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Akiharu Watanabe - One of the best experts on this subject based on the ideXlab platform.
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clinical comparison of branched chain amino acid l leucine l isoleucine l valine granules and oral nutrition for hepatic insufficiency in patients with Decompensated Liver Cirrhosis liv en study
Hepatology Research, 2005Co-Authors: Shunichi Sato, Kazuyuki Suzuki, Akiharu Watanabe, Hisataka Moriwaki, Yasutoshi Muto, Akinobu Kato, Masahiko Kato, Teiji NakamuraAbstract:This multicenter study compared the effects of branched-chain amino acid granules (Livact® Granules, LIV) and an enteral nutrient for chronic hepatic failure (Aminoleban® EN, EN) on serum albumin in patients with Decompensated Liver Cirrhosis. This study enrolled “patients with Decompensated Liver Cirrhosis associated with hepatic encephalopathy who were suffering from hypoalbuminemia in spite of adequate food intake,” a condition for which both drugs are indicated. Enrolled patients were randomized to the two groups according to the central registration method. This study continued for 24 weeks. Selected foods were supplied to each patient in principle so that caloric and protein intakes were standardized between the two groups. A total of 281 patients were enrolled. LIV was not inferior to EN concerning the primary efficacy endpoint changes in serum albumin.
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Effects of zinc deficiency/zinc supplementation on ammonia metabolism in patients with Decompensated Liver Cirrhosis.
Acta Medica Okayama, 2001Co-Authors: Yasuhiro Yoshida, Toshihiro Higashi, Kazuhiro Nouso, Harushige Nakatsukasa, Shinichiro Nakamura, Akiharu Watanabe, Takao TsujiAbstract:Hepatic encephalopathy is one of the major complications in Decompensated Liver Cirrhosis. The current study was conducted to clarify the mechanisms of zinc deficiency in Liver Cirrhosis and its involvement in hepatic encephalopathy via ammonia metabolism. Ten patients each with compensated or Decompensated Liver Cirrhosis and 11 healthy volunteers were enrolled in the study. Serum zinc levels and its daily urinary excretion were measured, an oral zinc-tolerance test was performed to examine zinc malabsorption, and the effects of diuretics on zinc excretion and of zinc supplementation on ammonia metabolism in the skeletal muscle were studied. The mean serum zinc levels in patients with Decompensated Liver Cirrhosis were found to be significantly lower than the levels in controls and patients with compensated Liver Cirrhosis. The serum zinc levels were inversely correlated with blood ammonia in the fasting state. In the oral zinc-tolerance test, the percent increase in serum zinc levels 120 and 180 min after ingestion was less in cirrhotic patients than in controls. A diuretic administration resulted in a significant reduction in serum zinc levels. An increased uptake of ammonia by and an increased release of glutamine from leg skeletal muscle after oral supplementation of zinc sulfate were evident. Taken together, zinc deficiency in Decompensated cirrhotic patients appears to be due to low absorption and to high urinary excretion, for which excessive diuretic administration is, in part, responsible, and zinc supplementation might play an important role in the prevention of hepatic encephalopathy by activating glutamine synthetase.
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effects of zinc deficiency zinc supplementation on ammonia metabolism in patients with Decompensated Liver Cirrhosis
Acta Medica Okayama, 2001Co-Authors: Yasuhiro Yoshida, Toshihiro Higashi, Kazuhiro Nouso, Harushige Nakatsukasa, Shinichiro Nakamura, Akiharu Watanabe, Takao TsujiAbstract:Hepatic encephalopathy is one of the major complications in Decompensated Liver Cirrhosis. The current study was conducted to clarify the mechanisms of zinc deficiency in Liver Cirrhosis and its involvement in hepatic encephalopathy via ammonia metabolism. Ten patients each with compensated or Decompensated Liver Cirrhosis and 11 healthy volunteers were enrolled in the study. Serum zinc levels and its daily urinary excretion were measured, an oral zinc-tolerance test was performed to examine zinc malabsorption, and the effects of diuretics on zinc excretion and of zinc supplementation on ammonia metabolism in the skeletal muscle were studied. The mean serum zinc levels in patients with Decompensated Liver Cirrhosis were found to be significantly lower than the levels in controls and patients with compensated Liver Cirrhosis. The serum zinc levels were inversely correlated with blood ammonia in the fasting state. In the oral zinc-tolerance test, the percent increase in serum zinc levels 120 and 180 min after ingestion was less in cirrhotic patients than in controls. A diuretic administration resulted in a significant reduction in serum zinc levels. An increased uptake of ammonia by and an increased release of glutamine from leg skeletal muscle after oral supplementation of zinc sulfate were evident. Taken together, zinc deficiency in Decompensated cirrhotic patients appears to be due to low absorption and to high urinary excretion, for which excessive diuretic administration is, in part, responsible, and zinc supplementation might play an important role in the prevention of hepatic encephalopathy by activating glutamine synthetase.
Takao Tsuji - One of the best experts on this subject based on the ideXlab platform.
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Effects of zinc deficiency/zinc supplementation on ammonia metabolism in patients with Decompensated Liver Cirrhosis.
Acta Medica Okayama, 2001Co-Authors: Yasuhiro Yoshida, Toshihiro Higashi, Kazuhiro Nouso, Harushige Nakatsukasa, Shinichiro Nakamura, Akiharu Watanabe, Takao TsujiAbstract:Hepatic encephalopathy is one of the major complications in Decompensated Liver Cirrhosis. The current study was conducted to clarify the mechanisms of zinc deficiency in Liver Cirrhosis and its involvement in hepatic encephalopathy via ammonia metabolism. Ten patients each with compensated or Decompensated Liver Cirrhosis and 11 healthy volunteers were enrolled in the study. Serum zinc levels and its daily urinary excretion were measured, an oral zinc-tolerance test was performed to examine zinc malabsorption, and the effects of diuretics on zinc excretion and of zinc supplementation on ammonia metabolism in the skeletal muscle were studied. The mean serum zinc levels in patients with Decompensated Liver Cirrhosis were found to be significantly lower than the levels in controls and patients with compensated Liver Cirrhosis. The serum zinc levels were inversely correlated with blood ammonia in the fasting state. In the oral zinc-tolerance test, the percent increase in serum zinc levels 120 and 180 min after ingestion was less in cirrhotic patients than in controls. A diuretic administration resulted in a significant reduction in serum zinc levels. An increased uptake of ammonia by and an increased release of glutamine from leg skeletal muscle after oral supplementation of zinc sulfate were evident. Taken together, zinc deficiency in Decompensated cirrhotic patients appears to be due to low absorption and to high urinary excretion, for which excessive diuretic administration is, in part, responsible, and zinc supplementation might play an important role in the prevention of hepatic encephalopathy by activating glutamine synthetase.
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effects of zinc deficiency zinc supplementation on ammonia metabolism in patients with Decompensated Liver Cirrhosis
Acta Medica Okayama, 2001Co-Authors: Yasuhiro Yoshida, Toshihiro Higashi, Kazuhiro Nouso, Harushige Nakatsukasa, Shinichiro Nakamura, Akiharu Watanabe, Takao TsujiAbstract:Hepatic encephalopathy is one of the major complications in Decompensated Liver Cirrhosis. The current study was conducted to clarify the mechanisms of zinc deficiency in Liver Cirrhosis and its involvement in hepatic encephalopathy via ammonia metabolism. Ten patients each with compensated or Decompensated Liver Cirrhosis and 11 healthy volunteers were enrolled in the study. Serum zinc levels and its daily urinary excretion were measured, an oral zinc-tolerance test was performed to examine zinc malabsorption, and the effects of diuretics on zinc excretion and of zinc supplementation on ammonia metabolism in the skeletal muscle were studied. The mean serum zinc levels in patients with Decompensated Liver Cirrhosis were found to be significantly lower than the levels in controls and patients with compensated Liver Cirrhosis. The serum zinc levels were inversely correlated with blood ammonia in the fasting state. In the oral zinc-tolerance test, the percent increase in serum zinc levels 120 and 180 min after ingestion was less in cirrhotic patients than in controls. A diuretic administration resulted in a significant reduction in serum zinc levels. An increased uptake of ammonia by and an increased release of glutamine from leg skeletal muscle after oral supplementation of zinc sulfate were evident. Taken together, zinc deficiency in Decompensated cirrhotic patients appears to be due to low absorption and to high urinary excretion, for which excessive diuretic administration is, in part, responsible, and zinc supplementation might play an important role in the prevention of hepatic encephalopathy by activating glutamine synthetase.
Yasuhiro Yoshida - One of the best experts on this subject based on the ideXlab platform.
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Effects of zinc deficiency/zinc supplementation on ammonia metabolism in patients with Decompensated Liver Cirrhosis.
Acta Medica Okayama, 2001Co-Authors: Yasuhiro Yoshida, Toshihiro Higashi, Kazuhiro Nouso, Harushige Nakatsukasa, Shinichiro Nakamura, Akiharu Watanabe, Takao TsujiAbstract:Hepatic encephalopathy is one of the major complications in Decompensated Liver Cirrhosis. The current study was conducted to clarify the mechanisms of zinc deficiency in Liver Cirrhosis and its involvement in hepatic encephalopathy via ammonia metabolism. Ten patients each with compensated or Decompensated Liver Cirrhosis and 11 healthy volunteers were enrolled in the study. Serum zinc levels and its daily urinary excretion were measured, an oral zinc-tolerance test was performed to examine zinc malabsorption, and the effects of diuretics on zinc excretion and of zinc supplementation on ammonia metabolism in the skeletal muscle were studied. The mean serum zinc levels in patients with Decompensated Liver Cirrhosis were found to be significantly lower than the levels in controls and patients with compensated Liver Cirrhosis. The serum zinc levels were inversely correlated with blood ammonia in the fasting state. In the oral zinc-tolerance test, the percent increase in serum zinc levels 120 and 180 min after ingestion was less in cirrhotic patients than in controls. A diuretic administration resulted in a significant reduction in serum zinc levels. An increased uptake of ammonia by and an increased release of glutamine from leg skeletal muscle after oral supplementation of zinc sulfate were evident. Taken together, zinc deficiency in Decompensated cirrhotic patients appears to be due to low absorption and to high urinary excretion, for which excessive diuretic administration is, in part, responsible, and zinc supplementation might play an important role in the prevention of hepatic encephalopathy by activating glutamine synthetase.
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effects of zinc deficiency zinc supplementation on ammonia metabolism in patients with Decompensated Liver Cirrhosis
Acta Medica Okayama, 2001Co-Authors: Yasuhiro Yoshida, Toshihiro Higashi, Kazuhiro Nouso, Harushige Nakatsukasa, Shinichiro Nakamura, Akiharu Watanabe, Takao TsujiAbstract:Hepatic encephalopathy is one of the major complications in Decompensated Liver Cirrhosis. The current study was conducted to clarify the mechanisms of zinc deficiency in Liver Cirrhosis and its involvement in hepatic encephalopathy via ammonia metabolism. Ten patients each with compensated or Decompensated Liver Cirrhosis and 11 healthy volunteers were enrolled in the study. Serum zinc levels and its daily urinary excretion were measured, an oral zinc-tolerance test was performed to examine zinc malabsorption, and the effects of diuretics on zinc excretion and of zinc supplementation on ammonia metabolism in the skeletal muscle were studied. The mean serum zinc levels in patients with Decompensated Liver Cirrhosis were found to be significantly lower than the levels in controls and patients with compensated Liver Cirrhosis. The serum zinc levels were inversely correlated with blood ammonia in the fasting state. In the oral zinc-tolerance test, the percent increase in serum zinc levels 120 and 180 min after ingestion was less in cirrhotic patients than in controls. A diuretic administration resulted in a significant reduction in serum zinc levels. An increased uptake of ammonia by and an increased release of glutamine from leg skeletal muscle after oral supplementation of zinc sulfate were evident. Taken together, zinc deficiency in Decompensated cirrhotic patients appears to be due to low absorption and to high urinary excretion, for which excessive diuretic administration is, in part, responsible, and zinc supplementation might play an important role in the prevention of hepatic encephalopathy by activating glutamine synthetase.
Toshihiro Higashi - One of the best experts on this subject based on the ideXlab platform.
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Effects of zinc deficiency/zinc supplementation on ammonia metabolism in patients with Decompensated Liver Cirrhosis.
Acta Medica Okayama, 2001Co-Authors: Yasuhiro Yoshida, Toshihiro Higashi, Kazuhiro Nouso, Harushige Nakatsukasa, Shinichiro Nakamura, Akiharu Watanabe, Takao TsujiAbstract:Hepatic encephalopathy is one of the major complications in Decompensated Liver Cirrhosis. The current study was conducted to clarify the mechanisms of zinc deficiency in Liver Cirrhosis and its involvement in hepatic encephalopathy via ammonia metabolism. Ten patients each with compensated or Decompensated Liver Cirrhosis and 11 healthy volunteers were enrolled in the study. Serum zinc levels and its daily urinary excretion were measured, an oral zinc-tolerance test was performed to examine zinc malabsorption, and the effects of diuretics on zinc excretion and of zinc supplementation on ammonia metabolism in the skeletal muscle were studied. The mean serum zinc levels in patients with Decompensated Liver Cirrhosis were found to be significantly lower than the levels in controls and patients with compensated Liver Cirrhosis. The serum zinc levels were inversely correlated with blood ammonia in the fasting state. In the oral zinc-tolerance test, the percent increase in serum zinc levels 120 and 180 min after ingestion was less in cirrhotic patients than in controls. A diuretic administration resulted in a significant reduction in serum zinc levels. An increased uptake of ammonia by and an increased release of glutamine from leg skeletal muscle after oral supplementation of zinc sulfate were evident. Taken together, zinc deficiency in Decompensated cirrhotic patients appears to be due to low absorption and to high urinary excretion, for which excessive diuretic administration is, in part, responsible, and zinc supplementation might play an important role in the prevention of hepatic encephalopathy by activating glutamine synthetase.
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effects of zinc deficiency zinc supplementation on ammonia metabolism in patients with Decompensated Liver Cirrhosis
Acta Medica Okayama, 2001Co-Authors: Yasuhiro Yoshida, Toshihiro Higashi, Kazuhiro Nouso, Harushige Nakatsukasa, Shinichiro Nakamura, Akiharu Watanabe, Takao TsujiAbstract:Hepatic encephalopathy is one of the major complications in Decompensated Liver Cirrhosis. The current study was conducted to clarify the mechanisms of zinc deficiency in Liver Cirrhosis and its involvement in hepatic encephalopathy via ammonia metabolism. Ten patients each with compensated or Decompensated Liver Cirrhosis and 11 healthy volunteers were enrolled in the study. Serum zinc levels and its daily urinary excretion were measured, an oral zinc-tolerance test was performed to examine zinc malabsorption, and the effects of diuretics on zinc excretion and of zinc supplementation on ammonia metabolism in the skeletal muscle were studied. The mean serum zinc levels in patients with Decompensated Liver Cirrhosis were found to be significantly lower than the levels in controls and patients with compensated Liver Cirrhosis. The serum zinc levels were inversely correlated with blood ammonia in the fasting state. In the oral zinc-tolerance test, the percent increase in serum zinc levels 120 and 180 min after ingestion was less in cirrhotic patients than in controls. A diuretic administration resulted in a significant reduction in serum zinc levels. An increased uptake of ammonia by and an increased release of glutamine from leg skeletal muscle after oral supplementation of zinc sulfate were evident. Taken together, zinc deficiency in Decompensated cirrhotic patients appears to be due to low absorption and to high urinary excretion, for which excessive diuretic administration is, in part, responsible, and zinc supplementation might play an important role in the prevention of hepatic encephalopathy by activating glutamine synthetase.
Kazuhiro Nouso - One of the best experts on this subject based on the ideXlab platform.
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Effects of zinc deficiency/zinc supplementation on ammonia metabolism in patients with Decompensated Liver Cirrhosis.
Acta Medica Okayama, 2001Co-Authors: Yasuhiro Yoshida, Toshihiro Higashi, Kazuhiro Nouso, Harushige Nakatsukasa, Shinichiro Nakamura, Akiharu Watanabe, Takao TsujiAbstract:Hepatic encephalopathy is one of the major complications in Decompensated Liver Cirrhosis. The current study was conducted to clarify the mechanisms of zinc deficiency in Liver Cirrhosis and its involvement in hepatic encephalopathy via ammonia metabolism. Ten patients each with compensated or Decompensated Liver Cirrhosis and 11 healthy volunteers were enrolled in the study. Serum zinc levels and its daily urinary excretion were measured, an oral zinc-tolerance test was performed to examine zinc malabsorption, and the effects of diuretics on zinc excretion and of zinc supplementation on ammonia metabolism in the skeletal muscle were studied. The mean serum zinc levels in patients with Decompensated Liver Cirrhosis were found to be significantly lower than the levels in controls and patients with compensated Liver Cirrhosis. The serum zinc levels were inversely correlated with blood ammonia in the fasting state. In the oral zinc-tolerance test, the percent increase in serum zinc levels 120 and 180 min after ingestion was less in cirrhotic patients than in controls. A diuretic administration resulted in a significant reduction in serum zinc levels. An increased uptake of ammonia by and an increased release of glutamine from leg skeletal muscle after oral supplementation of zinc sulfate were evident. Taken together, zinc deficiency in Decompensated cirrhotic patients appears to be due to low absorption and to high urinary excretion, for which excessive diuretic administration is, in part, responsible, and zinc supplementation might play an important role in the prevention of hepatic encephalopathy by activating glutamine synthetase.
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effects of zinc deficiency zinc supplementation on ammonia metabolism in patients with Decompensated Liver Cirrhosis
Acta Medica Okayama, 2001Co-Authors: Yasuhiro Yoshida, Toshihiro Higashi, Kazuhiro Nouso, Harushige Nakatsukasa, Shinichiro Nakamura, Akiharu Watanabe, Takao TsujiAbstract:Hepatic encephalopathy is one of the major complications in Decompensated Liver Cirrhosis. The current study was conducted to clarify the mechanisms of zinc deficiency in Liver Cirrhosis and its involvement in hepatic encephalopathy via ammonia metabolism. Ten patients each with compensated or Decompensated Liver Cirrhosis and 11 healthy volunteers were enrolled in the study. Serum zinc levels and its daily urinary excretion were measured, an oral zinc-tolerance test was performed to examine zinc malabsorption, and the effects of diuretics on zinc excretion and of zinc supplementation on ammonia metabolism in the skeletal muscle were studied. The mean serum zinc levels in patients with Decompensated Liver Cirrhosis were found to be significantly lower than the levels in controls and patients with compensated Liver Cirrhosis. The serum zinc levels were inversely correlated with blood ammonia in the fasting state. In the oral zinc-tolerance test, the percent increase in serum zinc levels 120 and 180 min after ingestion was less in cirrhotic patients than in controls. A diuretic administration resulted in a significant reduction in serum zinc levels. An increased uptake of ammonia by and an increased release of glutamine from leg skeletal muscle after oral supplementation of zinc sulfate were evident. Taken together, zinc deficiency in Decompensated cirrhotic patients appears to be due to low absorption and to high urinary excretion, for which excessive diuretic administration is, in part, responsible, and zinc supplementation might play an important role in the prevention of hepatic encephalopathy by activating glutamine synthetase.
