Sanfilippo syndrome (mucopolysaccharidosis type III) is a lysosomal disorder caused by a defect in the catabolism of heparan sulfate. Mucopolysaccharidosis type III is the most common type of all mucopolysaccharidoses. The pathogenic basis of the disease consists of the storage of undegraded substrate in the central nervous system. Progressive cognitive decline resulting in dementia and behavioural abnormalities are the main clinical characteristics of Sanfilippo syndrome. Mucopolysaccharidosis type III may be misdiagnosed as otherforms of developmental delay, attention deficit/hyperactivity disorder and autistic spectrum disorders because of lack of somatic symptoms, presence of mild and atypical forms of the disease. Patients with Sanfilippo syndrome may have comparatively low urinary glycosaminoglycans levels resulting in false negative urinary assay. Definitive diagnosis is made by enzyme assay on leucocytes and cultured fibroblasts. There is currently no effective treatment of mucopolysaccharidosis type III, though ongoing researches of gene, substrate reduction and intrathecal enzyme replacement therapies expect getting curative method to alter devasting damage of central nervous system in near future.
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Front Genet
January 2025
Genetics and Precision Medical Center, Wuhan Children's Hospital (Wuhan Maternal and Child Healthcare Hospital), Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Introduction: Mucopolysaccharidosis type VI (MPSVI), an autosomal recessive lysosomal storage disorder caused by pathogenic variants in gene. Usually, whole exome sequencing (WES) can identify these variants, and if WES failed to detect causative variants, whole-genome sequencing (WGS) may be considered to investigate deep intronic variations and structural alterations in patients.
Methods: Whole-exome sequencing (WES) and whole genome sequencing (WGS) were performed in a Chinese family having a boy with suspected diagnosis of MPS with macrocephaly, coarse facial features, broad forehead, thick lips, frontal bossing, craniosynostosis, blue spots, frequent upper respiratory infections, inguinal hernia, and dysostosis multiplex.
Mol Genet Metab
January 2025
Division of Medical Genetics, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, QC, Canada. Electronic address:
Mucopolysaccharidosis type II (MPS II), also known as Hunter syndrome, is an X-linked lysosomal storage disorder. It results from a deficiency of the enzyme iduronate-2-sulfatase (I2S), leading to the accumulation of glycosaminoglycans (GAGs) in various tissues and organs. Clinical manifestations include skeletal abnormalities, facial coarsening, organ enlargement, and developmental delays.
View Article and Find Full Text PDFCase Rep Dent
January 2025
Faculty of Dental Sciences, Beirut Arab University, Beirut, Lebanon.
Mucopolysaccharidosis (MPS) Type III (MPS III) or Sanfilippo syndrome is a rare autosomal recessive inherited metabolic disorder. This disorder is responsible for lysosomal storage disorder at the cellular aspect. Due to lysosomal enzyme perturbance leading to the alteration of macromolecule metabolisms, this cellular perturbance causes multiple severe systemic and mental outcomes.
View Article and Find Full Text PDFTurk Arch Pediatr
January 2025
Federal State Budgetary Scientific Institution, Research Center for Medical Genetics, Moscow, Russia.
Objective: The study aimed to evaluate the epidemiological, clinical, and molecular data of mucopolysaccharidosis type II (MPS II) patients and their outcomes using the national registry of patients in the Russian Federation (RF). Materials and Methods: In the retrospective cohort study, the authors included data from the Russian national registry of MPS II. Results: The prevalence of MPS II in RF is 0.
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