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At least 631 records · Page 35Linked to original sources
PubMed1983

[Hyperammonemia during total parenteral nutrition in children].

Twenty-one children presenting with severe malnutrition were fed with total parenteral nutrition using 2 different aminoacids solutes containing 19% and 42% branched chain aminoacids respectively. With the 42% branched chain aminoacids solute a dysregulation of ammonia metabolism and changes in protein synthesis were observed. Several factors probably accounted for these changes. An excessive intake of branched chain aminoacids in children with malnutrition, under parenteral nutrition, is therefore iatrogenic and inappropriate.

Amino Acids, Branched-Chain↗
PubMed1983

[Correlations among hypoxia, hypercapnia and hyperammonemia in patients with cor pulmonale decompensatum].

The correlation between ammonia concentration of the plasma and blood pH, blood gas values was examined in 28 patients with chronic cor pulmonale decompensatum. In cases with central nervous symptoms were found a significant negative correlation between ammonia concentration of the plasma and arterial oxygen saturation, a significant positive correlation between ammonia concentration of the plasma and paCO2, a significant negative correlation between ammonia concentration of the plasma and arterial blood-pH. In cases without central nervous symptoms, however, no significant correlations was established.

Ammonia↗
PubMed1983

[Neonatal hyperammonemia].

Experience with severe neonatal hyperammonaemia in the Newborn Intensive Care Unit of the Leuven University Hospital is reported and compared with the literature data. Among eleven patients seven presented with the transient neonatal hyperammonaemia-syndrome and four with a urea cycle defect. Prompt recognition of the transient neonatal hyperammonaemia syndrome is important because its prognosis is much better than that of the primary urea cycle defects presenting in the neonatal period.

Amino Acid Metabolism, Inborn Errors↗
PubMed1982

[Combined exchange transfusion and peritoneal dialysis treatment in a neonatal case of methylmalonic acidemia with severe hyperammonemia].

A case of methyl-malonic acidemia with severe neonatal hyperammoniemia is presented. Treatment during the first days of live with exchange-transfusion, with protein-free blood and peritoneal dialysis induced a decrease of blood ammonia values from 1360 to 270 micrograms/dl and the correction of systemic metabolic acidosis. Continuation of treatment by dietary means was followed by normalization of clinical status and almost total correction of the urinary excretion of methyl-malonic and propionic acids, but the patient died at 33 days of life due to an intercurrent infection. This case, together with a case previously reported of propionic acidemia with neonatal hyperammoniemia and prolonged survival, demonstrates that complementary treatment by means of exchange transfusion and peritoneal dialysis is mandatory in all cases of neonatal hyperammoniemia of metabolic origin, since survival without irreversible neurological damage is possible.

Amino Acid Metabolism, Inborn Errors↗
PubMedDate not supplied

Induced transient hyperammonemia in Rana hexadactyla with reference to the ammonia and urea excretion.

Different ammonia toxicity induced by ammonium acetate administration in frogs lead to variable excretion of ammonia and urea into the medium. When 11.45 mM/kg body weight of ammonium acetate was administered, ammonia excretion increased while urea excretion decreased. When 4.17 mM/kg body weight of ammonium acetate is administered, the urea excretion increased while ammonia excretion decreased. The possible metabolic conversion of ammonia and urea by the animal at high and low ammonium acetate administration has been discussed.

Ammonia↗
PubMed1978

[Hyperammonemia].

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Amino Acid Metabolism, Inborn Errors↗