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  • 1
    ISSN: 1573-2568
    Keywords: CHRONIC HEPATITIS ; HEPATITIS B VIRUS INFECTION ; HEPATITIS C VIRUS INFECTION ; AMYLASE ; LIPASE
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Serum amylase and lipase concentrations weredetermined in 78 patients with chronic liver diseases[26 chronic active hepatitis (CAH) and 52 livercirrhosis] and in 15 healthy subjects. Pancreaticisoamylase concentrations and macroamylase complexes wereassayed in hyperamylasemic sera. Serum amylase levelswere abnormally elevated in 27 patients (35%; 22 livercirrhosis, 5 CAH), whereas serum lipase levels were elevated in 16 patients (21%; 15 livercirrhosis, 1 CAH). In 9 of the 27 hyperamylasemicpatients, the hyperamylasemia was of pancreatic type.Macroamylasemic complexes were not detected inhyperamylasemic sera. Patients with liver cirrhosis had serumlevels of amylase and lipase significantly higher thanboth the healthy subjects and the patients with CAH,while no significant differences were found in serum levels of these enzymes in patients with CAH ascompared to the healthy subjects. A decreased livermetabolism of serum amylase and lipase in patients withchronic infective liver disease, especially in those having liver cirrhosis, may lead to anaccumulation of these enzymes in the blood.
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  • 2
    ISSN: 1573-2568
    Keywords: LIVER ; HEAT SHOCK PROTEIN ; OXIDATIVE STRESS
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Heat shock proteins are intracellular proteinsassociated with a generalized response of cells tostress. The purpose of this study was to assess RNAlevels of heat shock protein 70 and 90 in fed or fasted rat livers during ischemia-reperfusion.Northern blot analysis of heat shock proteins wasperformed. Adenosine triphosphate and glutathione wereassessed. In baseline conditions, livers of fasted ratsshowed a twofold increase in mRNA for both heat shockproteins and 38% and 43% reductions in adenosinetriphosphate and glutathione, respectively, whencompared with organs from fed rats. After ischemia,livers of fasted rats presented a twofold decrease inheat shock protein mRNA, while no changes were observedin livers of fed rats; reduced glutathione and adenosinetriphosphate decreased 55% and 50% in fasted livers and 25% and 20% in fed organs,respectively. After 120 min of reperfusion, heat shockprotein mRNA rose threefold in fasted livers, while aslight decrease was observed in the fed group; reduced glutathione and adenosine triphosphate returnedto 65% and 70% of baseline values in fasted livers and85% and 90% in fed organs, respectively. In conclusion,the nutritional status affects heat shock protein expression determined by reperfusion. Thereduced antioxidant status leading to increasedoxidative stress could be the mechanism underlying thephenomenon.
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  • 3
    ISSN: 1573-2568
    Keywords: hepatocyte ; ethanol ; cytosolic free calcium ; lactate dehydrogenase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The events implicated in the early phases of acute ethanol-induced hepatocyte injury and their relation with the nutritional status of the liver are not clearly defined. We aimed to determine the effect of ethanol on ATP and cytosolic free Ca2+ in hepatocytes isolated from fed or fasted rats. Cell injury was assessed by LDH release and trypan blue uptake, ATP by [31P]NMR spectroscopy, and cytosolic free Ca2+ with aequorin. In control conditions, cells from fasted animals had a lower ATP level (−52%) and a higher cytosolic free Ca2+ (+101%) than did those isolated from fed animals. Ethanol caused a dose-dependent cell injury in both groups. At all ethanol doses, greater damage occurred when using hepatocytes isolated from fasted rats. In both groups, a dose-dependent decrease in ATP content and a rise in cytosolic free Ca2+ were seen. The magnitude of these changes were significantly greater in the fasted group. In conclusion, these data showed that fasting affects the energy status and cytosolic free calcium level in hepatocytes; ethanol causes a dose-dependent cell injury that occurs in association with a fall in ATP and a rise in cytosolic free Ca2+ levels. The nutritional status of an animals is an important determinant of the severity of ethanol-induced damage to liver cells.
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  • 4
    ISSN: 1573-2568
    Keywords: T61 ; Tanax ; dimethylformamide ; hepatitis ; glutathione
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A case of acute hepatic failure following ingestion of the veterinary euthanasia drug T61 is described. Presenting symptoms were drowsiness, disorientation, muscle hypertonia, and upper limb myoclonus, which faded within a few hours. Two days later, acute liver failure occurred, manifested as encephalopathy, jaundice, and a severe coagulopathy. The hepatic damage was thought to be due to the solvent dimethylformamide, which is the only known hepatotoxin included in the preparation utilized in the suicide attempt. High-dose (1.2g/day) intravenous reduced glutathione was administered, with a rapid improvement of liver function. The patient was discharged after 17 days. Normalization of all liver function tests was achieved within two months. The favorable outcome in this case stands in contrast to the report of a previous case of lethal T61-induced hepatic failure. Although a different amount of dimethylformamide was ingested in each case (0.45 vs 0.60 ml/kg body wt) and individual differences in susceptibility to the effects of the hepatotoxic agent may have played a major role in these two cases, it is not unlikely that the infusion of high doses of glutathione to our patient contributed to her survival and hepatic recovery.
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  • 5
    ISSN: 1573-2568
    Keywords: bone mineral density ; bone resorption ; dual-energy x-ray absorptiometry ; liver cirrhosis ; osteoporosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Bone loss is an established complication of cholestatic liver cirrhosis, while little is known about bone mass and metabolism in noncholestatic liver cirrhosis. The aim of the present study is, therefore, to evaluate bone mass and mineral metabolism in patients with liver cirrhosis secondary to viral hepatitis. Bone mineral density measurement at lumbar and femoral levels and the evaluation of bone and mineral metabolism and gonadal function were performed in 31 patients with liver cirrhosis and 37 healthy volunteers. Lumbar and femoral bone mineral density values were significantly lower in patients than in healthy volunteers. Prevalence and severity of bone loss increased according to the severity of liver disease. All serum indices of bone and mineral metabolism and of gonadal function showed a similar behavior, but a significant increase of bone resorption was present in all Child-Pugh classes. In particular, class A patients showed normal mean bone mineral density values but increased serum levels of the telopeptide of type I collagen. Liver cirrhosis predisposes to bone loss regardless of the presence of cholestasis. The severity of metabolic osteopathy worsens as liver function does. The underlying mechanism is represented by an increased bone resorption.
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