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)

Amino acid imbalance ratio was determined in apparently healthy Pakistanis and patients with hepatitis and cirrhosis of the liver. The ratio was normal in 75% of the patients with actue viral hepatitis but in only 5% with cirrhosis of the liver. The ratio was abnormal in 25% cases of acute viral hepatitis possibly due to aminoaciduria. The abnormal ratio in cirrhosis of the liver indicated the functional capacity for albumin synthesis and correlated well with serum albumin concentration.
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PMID:Aminoacid imbalance ratio in liver disease. 82 73

Amino acid imbalance ratio was determined in apparently healthy Pakistanis and patients with hepatitis and cirrhosis of the liver. The ratio was normal in 75% of the patients with acute viral hepatitis but in only 5% with cirrhosis of the liver. The ratio was abnormal in 25% cases of acute viral hepatitis possibly due to aminoaciduria. The abnormal ratio in cirrhosis of the liver indicated the functional capacity for albumin synthesis and correlated well with serum albumin concentration.
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PMID:Aminoacid imbalance ratio in liver disease. 82 59

Fifty-six patients with moderate to severe neonatal hepatitis were followed for 12 to 78 months. Two died from causes other than hepatitis itself and were free from liver disease at the time of death. Of the remaining 54 patients, seven died of hepatitis, two are living with chronic liver disease and psychomotor retardation, and 45 are living without liver disease. High peak bilirubin levels and liver histologic findings of periportal fibrosis, moderate to severe portal inflammation, and/or diffuse giant cell transformation appear to be major factors predictive for poor outcome. Cytomegalovirus (CMV) infection was a common associated infection. Evidence of CMV infection was found in 22 (49%) of the 45 patients studied. Three of them died, and one is still living with cirrhosis of the liver. Metabolic disorders such as alpha-1-antitrypsin deficiency, galactosemia, and aminoaciduria and/or aminoacidemia were carefully screened but were not found in these cases. A fatal case had a sibling who had died of a similar disease course. Chinese infants may have metabolic and familial cholestasis diseases requiring further investigation.
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PMID:Neonatal hepatitis: a follow-up study. 282 43

Rats were injected intraperitoneally with copper-lactate daily for over 160 days (total dose of 30 mg copper in each animal). At 120 to 160 days of copper administration, animals developed symptoms similar to those of Wilson's disease, i.e., kidney functional disturbances, proteinuria, aminoaciduria, decreased blood ceruloplasmin oxidase activity and increased urinary copper excretion. Cirrhosis was found in some animals. Tubular necrosis of the kidneys, liver fibrosis and tigrolysis of thalamic nerve cells were also found. Copper depositions were observed in liver parenchymal cells, renal tubular epithels, thalamus glia cells and on the Descemet's membrane of the cornea. The similarities between induced copper- intoxication in rats and Wilson's disease are discussed.
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PMID:Laboratory and histological similarities between Wilson's disease and rats with copper toxicity. 645 May 19

A fifteen-month-old boy, born to consanguineously married couple, presented with asymptomatic hepatomegaly. Investigations revealed mildly deranged liver functions, necroinflammatory changes and cirrhosis on liver biopsy, a markedly raised alpha feto protein and tyrosine levels in plasma and a generalized aminoaciduria. His diagnosis of hereditary tyrosinemia was established on findings of raised serum and urine succinylacetone and a deficient activity of fumaryl acetoacetate hydroxylase enzyme. Prenatal diagnosis of hereditary tyrosinemia was performed in a subsequent pregnancy in this family from India.
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PMID:Tyrosinemia type I--diagnostic issues and prenatal diagnosis. 1651 30

A homozygous mutation in the complex III chaperone BCS1L causes GRACILE syndrome (intrauterine growth restriction, aminoaciduria, cholestasis, hepatic iron overload, lactacidosis). In control and patient fibroblasts we localized BCS1L in inner mitochondrial membranes. In patient liver, kidney, and heart BCS1L and Rieske protein levels, as well as the amount and activity of complex III, were decreased. Major histopathology was found in kidney and liver with cirrhosis and iron deposition, but of iron-related proteins only ferritin levels were high. In placenta from a GRACILE fetus, the ferrooxidases ceruloplasmin and hephaestin were upregulated suggesting association between iron overload and placental dysfunction.
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PMID:Characterization of complex III deficiency and liver dysfunction in GRACILE syndrome caused by a BCS1L mutation. 2058 Sep 47