hyperlysinemias/urea

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Propionic acidemia and hyperlysinemia in a case with ornithine transcarbamylase (OTC) deficiency.

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A female infant with episodic hyperammonemia due to a disorder of the urea cycle and who had hyperlysinemia and an unusual elevation of short chain fatty acids, mainly propionate, is described. Both occurred apparently only during attacks of hyperammonemia. Propionic acidemia was ruled out by enzyme

Clinical and biochemical studies on periodic hyperammonemia with hyperlysinemia and homocitrullinuria.

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An 18-year-old mentally and physically retarded boy, suffering from episodes of anorexia, vomiting, coma and convulsion which have been severer with advance in age, had periodic hyperammonemia, hyperlysinemia and homocitrullinuria. Blood cell arginase activity of the patient on normal diet was

Plasma lysine concentration and availability of 2-ketoglutarate in liver mitochondria.

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Defects of lysine metabolism are rare, but hyperlysinemia is a concomitant of many inborn errors of metabolism, including urea cycle abnormalities, pyruvate carboxylase deficiency and L-2-hydroxyglutaric aciduria. We have hypothesized that mitochondrial lysine degradation is regulated by

[Inborn errors of lysine metabolism].

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A wide variety of inborn errors of lysine catabolism have been described. They include: abnormalities of the mitochrondrial catabolism via the "saccharopine pathway", abnormalities of the peroxisomal catabolism via the pipecolic pathway, and "lysine intolerance with periodic ammonia intoxication"

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