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Children with the more severe form of MPS IV may not live beyond their twenties or thirties. Cause
Morquio syndrome is inherited from an autosomal recessive inherited gene. Every person has two copies of the genes needed to break down keratan sulfate, but only one healthy copy is needed. Both parents pass down one defective copy to their child, resulting in a child with no functional copies of the gene. As such, the body is incapable breaking down keratan sulfate for disposal. The incompletely broken down GAGs remain stored in cells in the body, causing progressive damage. Babies may show little sign of the disease, but as more and more cells become damaged, symptoms start to appear. Diagnosis
Classification
This syndrome has two forms, A and B, referred to as Morquio A and Morquio B syndrome or MPS IVA and MPS IVB. The two forms are distinguished by the gene product involved; Type A involves a malfunction in the GALNS gene, while Type B involves a malfunction of the GLB1 gene. Treatment
The treatment for Morquio syndrome consists of prenatal identification and of enzyme replacement therapy. On 12 February 2014, the US Food and Drug Administration approved the drug elosulfase alfa (Vimizim) for treating Type A. Currently, there is no treatment for Type B.

Prognosis
The lifespan of patients with Morquio syndrome is variable and depends on the subtype. Type A is generally severe, with a life expectancy in the 20s to 30s.