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Mowat-Wilson Syndrome

OMIM ID:

autosomal dominant

Mowat-Wilson Syndrome

Alternate Names

Hirschsprung disease-mental retardation syndrome

Defective Genes

ZEB2

Clinical Characteristics

Ocular Features

Most reports of Mowat-Wilson disorders provide only incomplete ocular findings and the full phenotype remains to be described.  Most of the reported findings are part of the facial phenotype, such as downward slanting palpebral fissures, and ‘wedge-shaped’ eyebrows with the medial portion visibly wider than the temporal region.  Hypertelorism, strabismus and telecanthus have also been noted.  However, optic nerve atrophyor aplasia, RPE atrophy, microphthalmia, ptosis, and cataracts are sometimes present while strabismus is more common.  Iris and other uveal colobomas may be present and at least one patient has been reported with retinal aplasia.  There may be considerable asymmetry in the features among the two eyes.

Systemic Features

This is a highly complex dysmorphic developmental disorder with unusual progression of facial features.  Birth weight and length are usually normal but later there is general somatic and mental growth delay with microcephaly (pre- and post natal), short stature, intellectual disability, and epilepsy (70%).  Hypotonia has been noted at birth.  A significant proportion (~50%) of patients have Hirschsprung disease with megacolon.  Congenital heart defects are common, many involving septal openings.  Hypospadias is often present with or without other genitourinary anomalies.  Teeth are often crowded and crooked.  The earlobes may be flattened and may have a central depression.

The facial features are present in early childhood but as they mature the upper half of the nasal profile becomes convex, while the nasal tip becomes longer and overhangs the philtrum.  The eyes appear more deeply set.  The chin lengthens and prognathism becomes apparent.  IQ levels cannot be determined but many individuals exhibit behavioral or emotional disturbances.

Genetics

Inheritance

Heterozygous mutations in ZEB2 (2q22.3) are responsible for most cases (81%) of this disorder.  A large number of molecular mutations, many of the nonsense type, have been reported. About 2-4% of patients have cytogenetic alterations involving the 2q22 region.

Another disorder with microcephaly, intellectual disability and Hirschsprung disease is Goldberg-Shprintzen syndrome (609460) with mutations in the KIAA1279 gene.

Pedigree

Autosomal dominant

Autosomal dominant disorders require only one mutation for the disease to be expressed.  Since an affected parent has two chromosomes, only one of which has the mutant gene, parents can expect that half (50%) of their children will receive that one and inherit the disease.  It is common for individuals that inherit the mutation, however, to not have evidence of the disease (nonpenetrance).

Image
Sample pedigree of autosomal dominant inheritance

Autosomal dominant inheritance leads to a vertical pattern of transmission

Treatment & Management

Treatment may be directed at specific defects but there is no treatment for the general disorder. Individuals can live to adulthood. Treatment is largely symptomatic.  Physical and speech treatment can be helpful if initiated early.

Publications

Displaying 1 - 6 of 6

Clinical and Mutational Spectrum of Mowat–Wilson Syndrome

PubMedID: 16053902

Clinical spectrum of eye malformations in four patients with Mowat–Wilson syndrome

PubMedID: 25899569

Mowat–Wilson syndrome: Facial phenotype changing with age: Study of 19 Italian patients and review of the literature

PubMedID: 19215041

Ophthalmologic Abnormalities in Mowat-Wilson Syndrome and a Mutation inZEB2

PubMedID: 22486326

Phenotype and genotype of 87 patients with Mowat–Wilson syndrome and recommendations for care

PubMedID: 29300384

The behavioral phenotype of Mowat–Wilson syndrome

PubMedID: 22246645