The Mucopolysaccharidoses and
Mucolipidoses Treatment Program

Under the direction of medical geneticist Barbara K. Burton, MD, the Mucopolysaccharidoses and Mucolipidoses Treatment Program provides comprehensive care and assists patients and families in the management of these complex conditions. The program's mission is to maximize the quality of life of our patients by providing outstanding, compassionate care.

What are mucopolysaccharidoses?

a 7-year-old boy

A 7-year-old boy with MPS II.

Mucopolysaccharidoses (MPS) are a group of genetic disorders each of which is caused by the deficiency of an enzyme (a protein that produces chemical reactions in the body) that breaks down one or more types of mucopolysaccharides, also referred to as glycosaminoglycans (GAGs). GAGs are long, repeating chains of complex sugar molecules that are normal chemical components of bones, cartilage, and many other tissues within the body. They are constantly being “turned over,” meaning that new GAGs are produced as others are broken down. If the GAGs cannot be broken down normally, they accumulate in excess in various tissues of the body resulting in the clinical features associated with an MPS disorder.

Changes in specific genes result in the deficiency or absence of the enzyme. The MPS disorders are categorized into several groups based on the clinical features and specific enzyme deficiency. An individual is usually suspected of having an MPS disorder after developing characteristic physical findings. The diagnosis is further confirmed by laboratory testing. Clinical features of these conditions may vary depending on the specific diagnosis.

Find more details on the specific MPS disorders in the associated pages in this section.

What are mucolipidoses?

Mucolipidoses (ML) are a group of genetic disorders in which both glycosaminoglycans (GAGs) and another group of substances called sphingolipids build up in the body. GAGs are long, repeating chains of complex sugar molecules, and sphingolipids are fats. ML disorders may also be referred to as “targeting defects” because affected individuals are lacking the enzyme (a protein that produces chemical reactions in the body) that “targets” other enzymes to the lysosome (a sac-like structure found in a cell).

ML disorders are different from mucopolysaccharidoses (MPS). In MPS, the absence or deficiency of one specific enzyme results in an excess of sugars or GAGs in an individual's tissues and in the urine. In ML, individuals are lacking multiple enzymes in their lysosomes within their cells because of this targeting defect.

Changes in specific genes results in the deficiency or absence of the targeting enzyme. The ML disorders are categorized into four groups based on the clinical features and enzyme deficiencies. ML-II and ML-III are the more common forms of ML. An individual is usually suspected of having an ML disorder based on clinical features. The diagnosis is further confirmed by laboratory testing.

Carrier testing and prenatal testing for MPS and ML

Prenatal diagnosis is available for all MPS and ML disorders. Amniocentesis (a procedure in which amniotic fluid is taken from around the fetus) can be used to obtain fetal cells which are then cultured and used for enzyme analysis or genetic testing by DNA analysis. In addition, chorionic villus sampling (the extraction of a small sample of tissue from the developing placenta) can be performed in the first trimester of pregnancy in order to make a diagnosis. Pre-implantation genetic diagnosis is possible in some cases, using in vitro fertilization, if the mutation or mutations responsible for the disorder in a family have previously been identified. Carrier testing for MPS and ML disorders can usually be accomplished, either by enzymatic or molecular (DNA-based) analyses, depending on the specific circumstances.



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