Rapid Diagnosis of Methylmalonic and Propionic Acidemias

Abstract
Methylmalonic acidemias (MMAs) and propionic acidemias (PAs) comprise a group of congenital disorders of branched-chain amino acid metabolism (1). PA is caused by deficiency of propionyl-CoA carboxylase, whereas MMA results from deficiency of either methylmalonyl-CoA mutase or defects in the production of adenosylcobalamin. Deficiency of vitamin B12, a cofactor for methylmalonyl-CoA mutase, will also produce signs and symptoms consistent with MMA (2)(3)(4). Other biochemically closely related disorders are the cobalamin (Cbl) defects, classified as forms A through G (5). Clinical signs and symptoms include failure to thrive, metabolic acidosis, persistent ketotic episodes, hypoglycemia, hypotonia, hyperammonemia, and neurologic symptoms (6). Children with PA, MMA, or Cbl disorders often present with acute illness as neonates or infants. Treatment of MMA and PA includes careful monitoring and limitation of branched-chain amino acid intake (4) as well as possible supplementation with biotin, vitamin B12, and l-carnitine (7).

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