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disorders can present with profound metabolic acidosis and intermittent lethargy, vomiting, tachypnea, tremors, twitching, convulsions, and coma, with early death in about half the patients and developmental retardation in those who survive Rare subtypes of methylmalonic acidemia respond to vitamin B12 Isovaleric acidemia is characterized by a striking odor of stale perspiration, which has given it the sobriquet sweaty foot syndrome Numerous metabolic defects, most commonly of pyruvate decarboxylase and pyruvate dehydrogenase, are responsible for the accumulation of lactic and pyruvic acids The enzymatic defect of isovaleric acidemia has also been demonstrated in a recurrent form of episodic cerebellar ataxia and athetosis and in a persistent form in mitochondrial encephalopathies (Leigh disease), as described further on in this chapter A separate and rare de ciency of aromatic L-amino acid decarboxylase has been described; the chemical signature is of low levels of almost all catecholamines This defect is associated with a peculiar movement disorder of oculogyric crises, dystonia and athetosis and autonomic failure (see Swoboda et al) A type II glutaric acidemia has also been observed in the neonatal period and causes episodes of acidosis with vomiting and hyperglycemia Multiple congenital anomalies of brain and somatic structures and cardiomyopathy are conjoined A diet low in the speci c toxic amino acid and supplements of carnitine and ribo avin are recommended, but the effects are unclear In the nonketotic form of hyperglycinemia, there are high levels of glycine but no acidosis The notable diagnostic nding is an elevation of the CSF glycine, several times higher than that of the blood The effects on the nervous system are more devastating than in the ketotic form In reported cases (the authors and our colleagues have seen several), the neonate is hypotonic, listless, and dyspneic, with dysconjugate eye movements, opisthotonic posturing, myoclonus, and seizures A few such neonates survive to infancy but are extremely retarded and helpless Spongy degeneration of the brain has been reported both in this disease and in the ketotic form (Shuman et al) No treatment has been effective in severe cases In an atypical milder form, with neurologic abnormalities that appear in later infancy or childhood, reduction of dietary protein and administration of sodium benzoate in doses up to 250 mg/ kg per day have been bene cial The use of dextromethorphan, which blocks glycine receptors, is said to be effective in preventing seizures and coma Inherited Hyperammonemias These are a group of six diseases caused by inborn de ciencies of the enzymes of the Krebs-Henseleit urea cycle; they are designated as N-acetyl glutamate synthetase, carbamyl phosphate synthetase (CPS), ornithine transcarbamylase (OTC), argininosuccinic acid synthetase (citrullinemia), argininosuccinase de ciency, and arginase de ciency Hyperornithinemia-hyperammonemia-homocitrullinemia (HHH) and intrinsic protein intolerance are closely related disorders They are identi ed by the nding of a persistent or episodic elevation of ammonia levels in the blood A detailed account of these inherited hyperammonemic syndromes is contained in the review by Brusilow and Horwich The pattern of inheritance of each of these disorders is autosomal recessive except for OTC de ciency, which is X-linked dominant Their clinical manifestations are a common expression of an accumulation of ammonia or of urea cycle intermediates in the brain; they differ only in severity, in accordance with the degree of completeness of the enzymatic de ciency and with the age of. generate pdf in mvc using itextsharp MVC To PDF | Convert Files Easily In C# | Iron PDF
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