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Mucopolysaccharidosis (MPS) clinical trials

View clinical trials related to Mucopolysaccharidosis (MPS).

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NCT ID: NCT05155488 Completed - Clinical trials for Mucopolysaccharidosis (MPS)

A Study to Improve the Awareness of Mucopolysaccharidosis Type II in Brazil

Start date: December 6, 2021
Phase:
Study type: Observational

The main aims of the study are to learn about the percentage of mucopolysaccharidosis type II (MPS II) in adults in Brazil as well as about the diagnosis process. No study medicines will be provided to participants in this study. The data available for participants diagnosed with MPS II in DATASUS (a database of the Informatics Department of Brazilian Health System) will be reviewed. No clinic visits will be required as part of participation in this study.

NCT ID: NCT01822184 Completed - Hunter Syndrome Clinical Trials

Observational Study to Evaluate Neurodevelopmental Status in Pediatric Patients With Hunter Syndrome (MPS II)

Start date: January 18, 2013
Phase:
Study type: Observational

Hunter syndrome (Mucopolysaccharidosis II, [MPS II]) is a rare, genetically linked lysosomal storage disease (LSD) caused by deficiency of the enzyme, iduronate-2-sulfatase (I2S). Most MPS II patients will present with some degree of neurodevelopmental involvement, ranging from severe cognitive impairment and behavioral problems to mildly impaired cognition. This is an observational study; no investigational treatment will be administered. The primary objective of this study is to evaluate the neurodevelopmental status of pediatric patients with MPS II over time and to gain information to guide future treatment studies in this patient population.

NCT ID: NCT01155778 Completed - Clinical trials for Mucopolysaccharidosis (MPS)

Safety, Tolerability, Ascending Dose and Dose Frequency Study of rhHNS Via an IDDD in MPS IIIA Patients

Start date: June 1, 2010
Phase: Phase 1/Phase 2
Study type: Interventional

Sanfilippo syndrome, or Mucopolysaccharidosis (MPS) III, is a rare lysosomal storage disease (LSD) caused by loss in activity of 1 of 4 enzymes necessary for degradation of the glycosaminoglycan (GAG) heparan sulfate (HS) in lysosomes. MPS IIIA results from deficiency of the enzyme heparan N-sulfatase (sulfamidase). MPS IIIA symptoms arise on average at 7 months of age, with the average age of diagnosis at 4.5 years for the majority of patients. The central nervous system (CNS) is the most severely affected organ system in patients with MPS IIIA, evidenced by deficits in language development, motor skills, and intellectual development. In addition, there are abnormal behaviors including but not limited to aggression and excess motor activity/hyperactivity that contribute to disturbances in sleep.Overall, individuals with MPS IIIA have a marked developmental delay and significantly reduced lifespan of 15 years of age on average. The purpose of this study is to determine the safety and tolerability of rhHNS via ascending doses administered via an a surgically implanted intrathecal drug delivery device (IDDD) intrathecal (IT) route once monthly (or every two weeks) for 6 months in patients with MPS IIIA.