Mucopolysaccharidosis IVA within Tunisian patients: Confirmation of the two novel GALNS gene mutations

Pathol Biol (Paris). 2012 Jun;60(3):190-2. doi: 10.1016/j.patbio.2011.03.001. Epub 2011 Nov 9.

Abstract

Mucopolysaccharidosis type IVA or Morquio A disease is an autosomal recessive disease resulting from a deficiency of the lysosomal enzyme N-acetylgalactosamine-6-sulfate-sulfatase, which hydrolyses N-acetylgalactosamine-6-sulfate and galactose-6-sulfate in glycosaminoglycans. Phenotypes in Morquio A disease vary from the classical form with severe bone dysplasia, heart valve involvement, corneal opacity, short trunk dwarfism and a life span of 20 to 30 years, to attenuated forms with normal life span, mild bone involvement and mild visceral organ involvement. Unlike the other forms of mucopolysaccharidoses, Morquio A disease is characterized by normal intelligence.

Aim of the study: The aims of this study were to determine if the novel GALNS anomalies IVS1+1G-A and G66R identified in Tunisia are mutations or polymorphisms.

Patients and methods: This study was carried out on six Morquio A patients recruited from many regions of Tunisia. We have used SCCP, sequencing and enzymatic digestion.

Results: IVS1+1G-A and G66R were two deleterious mutations and not polymorphisms.

Conclusion: Screening of mutations and polymorphisms in GALNS gene provide useful information on genotype/phenotype correlations. It should also facilitate more accurate genetic counselling of newly diagnosed cases and their family members.

MeSH terms

  • Adult
  • Base Sequence
  • Chondroitinsulfatases / genetics*
  • DNA Mutational Analysis
  • Genetic Association Studies
  • Humans
  • Molecular Sequence Data
  • Mucopolysaccharidosis IV / epidemiology
  • Mucopolysaccharidosis IV / genetics*
  • Mutation / physiology
  • Polymorphism, Genetic*
  • Polymorphism, Single-Stranded Conformational / physiology
  • RNA Splice Sites / genetics
  • Tunisia / epidemiology
  • Validation Studies as Topic
  • Young Adult

Substances

  • RNA Splice Sites
  • Chondroitinsulfatases
  • GALNS protein, human