Results 171 to 180 of about 12,857 (206)
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Valproate‐induced hyperammonemia

Annals of Neurology, 1982
AbstractA patient with carbamyl phosphate synthetase deficiency had four episodes of hyperammonemia, up to 226 μM, associated with valproate (VPA) treatment. These were accompanied by vomiting, lethargy, and coma. A group of epileptic patients receiving VPA remained asymptomatic but had significantly higher mean plasma ammonium levels when compared to ...
M L, Batshaw, S W, Brusilow
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Hyperammonemia in Multiple Myeloma

Acta Haematologica, 2009
Two patients with multiple myeloma who appeared to be producing ammonia are reported. Both patients showed hyperammonemia and amino acid disturbances, such as a low Fischer ratio. One patient had Bence Jones protein (λ) type myeloma and became comatose, but the hyperammonemia and disturbance of consciousness were improved by chemotherapy for the ...
H, Matsuzaki   +6 more
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Hyperammonemia in Marasmic Children

Journal of Tropical Pediatrics, 1994
The amino acids citrulline, ornithine and arginine, total serum proteins, serum enzymes glutamic oxalacetic and glutamic pyruvic transaminases, blood ammonia and urea were measured in 20 marasmic children with manifest psychomotor changes, before and after nutritional rehabilitation, as well as in 10 healthy age-matched children.
M R, Morsy   +5 more
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Hyperammonemia and Perinatal Asphyxia

Pediatrics, 1981
In a recent article Goldberg et al1 presented data on 12 asphyxiated newborn infants with high ammonia levels concomitant with abnormal liver function tests. They pointed out that the liver dysfunction, probably secondary to the ischemic-hypoxic injury, might have contributed to ammonia elevation by decreasing urea biosynthesis.
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Carbamazepine-induced hyperammonemia

American Journal of Health-System Pharmacy, 2009
A case of carbamazepine-induced hyperammonemia is presented.A 26-year-old man with bipolar disorder, seizures, and mild mental retardation secondary to a traumatic brain injury began treatment with carbamazepine for aggression and seizure control. After three weeks of carbamazepine therapy, the patient arrived at the emergency department (ED) with ...
Erin N, Adams   +2 more
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The hyperinsulinism/hyperammonemia syndrome

Reviews in Endocrine and Metabolic Disorders, 2010
The hyperinsulinism/hyperammonemia (HI/HA) syndrome is the second most common form of congenital hyperinsulinism (HI). Children affected by this syndrome have both fasting and protein sensitive hypoglycemia combined with persistently elevated ammonia levels.
Andrew A, Palladino, Charles A, Stanley
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Hyperammonemia, Bane of the Brain

Clinical Pediatrics, 2004
Ammonia, normally produced from catabolism of amino acids, is a deadly neurotoxin. As such, the concentration of free ammonia in the blood is very tightly regulated and is exceeded by two orders of magnitude by its physiologic derivative, urea. The normal capacity for urea production far exceeds the rate of free ammonia production by protein catabolism
Robert M, Cohn, Karl S, Roth
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Treatment of Congenital Hyperammonemias

Enzyme, 2017
A rapid recognition of congenital hyperammonemia, a clear diagnostic workup and institution of a combined treatment without delay, by restriction of nitrogen supply, adequate caloric supply, substitution of missing metabolites, and use of alternate routes of nitrogen excretion will help to control hyperammonemic crises and improve the prognosis.
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Glutamate transporters in hyperammonemia

Neurochemistry International, 2002
Evidence suggests that increases in brain ammonia due to congenital urea cycle disorders, Reye Syndrome or liver failure have deleterious effects on the glutamate neurotransmitter system. In particular, ammonia exposure of the brain in vivo or in vitro preparations leads to alterations of glutamate transport.
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Electroencephalographic changes and hyperammonemia

Electroencephalography and Clinical Neurophysiology, 1958
Resume Sept patients souffrants de differentes maladies et dont l'etat de conscience variait entre un etat de vigilance normale jusqu'au coma profond ont montre des ondes ⪡ triphasiques ⪢ dans leur trace EEG. Tous les 7 malades avaient une perturbation commune, c'est-a-dire une elevation de l'ammonium sanguin. L'auteur tire les conclusions suivantes:
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