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Biomedical subjects

C O Record

Publications and source records attributed to C O Record.

123 records · Page 7Linked to original sources
PubMed1976

Plasma and brain amino acids in fulminant hepatic failure and their relationship to hepatic encephalopathy.

Amino acid concentrations were determined in plasma, whole blood, cerebrospinal fluid and brain tissue of 45 patients with grade 3 or 4 coma due to fulminant hepatic failure. The concentration of 15 of the 19 amino acids determined were significantly increased in blood and the increases were greatest for the amino acids concerned with neurotransmitter metabolism. There was no correlation, however, between the plasma concentration of these amino acids and changes in the grade of hepatic coma. The plasma concentrations of the branched chain amino acids were normal except in those patients who subsequently recovered in whom levels were slightly decreased. Phenylalanine- tyrosine and methionine were among the 15 out of 18 amino acids which were significantly increased in cerebrospinal fluid and among the 15 out of 21 amino acids which were significantly increased in the brain. The increase in tryptophan was associated with a significant elevation in brain 5-hydroxyindoleacetic acid concentration suggesting an increase in 5-hydroxytryptamine turnover in hepatic coma. Brain to plasma ratios of most amino acids in hepatic coma patients were similar to control subjects suggesting that plasma concentration is the main factor controlling the cerebral concentration. However, for the branched chain amino acids, cerebrospinal fluid and brain concentrations were increased when plasma concentrations were normal suggesting an increase in brain uptake.

Amino Acids↗
PubMed1975

Disturbances in glucose metabolism in patients with liver damage due to paracetamol overdose.

1. Intravenous glucose tolerance test were performed in fourteen patients with mild or moderate liver damage due to paracetamol overdose. 2. In patients managed conservatively there was glucose intolerance associated with a diminished early insulin response to glucose, suggesting inadequate nutrition in the period between the overdose and the glucose tolerance test. 3. Patients given intravenous glucose supplements to maintain nutrition were also glucose intolerant and, in these, insulin responses to glucose were normal. The decreased fractional disappearance rate was partly due to an increase in glucose distribution space and partly due to a decrease in absolute glucose disappearance rate. 4. Impaired gluconeogenesis was suggested by mild fasting hypoglycaemia in four patients and raised fasting blood lactate concentrations. Serum growth hormone concentrations showed a paradoxical increase after glucose. 5. All these variables had returned to normal in four patients re-tested after recovery.

Acetaminophen↗
PubMed1975

Acid-base and metabolic disturbances in fulminant hepatic failure.

In 28 patients with fulminant hepatic failure alkalaemia was present in 49 of a total of 65 observations. Alkalaemia was due primarlily to a low Pa, C02 in 30 instances and to raised plasma bicarbonate in 16 instances. Blood lactate, pyruvate, and acetoacetate were significantly raised, and in individual cases, blood citrate, succinate, and fumarate were elevated. Blood citrate rose progressively as the clinical condition worsened. Metabolic acidosis was only present in four patients. In three of these patients, all of whom had taken an overdose of paracetamol, the acidosis was severe, present before the onset of clinical heparic failure, and associated with hypoglycaemiaand mild hypotension. In two of these patients the acidosis was shown to be due to accumulation of lactic acid. Plasma free fatty acid concentrations were elevated out of proportion to the degree of ketosis.

Acetoacetates↗
PubMed1972

Metabolic studies in experimental liver disease resulting from D(+)-galactosamine administration.

1. In confirmation of previous work, administration of d(+)-galactosamine (0.5-0.75g/kg body wt.) to rats caused a hepatitis with histological evidence of liver damage and a 9-fold rise in aspartate aminotransferase activity in serum. 2. There was a significant elevation of blood lactate and pyruvate concentrations in 24h-starved rats treated with galactosamine but no change in the [lactate]/[pyruvate] ratio. 3-Hydroxybutyrate and acetoacetate concentrations in blood were decreased. 3. The changes in the concentrations of lactate, pyruvate and ketone bodies in the freeze-clamped liver were parallel to those observed in the blood. 4. In the livers of 24h-starved galactosamine-treated rats there were large increases in the concentrations of alanine (3-fold), citrate (5-fold), 2-oxoglutarate (4-fold), with smaller increases in malate, glutamate and aspartate. There was a 4-fold rise in the value of the mass-action ratio of the alanine aminotransferase system in the livers of galactosamine-treated rats when compared to controls. 5. There was a significant decrease in the activities of aspartate and alanine aminotransferases in the cytoplasm and the soluble fraction of sonicated homogenates of the livers of rats treated with galactosamine. The activity of phosphoenolpyruvate carboxylase was decreased by 75% of the control value. 6. Glucose synthesis from lactate in perfused livers from galactosamine-treated rats was inhibited 39% when compared with controls. 7. The results indicate that the conversion of lactate into glucose is decreased in the livers of galactosamine-treated rats and that this decrease may be due to the loss of phosphoenolpyruvate carboxylase from damaged hepatocytes.

Acetoacetates↗
PubMed1971

Candida endocarditis treated with 5-fluorocytosine.

Three patients with endocarditis due to Candida species were treated with 5-fluorocytosine. One had endocarditis imposed on senile aortic sclerosis and survived and two had infections on prosthetic valves and died. In the latter two patients chemotherapy failed to eradicate the infection and was associated with marrow depression and possibly hepatic necrosis.

Aged↗