ArticleJournal of inherited metabolic disease2008
Incidence of 3-hydroxy-3-methylglutaryl-coenzyme A lyase (HL) deficiency in Brazil, South America.
Article in Journal of inherited metabolic disease, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 23 citations in OpenAlex.
- Disruption of Mitochondrial Quality Control in Inherited Metabolic Disorders.Molecular neurobiology · 2025Review
- Treatment of HMG-CoA Lyase Deficiency-Longitudinal Data on Clinical and Nutritional Management of 10 Australian Cases.Nutrients · 2023Review
- Hepatic Manifestations of 3-Hydroxy-3-Methylglutaryl-Coenzyme-A Lyase Deficiency in Saudi Patients: Experience of a Tertiary Care Center.Journal of pediatric genetics · 2021Article
- A newborn screening approach to diagnose 3-hydroxy-3-methylglutaryl-CoA lyase deficiency.JIMD reports · 2020Article
- 3-hydroxy-3-methylglutaryl-coenzyme A lyase deficiency: one disease - many faces.Orphanet journal of rare diseases · 2020Article
- More Than One HMG-CoA Lyase: The Classical Mitochondrial Enzyme Plus the Peroxisomal and the Cytosolic Ones.International journal of molecular sciences · 2019Review
- Screening for organic acidurias and aminoacidopathies in high-risk Brazilian patients: Eleven-year experience of a reference center.Genetics and molecular biology · 2019Article
- Disturbance of redox homeostasis as a contributing underlying pathomechanism of brain and liver alterations in 3-hydroxy-3-methylglutaryl-CoA lyase deficiency.Journal of inherited metabolic disease · 2015Review
- Increased oxidative stress in patients with 3-hydroxy-3-methylglutaric aciduria.Molecular and cellular biochemistry · 2015Article
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
3-Hydroxy-3-methylglutaryl-CoA lyase (HL) deficiency (3-hydroxy-3-methylglutaric aciduria, 3-HMG) is a rare autosomal recessive inborn error of metabolism involving the final step of leucine degradation. HL is the key enzyme for the production of glucose-sparing ketone bodies for brain. Positive biochemical findings are metabolic acidosis, hyperammonaemia, and hypoketotic hypoglycaemia in the neonatal period or infancy. In the present study we report 15 Brazilian patients with HL deficiency and present their clinical and biochemical findings. Urine from all patients contained large amounts of 3-hydroxy-3-methylglutaric, 3-methylglutaconic, 3-hydroxyisovaleric and 3-methylglutaric acids, and 3-methylcrotonylglycine was also observed in 13 patients. The main features at clinical presentation were hypoglycaemia (12 patients), seizures (10 patients), metabolic acidosis (9 patients), vomiting (6 patients), and hepatomegaly (5 patients). All but two patients were of Portuguese ancestry. HL deficiency comprised 7.3% of total organic acidurias detected in our laboratory during a 13-year time span, indicating a high incidence of this disorder in Brazil. Limited molecular characterization (4/15 patients only) revealed two mutations common for individuals of Portuguese/Spanish (Iberian Peninsula) ancestry (E37X and V168fs(-2)). Our findings increase the number of HL-deficient patients and reinforce the characteristic phenotypic picture of the disease. Effective dietary interventions based on mild protein restriction and avoidance of fasting and possibly alternative C5 ketone body generating therapy for this disorder may provide further impetus and rationale for expanded newborn screening of HL deficiency.
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