1987Acta PaediatricaRequires access

Recent Advances in the Inherited Methylmalonic Acidemias

M J Mahoney, David Bick

Open publisher page 34 citations

Abstract

Methylmalonic acidemia results from decreased activity of methylalonyl-CoA mutase, an enzyme required for the catabolism of four amino acids. A cobalamin (vitamin B12) compound is required as coenzyme. Several inherited mutations of the mutase apoenzyme or of cobalamin coenzyme synthesis have been identified. Clinical disease is most commonly recognized as a severe protein intolerance state although a wide range of symptoms has been appreciated. Current therapy emphasizes strict dietary management and use of vitamin B12 in cobalamin responsive patients.

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What this paper is about

Methylmalonic acidemia results from decreased activity of methylalonyl-CoA mutase, an enzyme required for the catabolism of four amino acids. A cobalamin (vitamin B12) compound is required as coenzyme. Several inherited mutations of the mutase apoenzyme or of cobalamin coenzyme synthesis have been identified. Clinical disease is most commonly recognized as a severe protein intolerance state although a wide range of symptoms has been appreciated. Current therapy emphasizes strict dietary management and use of vitamin B12 in cobalamin responsive patients.

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Available abstract

Methylmalonic acidemia results from decreased activity of methylalonyl-CoA mutase, an enzyme required for the catabolism of four amino acids. A cobalamin (vitamin B12) compound is required as coenzyme. Several inherited mutations of the mutase apoenzyme or of cobalamin coenzyme synthesis have been identified. Clinical disease is most commonly recognized as a severe protein intolerance state although a wide range of symptoms has been appreciated. Current therapy emphasizes strict dietary management and use of vitamin B12 in cobalamin responsive patients.

Key concepts: Cobalamin, Methylmalonic acidemia, Mutase, Medicine, Catabolism, Vitamin B12, Biochemistry, Enzyme

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