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)

The diagnosis of liver cirrhosis depends on assessing fibrosis and architectural alterations of the liver. In a needle biopsy specimen the connective tissue is often inadequately sampled, which leads to an uncertain diagnosis. Parenchymal features alone are currently insufficient. We, therefore, carried out a comprehensive morphometric study to detect parenchymal structures that may be useful in the diagnosis and prognosis of cirrhosis. Five human liver biopsy specimens were selected from each of four alcoholic disease groups: fatty liver, alcoholic hepatitis, cirrhosis with greater-than-5-yr survival, and cirrhosis with less-than-2-yr survival. Volume fractions (Vv) and surface densities (Sv) were determined stereologically for parenchymal and hepatocellular compartments in electron micrographs. The differences between noncirrhosis and cirrhosis were (a) a doubling of the Vv of parenchymal interstitial space, (b) a nearly 25% increase in the Sv of hepatocyte plasma membrane, (c) a nearly 50% increase in the Sv of hepatocyte RER, and (d) a decrease in the Sv of the outer mitochondrial membrane. The significant difference between the greater than 5-yr and the less than 2-yr survivors of cirrhosis was the marked decrease in hepatocyte nuclear Vv in the latter group. Statistical analysis of our data showed that optimal sampling is achieved with as few as three micrographs from one block of tissue per biopsy specimen.
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PMID:Morphometry of liver parenchyma in needle biopsy specimens from patients with alcoholic liver disease: preliminary variables for the diagnosis and prognosis of cirrhosis. 266 43

Purpose of this study was to elucidate the difference in severity of alcoholic liver diseases (ALD), especially of alcoholic hepatitis (AH) between female and male. We have experienced 15 female and 113 male patients with ALD laparoscopically and histologically proved during the past 10 years. In female patients, histological analysis revealed 8 cases of cirrhosis, 2 each cases of AH, fibrosis and chronic hepatitis, and 1 case of fatty liver. Occurrence of AH in female (13%) was significantly higher than male in which AH was seen in 3 cases (3%) (p less than 0.05). Duration of alcoholic abuse in female AH patients was shorter than male AH patients (5.5 +/- 0.5 years vs 24.0 +/- 2.9 years). Total alcohol consumed in female AH patients was less than male AH patients (256 +/- 52 kg vs 1560 +/- 703 kg). Abnormality in liver function tests including hepaplastin test, serum bilirubin, transaminases, lactate dehydrogenase, alkaline phosphatase, gamma-glutamyltranspeptidase, immunoglobulins was outstanding in female patients compared with male patients. Histological findings such as hepatocellular ballooning, neutrophilic infiltration, fatty change and wiremesh fibrosis were intensive in female patients compared with male patients. In conclusion, there were much more severe ALD like AH or cirrhosis in female than male patients. In female AH patients duration of alcoholic abuse was shorter and total alcohol consumed was less than male AH patients. And it was suggested that female AH is clinically and pathologically getting severe compared with male AH.
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PMID:[Sex difference in alcoholic liver disease: with special reference to the severity of alcoholic hepatitis]. 280 7

The liver is the main organ for alcohol metabolism and is therefore predisposed for various functional changes and irreversible alterations. The alcoholic fatty liver represents the early stage of alcohol-induced liver diseases and is completely reversible upon consequent alcohol abstinence. Already at this early stage a significant increase of gamma-glutamyltransferase activities is commonly found in the serum, which can mainly be attributed to an enzyme induction in the endoplasmic reticulum of the liver cell. Other stages of alcohol-induced liver diseases include the alcoholic hepatitis and the liver cirrhosis, which have a better prognosis upon consequent alcohol abstinence compared to continuous alcohol consumption. Many therapeutic studies with various drugs have been carried out in patients with alcohol-induced liver diseases, but at present a treatment with drugs in a sufficiently great number of patients has not been firmly established. The most important medical goal is to establish the diagnosis of alcohol-induced liver diseases already at the early stage of the fatty liver in order to initiate the necessary therapeutic measures with the aim of a consequent alcohol abstinence.
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PMID:[The liver and alcohol]. 285 Jun 81

The occurrence and intensity of staining for specific antibodies against the aminoterminal propeptide of type III procollagen (PIIIP), which is indicative of the synthesis and the degradation of that collagen type, was studied in sections from normal and alcoholic livers and compared with serum PIIIP levels, serum antipyrine clearance, fibronectin distribution and morphology as revealed by conventional stains and electronmicroscopy. Positive staining for PIIIP and fibronectin was observed in the perisinusoidal space of the normal liver and in portal tracts. In alcohol-induced fatty liver positive staining increased around the central veins, in alcoholic hepatitis increased staining reaction was seen to a limited extent in areas of cell injury. Extensive reticulin and PIIIP-positive areas were found in the periportal interstitium of the cirrhotic livers and in large fibrotic areas extending into the surrounding parenchyma in cases of active disease. The results show a distinct relationship between collagen type III metabolism, morphologically detectable hepatic injury and liver cell function tests, with tissue deposition occurring later in the disease process than biochemically detectable serum collagen levels and signs of altered liver cell function.
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PMID:Interstitial collagen in alcoholic human liver. 298 Jul 43

The activities of three enzymes catalyzing the production or degradation of phosphatidylcholine, a major structural phospholipid of cell membranes, were assessed in hepatocyte membrane microsomal preparation from patients with various types of liver disease. Choline phosphotransferase activity of preparation from patients with chronic aggressive, chronic active, chronic persistent, alcoholic hepatitis and cirrhosis accompanied by marked necrosis and relatively slight fibrosis was markedly decreased, compared with normal liver; the activity from patients with fatty liver and chronic inactive hepatitis was slightly decreased. Specimens from patients with acute transient hepatitis were not significantly different from normal. Methyltransferase and phospholipase A2 activities tended to parallel that of choline phosphotransferase, although the degree of changes was generally less marked. Our studies indicate that enzyme activities that are critical for hepatic cell membrane integrity and activity are attenuated in liver specimens from patients with disease in which there is marked hepatic cell necrosis.
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PMID:Phospholipid transmethylation and choline phosphotransferase in microsomal fraction of human diseased liver. 301 86

From these discussions, it is apparent that: Alcoholic liver disease is increasing at a rapid rate in conjunction with an increase of annual gross and per capita consumption of alcohol. Alcoholic hepatitis and alcoholic hyaline are much less common in Japan compared to western countries. Alcoholic hepatic fibrosis and chronic hepatitis are the common types of alcoholic liver disease in Japan. Alcoholic hepatic fibrosis may be a pathological process or entity independent of fatty liver, alcoholic hepatitis, and alcoholic cirrhosis. It is not clear at the present time whether heavy alcohol consumption per se or non-A, non-B hepatitis virus is the cause of chronic hepatitis seen in HBsAg negative alcoholics.
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PMID:Alcoholic liver disease in Japan. 302 74

In liver biopsy material of eighty-nine patients with suspected liver disease the drug-metabolizing function was investigated. The capacity of the liver to oxidatively metabolize drugs was assessed by determination of cytochrome P-450 dependent monooxygenase activity in vitro. The biotransformational function of these microsomal enzymes was tested with compounds representing the activity of oxidative drug metabolism (7-ethoxycoumarin, p-nitroanisol and cytochrome c). From the eight-nine patients sixty-one had various liver diseases not related to ethanol and twenty-eight abused ethanol. When both groups were matched for age, sex, smoking, treatment with sedatives, drugs and degree of liver damage the alcoholic group had significantly higher activities of 7-ethoxycoumarin O-deethylase (EOD: 76.9 +/- 31.1 pmol min-1 mg-1 protein, mean +/- SD) than the non-alcoholic liver disease group (42.7 +/- 14.1). The inducing effect of ethanol was most striking on the EOD activity, less for the O-demethylation of p-nitroanisol (PNA) and not present for the NADPH-cytochrome c reductase. The induced patients were analysed in detail to find out which factors were responsible for the observed scatter of enzyme activities within the alcoholic group. Alcoholics with fatty liver (n = 7) had the highest EOD activities (108.9 +/- 25.0), patients with alcoholic hepatitis (n = 10) had significantly less activity (66.0 +/- 1.9) than the former group. However, alcoholics without liver damage (n = 6) had activities not significantly different (46.0 +/- 15.8) from controls (39.4 +/- 9.1). These subgroups among the alcoholics were comparable in terms of sex, age, smoking and drinking habits.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inducing efficacy of ethanol on hepatic drug metabolizing enzymes in patients. 309 41

Liver biopsies from nine patients with maturity-onset diabetes and fatty liver hepatitis were semiquantitatively assessed, and the findings compared with those in alcoholic hepatitis. Overall appearances were similar, but the lesion in some diabetics was periportal rather than perivenular in location, and nuclear vacuolation of hepatocyte nuclei was always present. The inflammatory infiltrate often included neutrophil leucocytes, as in the alcoholic. In three patients with multiple biopsies, progression appeared to be slow, but one patient developed cirrhosis.
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PMID:The pathology of diabetic hepatitis. 263 85

The presence of liver membrane antibody in IgG and IgA was investigated by radioimmunoassay using isolated rabbit hepatocytes as target cells. This technique was more sensitive than the immunofluorescent method. IgG liver membrane antibodies were positive in 24% of patients with alcoholic liver disease. IgA liver membrane antibodies were detected in 58% of patients with alcoholic liver disease, whereas they were detected only in 21% of those with nonalcoholic liver disease, except for cases of autoimmune chronic active hepatitis. In alcoholic liver disease, IgA liver membrane antibodies were detected at a high frequency in a group of patients with alcoholic hepatitis and active cirrhosis (94%) as compared with that of fatty liver, hepatic fibrosis, and inactive cirrhosis (42%). These results suggest that alcoholic liver disease is characterized in part by a humoral immune response of IgA liver membrane antibodies.
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PMID:Differences of liver membrane antibody frequency in alcoholic liver disease. Detection of IgG and IgA classes using radioimmunoassay. 328 54

The effect of oral testosterone treatment (200 mg tid) on liver morphology was examined in a double-blind, placebo controlled study including men with alcoholic cirrhosis (n = 126). Liver biopsies obtained before randomization showed micronodular cirrhosis in 119 patients (94%), alcoholic hepatitis in 64 (51%), and fatty liver in 104 (83%). These and other morphological findings did not differ significantly in the patients randomized to testosterone (n = 76) and to placebo (n = 50) (skewed randomization 3:2). Follow-up liver specimens (biopsies or autopsies) obtained after a median treatment duration of 30 months demonstrated a significant (p less than 0.01) increase in the prevalence of macronodular cirrhosis (from 6 to 51%) and a significant (p less than 0.01) decrease in the prevalence of alcoholic hepatitis (to 21%) and of fatty liver (to 52%). Testosterone treatment did not significantly influence the prevalence of these changes. Further, testosterone treatment had no significant effect on the prevalence of other morphological changes, including vascular and malignant changes. However, in the testosterone-treated group one patient developed diffuse sinusoidal dilation and one patient showed Budd-Chiari's syndrome. The degree of fatty liver and of alcoholic hepatitis in follow-up liver specimens were significantly (p less than 0.002) higher among patients who consumed ethanol during follow-up than in patients who abstained (76 versus 22% and 30 versus 6%). In conclusion, this study does not establish any indication or any contraindication in terms of hepatic histopathology with the possible exception of hepatic venous thrombosis for the use of oral testosterone treatment in men with alcoholic cirrhosis.
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PMID:No effect of long-term oral testosterone treatment on liver morphology in men with alcoholic cirrhosis. 330 Feb 74


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