[Clinical features and genetic analysis of a child with glycogen storage disease type VI]

Zhonghua Yi Xue Yi Chuan Xue Za Zhi. 2022 Oct 10;39(10):1099-1102. doi: 10.3760/cma.j.cn511374-20211005-00799.
[Article in Chinese]

Abstract

Objective: To explore the clinical features and genetic etiology of a child with glycogen storage disease VI (GSD-VI).

Methods: Clinical data and laboratory results of the patient were collected. Whole exome sequencing (WES) was carried out for the patient. Candidate variant and its parental origin was verified by Sanger sequencing.

Results: The patient was a 3-year-and-9-month old boy whom has featured abdominal distention, hepatomegaly, short stature and elevated hepatic transaminase. WES revealed the he has harbored compound heterozygous variants of the PYGL gene, namely c.697G>A (p.Gly233Ser) and c.320dupA (p.Asn107fs). Sanger sequencing has verified that the two variants have derived from his father and mother, respectively. The c.320dupA (p.Asn107fs) variant was unreported previously.

Conclusion: The compound heterozygous variants of the PYGL gene probably underlay the GSD-VI in this patient. Above finding has enriched the spectrum of PYGL gene variants and provided a basis for the treatment and genetic counseling.

Publication types

  • Case Reports

MeSH terms

  • Child
  • Exome Sequencing
  • Genetic Testing
  • Glycogen Storage Disease Type VI* / genetics
  • Humans
  • Infant
  • Male
  • Mutation
  • Transaminases / genetics

Substances

  • Transaminases