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)

An anomalous zymogram of lactate dehydrogenase (LDH) in the serum from a patient with liver cirrhosis was reported. Agar-gel electrophoresis of serum showed an extra LDH band close to the anodic side of LDH5 and a wide band of LDH5. Gel filtration of patient's serum in Sephadex G-200 demonstrated an abnormal LDH fraction eluted between immunoglobulin G (IgG) and macroglobulin in addition to a normal LDH component. Chromatographically abnormal LDH was demonstrated on agar gel as extra and wide LDH5 bands and resembled closely human hepatic LDH in various physico-chemical properties such as inhibition by urea or substrate, stability against heat, and Michaelis-Menten's constant. Immunological analyses demonstrated that abnormal LDH could be in the state combined with IgG. Molecular weight of the complex estimated by gel filtration was approximately 300,000. Mixtures of the heated patient's serum with normal or patient's hepatic LDH showed abnormal LDH fraction by gel filtration, whereas abnormal fraction was not demonstrated when heated normal serum was mixed with normal or the patient's hepatic LDH. These results strongly suggest that the occurrence of anomalous LDH zymogram in patient's serum is due to a formation of LDH-IgG complex, which is based on the binding of essentially normal hepatic LDH and abnormal IgG.
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PMID:Macromolecular lactate dehydrogenase linked to serum IgG of a patient with liver cirrhosis. 13 87

A mixture with essential and nonessential amino acids high in branched chain amino acids and low in aromatic amino acids (Fischer solution), and another synthetic mixture of branched chain amino acids containing 3 amino acids associated with the urea cycle (Hep-OU) were infused to control subjects and patients with severe hepatic disease. Alterations in serum aminograms, blood ammonia levels and electroencephalograms following the infusion were studied and compared with those obtained by a commercially available amino acid mixture. Short-term or continuous infusion of a commercially available amino acid solution to cirrhotic patients caused an increase in methionine, phenylalanine and tyrosine and a decrease in branched chain amino acids. These post-infusion results were similar to the patterns seen in hepatic encephalopathy. In cirrhotic patients, infusion of Fischer solution which contains small quantities of methionine and phenylalanine produced an increase in the concentrations of these 2 amino acids, probably because of impaired utilization by the injured liver. No marked alterations in serum aminograms, however, were observed in cirrhotic patients either immediately after, or 3 h after, the end of the Hep-OU infusion. Reduction of methionine, tyrosine and phenylalanine levels and elevation of the molar ratio of (valine + leucine + isoleucine)/(phenylalanine + tyrosine) were significant. The infusion of Hep-OU to patients with liver cirrhosis or subacute hepatitis resulted in clinical and neurological improvements and the restoration of the molar ratio of branched chain amino acids/aromatic amino acids.
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PMID:An approach to nutritional therapy of hepatic encephalopathy by normalization of deranged amino acid patterns in serum. 15 28

The activities of urea-cycle enzymes were measured in liver biopsies of patients suffering from chronic-persistent hepatitis (CPH), chronic-active hepatitis (CAH) and liver cirrhosis. Most of the activities of urea-cycle enzymes did not differ in the case of CPH as compared to controls. Chronic-active hepatitis and liver cirrhosis are associated with a significant (p less than 0.05) decrease of enzyme activity as compared to normal persons. Most of the urea-cycle enzymes are significantly decreased in patients with CAH in comparison with CPH. No significant differences can be demonstrated in the case of CAH as compared to patients with complete cirrhosis. In conclusion, progression of chronic liver disease is associated with increasing alterations of enzyme activities catalyzing a liver specific metabolic pathway. The decrease of the activities of the key enzymes of the urea cycle (Carbamylphosphate-Synthetase and Arginino-succinate-Synthetase) is nearly identical both in CAH and liver cirhosis, although CAH may be a reversible disease. Therefore, marked alterations in the metabolic pathway of ammonia detoxification seem to preceed the histological manifestation of irreversible liver damage.
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PMID:Activities of urea-cycle enzymes in chronic liver disease. 22 5

According to the present studies it is shown that arginine ketoglutarate in sufficiently high dosage (3x3 g daily by mouth) produces a significant lowering of plasma ammonia and free serum phenols with a high-protein diet in patients with liver cirrhosis, compared to a previous day without this substance. The ammonia reduction can be explained by a significant increase in urea synthesis, measured by the urea nitrogen content of the 24-hour urine. The simultaneous lowering of pathologically raised serum levels of free phenols can be explained by an improved oxidative decomposition of these substances. No stimulation of insulin secretion worthy of note occurred after oral administration of 9 g arginine ketoglutarate.
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PMID:[Effect of arginine ketoglutarate on the detoxifying capacity of the liver in cirrhosis of the liver (author's transl)]. 40 72

Three patients with cirrhosis, ascites, and dilutional hyponatremia were treated with demeclocycline in an attempt to correct the abnormal water retention. Demeclocycline administration (600 to 900 mg/day for 8 to 9 days) resulted in [a] increased blood urea nitrogen and plasma creatinine concentrations; [b] reduction of the inulin clearance by between 63% to 78% and of paraaminophippurate clearance by 36% to 77%; and [c] an impairment of the renal concentrating ability. Urine osmolality decreased to hypotonic levels, but polyuria did not appear, probably because it was prevented by the reduction of the glomerular filtration rate. Renal failure was reversible on withdrawal of demeclocycline. No other causes than demeclocycline administration could be found to explain the reduction of the glomerular filtration rate and the estimated renal plasma flow.
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PMID:Renal failure associated with demeclocycline in cirrhosis. 40 25

Following ureterosigmoidostomy, encephalopathy with hyperammonemia may occur in the presence of cirrhosis, and the same complication was also observed in a few patients without liver damage. This suggests overloading of normal liver ureagenisis by an increased portal ammonia supply. To test this hypothesis and to try to produce an experimental model of chronic hyperammonemia without portal or hepatic damage, ureterocolostomies were performed in rats. These rats were compared with sham operated upon rats and with rats having chronic uremia induced by subtotal nephrectomy. Rats having a ureterocolostomy had chronic, but moderate, systemic hyperammonemia without any histologic hepatic damage and without gross behavioral modifications and slight uremia with only inconstant pyelonephretic lesions. In these rats, hyperammonemia results from hepatic overloading by the increased portal ammonia supply which is a consequence of both intestinal absorption of some urinary ammonia and increased intestinal ammoniagenesis induced by hydrolysis of urinary and circulating urea.
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PMID:Hyperammonemia following ureterocolostomy in the rat. 46 48

The effect on free plasma amino acids before and after infusion of 1 mg glucagon was studied at rest after an overnight fast in seven patients with compensated liver cirrhosis and in seven healthy controls. Total aminoacidaemia in cirrhotic patients is significantly higher than in controls. Elevated basal levels in cirrhotics are found particularly in tyrosine, citrulline, tryptophane, threonine, phenylalanine, and methionine whereas ornithine and serine levels are decreased. Save for the redox couple cystine-cysteine which increases, glucagon elicits an decrease in most amino acids that is proportionate to their initial level. Total aminoacidaemia decreases in controls and cirrhotics by 14.6 and 9.1 per cent respectively. Serum ammonia level rises significantly in both groups, urea increases only in controls, uricaemia remains virtually unchanged.
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PMID:The effect of glucagon on free plasma amino acids in cirrhotics and healthy controls. 63 37

The sensory modalities of taste and smell were evaluated in eight patients with cirrhosis that was proved by biopsy specimens and in 13 control subjects. Additionally, the following serum levels were determined in these same subjects: zinc, copper, magnesium, calcium, manganese, and selenium. Fourteen concentrations each of sucrose, sodium chloride, urea, and hydrochloric acid were used to evaluate taste acuity. Smell was evaluated with 11 concentrations each of nitrobenzene, thiophene, and pyridine. These studies show that decreased acuity of taste and smell occurred in conjunction with cirrhosis in the patients who were tested. There were no trace element abnormalities that consistently correlated with decreased acuity in perception of the individual test substances.
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PMID:Decreased taste and smell acuity in cirrhosis. 64 37

Twelve patients with otherwise uncomplicated acute viral hepatitis (two were HBsAg-positive) developed renal failure. Apart from dehydration due to repeated vomiting in one patient, no factor responsible for precipitating renal failure could be identified. The clinical course was characterised by renal failure with plasma urea concentrations reaching maximum values of 26-69 mmol/l (175-416 mg/100 ml). Ten patients needed dialysis for up to two weeks. Seven patients recovered completely, while the other five died from sepsis. The types of renal failure were similar to those described in fulminant hepatic failure and cirrhosis--namely, functional renal failure in five patients and acute tubular necrosis in seven. Two of the patients with functional renal failure later developed tubular necrosis. The mechanism responsible for renal failure in acute viral hepatitis is uncertain, though endotoxaemia may contribute.
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PMID:Renal failure in otherwise uncomplicated acute viral hepatitis. 68 5

The value and effects of treating renal failure by dialysis are analyzed in a series of 84 patients with various types of liver disease. Although none of the 25 patients with cirrhosis survived, six of 50 with fulminant hepatic failure recovered completely as did seven of nine patients with renal failure secondary to extrahepatic biliary tract obstruction or with liver and renal damage following episodes of severe hypotension. Dialysis was required for seven weeks before diuresis occurred in one patient in the latter group. Both peritoneal and hemodialysis satisfactorily controlled plasma urea and creatinine levels, except in patients with fulminant hepatic failure in whom this was only achieved by hemodialysis. Complications of dialysis were most common in patients with cirrhosis and fulminant hepatic failure and included hypotension, gastrointestinal bleeding, and intraperitoneal sepsis. Overall, the results show that dialysis is only worth attempting in those patients in whom recovery of the underlying liver lesion is possible, and even then treatment for prolonged periods may be necessary.
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PMID:Dialysis in the treatment of renal failure in patients with liver disease. 88 9


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