Ten years of screening for congenital disorders of glycosylation in Argentina: Case studies and pitfalls

Background: Congenital Disorders of Glycosylation (CDG) are genetic diseases caused by hypoglycosylation of glycoproteins and glycolipids. Most CDG are multisystem disorders with mild to severe involvement. Methods: We studied 554 patients (2007–2017) with a clinical phenotype compatible with a CDG....

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Detalles Bibliográficos
Autores: Asteggiano, Carla Gabriela, Papazoglu, Gabriela Magali, Bistue Millon, Maria Beatriz, Peralta, Maria Fernanda, Azar, Nydia Beatríz, Spécola, Norma, Guelbert, Norberto Bernardo, Suldrup, Niels, Pereyra, Marcela, Dodelson de Kremer, Raquel
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2018
País:Argentina
Institución:Consejo Nacional de Investigaciones Científicas y Técnicas
Repositorio:CONICET Digital (CONICET)
Idioma:inglés
OAI Identifier:oai:ri.conicet.gov.ar:11336/164486
Acceso en línea:http://hdl.handle.net/11336/164486
Access Level:acceso abierto
Palabra clave:CDG
Glycosilation
IEF
NGS
https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
Descripción
Sumario:Background: Congenital Disorders of Glycosylation (CDG) are genetic diseases caused by hypoglycosylation of glycoproteins and glycolipids. Most CDG are multisystem disorders with mild to severe involvement. Methods: We studied 554 patients (2007–2017) with a clinical phenotype compatible with a CDG. Screening was performed by serum transferrin isoelectric focusing. The diagnosis was confirmed by genetic testing (Sanger or exome sequencing). Results: A confirmed abnormal pattern was found in nine patients. Seven patients showed a type 1 pattern: four with PMM2-CDG, two with ALG2-CDG, and one with classical galactosemia. A type 2 pattern was found in two patients: one with a CDG-IIx and one with a transferrin protein variant. Abnormal transferrin pattern were observed in a patient with a myopathy due to a COL6A2 gene variant. Conclusions: CDG screening in Argentina from 2007 to 2017 revealed 4 PMM2-CDG patients, 2 ALG2-CDG patients with a novel homozygous gene variant and 1 CDG-IIx.