PubMed:9709714 JSONTXT

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{"target":"https://pubannotation.org/docs/sourcedb/PubMed/sourceid/9709714","sourcedb":"PubMed","sourceid":"9709714","source_url":"http://www.ncbi.nlm.nih.gov/pubmed/9709714","text":"Reversal of severe hypertrophic cardiomyopathy and excellent neuropsychologic outcome in very-long-chain acyl-coenzyme A dehydrogenase deficiency.\nVery-long-chain acyl-coenzyme A dehydrogenase (VLCAD) deficiency is a disorder of fatty acid beta oxidation that reportedly has high rates of morbidity and mortality. We describe the outcome of a 5-year-old girl with VLCAD deficiency who was first seen at 5 months of age with severe hypertrophic cardiomyopathy, hepatomegaly, encephalopathy, and hypotonia. Biochemical studies indicated VLCAD deficiency caused by a stable yet inactive enzyme. Molecular genetic analysis of her VLCAD gene revealed a T1372C (F458L) missense mutation and a 1668 ACAG 1669 splice site mutation. After initial treatment with intravenous glucose and carnitine, the patient has thrived on a low-fat diet supplemented with medium-chain triglyceride oil and carnitine and avoidance of fasting. Her ventricular hypertrophy resolved significantly over 1 year, and cognitively, she is in the superior range for age. Clinical recognition of VLCAD deficiency is important because it is one of the few directly treatable causes of cardiomyopathy in 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