognised by their dose-dependent and experimental reproducibility, properties which are not shared by agents which produce hepatic injury only in idiosyncratic hosts. Intrinsic hepatotoxins may be categorised as direct or indirect. Direct hepatotoxins injure the hepatocyte by direct physiochemical alteration and as a consequence produce metabolic defects. Indirect hepatotoxins selectively block metabolic pathways and, by producing a precise biochemical lesion, lead to structural changes. They may lead to hepatic steatosis or necrosis (cytotoxic indirect hepatotoxins) or block bile flow (cholestatic indirect hepatotoxins). Direct hepatotoxins are rarely encountered as drugs. Overdoses of some drugs and antineoplastic agents appear to be indirect cytotoxic hepatotoxins, and the C-17 alkylated anabolic and contraceptive steroids are indirect, cholestatic hepatotoxins. Idiosyncracy of the host is the mechanism for most types of drug-induced hepatic injury. It may reflect allergy to the drug or a metabolic aberration of the host permitting the production of hepatotoxic metabolites.
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PMID:Drug-induced liver disease. 35 64

IgA bound in vivo was shown by immunofluorescence on the plasma membrane of isolated hepatocytes from subjects with normal liver and patients with liver cirrhosis, chronic active hepatitis or fatty liver. IgA in sera with elevated IgA concentrations, especially from cases with alcoholic cirrhosis, was bound in vitro to isolated hepatocytes from rabbit and mouse. This was not due to the high IgA concentration per se. Moreover, polyclonal polymeric serum-type and secretory IgA, and three of ten polymeric monoclonal IgA preparations, showed similar binding properties. Conversely, purified polyclonal and monoclonal monemeric IgA did not show affinity for the hepatocytes. The binding of polymeric IgA did not seem to depend on the proportion of dimers and larger polymers, kappa- or lambda-type light chains, heavy-chain subclasses, content of J chain or affinity for secetory component. The in vivo binding of IgA by hepatocytes is probably a physiological phenomenon which in part may explain the normal clearance of polymeric IgA from serum.
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PMID:In vivo and in vitro binding of IgA to the plasma membrane of hepatocytes. 36 35

Chronic hepatitis is one of liver diseases with arguments from the clinical and histopathological aspects. Histopathological examinations were made on 687 biopsy cases clinically diagnosed as chronic hepatitis. Histopathological classification was based on our own criteria by referring to discussions in the series of Inuyama symposia on hepattis and others. The correlation between histological diagnosis and clinical data was also examined. Histopathological diagnoses made of the 687 cases were classified as follows; normal liver or liver with no pathognomonic changes of 77 cases (11.2%), non-specific reactive hepatitis of 56 cases (8.0%), viral hepatitis of 488 cases (71.0%), alcoholic hepatitis of 25 cases (3.6%), fatty liver of 23 cases (3.3%), massive liver necrosis of 3 cases, liver fibrosis of 2 cases, congestive liver of 1 case, and unclassified 12 cases due to inadequate specimens or other reasons. Among 488 viral hepatitis cases, histological stages were as follows; acute hepatitis (38 cases, 7.8%), persistent hepatitis (23 cases, 4.7%), chronic inactive hepatitis (142 cases, 29.1%), chronic active hepatitis (165 cases, 33.8%), chronic hepatitis with subloblar necrosis (33 cases, 6.8%), precirrhosis (51 cases, 10.5%), cirrhosis (27 cases, 5.5%). The relationship between histological aspects and clinical features was discussed by sex, age, and others. Of 41 follow up cases, significant values of histological type, presence of HB ag., or alcoholic were discussed as for the causative factors evolving liver cirrhosis.
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PMID:[Chronic hepatitis--clinicopathological studies of 687 cases (author's transl)]. 46 98

In 1976 we undertook to evaluate the incidence of chronic liver lesions in 161 patients treated in hospital during the years 1970-1975 for their serologically established acute viral hepatitis type B (AVH-B). At systematic control examination mode in 1976, after a period from 1-5 years since the acute onset of disease, it was established that in 133 individuals (82.6%) the antigen HBs had disappeared from blood and the BLT had become normal. Persistent HBs antigenemia was established in 20 (12.4%) individuals. In 15 (9.2%) patients persistent HBs antigenemia was accompanied by pathologic BLT, in 5 (3.1%) cases liver function became returned to normal yet with the persistent HBs antigenemia after their recovery from A VH-B. In 8 (4.9%) patients pathologic BLT persisted although HBsAg had disappeared from blood. Among 28 persons with persistent pathological BLT or with persistent HBs antigenemia out of a total of 161 patients who had had A VH-B, there were 11 (6.8%) cases with the bioptically proved CPHf, 8 (5.0%) cases with CPH, 5 (3.1%) cases with CAH, while 4 (2.5%) patients showed fatty liver metamorphosis or had by light microskopy completely normal liver. CAH was established only in cases with persistent BHs antigenemia and pathological BLT. The incidence of the chronic liver lesion and of the persistent antigenemia was among our patients who had had A VH-B in inverse ratio to the intensity of their initial infection. Our study suggests that no prodisposition for persistent HBs antigenemia is created by the prednisolone therapy.
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PMID:Sequeale of acute viral hepatitis type B. 90 72

General views concerning bed rest, diet and working capability in liver disease have changed during the last years. Rigorous bed rest in acute viral hepatitis is necessary only for short periods of time; it is necessary in chronic liver disease only in rare cases and during the terminal stage, respectively. A liver diet does not exist. Normal palatable nutrition is completely adequate in liver disease. Restriction of protein and sodium chloride intake is indicated only in cases with incumbent coma or with ascites. Patients suffering from acute viral hepatitis are incapable of working; however, they can go back to work a few weeks after the acute stage. Estimation of disability to work in patients with chronic liver disease may be difficult; no general rules can be given; in chronic active hepatitis disability is proportional to the activity of the disease and may range from 20-100%. Fatty liver without inflammatory changes does not influence working capability.
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PMID:[Bed rest, diet and working capability in liver disease (author's transl)]. 92 79

Investigation of humoral immunity against hepatocellular membrane antigens in patients with chronic active hepatitis and other liver diseases showed two different immunofluorescence patterns of IgG on hepatocyte membranes. A linear pattern was seen in HBsAg-negative hepatitis, but HBsAg-positive cases and some of protracted, acute hepatitis B had a granular pattern. In patients with IgG bound to hepatocytes, continuing necrosis of parenchymal liver cells was seen. Conversely, hepatocytes without bound IgG were found in cases of chronic active hepatitis in remission, acute viral hepatitis without HBsAg and chronic persistent hepatitis, in "healthy" HBsAg-carriers and in patients with fatty liver or alcoholic cirrhosis. A liver-membrane autoantibody in serum, proved by fixation on membranes of isolated rabbit hepatocytes, could be demonstrated only in HBsAg-negative chronic active hepatitis with elevated IgG-concentrations. The results support the existence of different pathogenetic types of chronic active hepatitis, a so-called autoimmune type and a hepatitis virus-B-induced type.
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PMID:Detection of a liver-membrane autoantibody in HBsAg-negative chronic active hepatitis. 110 36


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