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Syndrome
Synopsis: Prader-Willi Syndrome
by Beth A. Pletcher, MD, November 1999
Patients are usually referred for
possible Prader-Willi syndrome (PWS) when an astute clinician sees
a child with obesity and developmental delay. While the clinical
features vary a great deal between individuals, there are some helpful
clues that might assist in the identification of children with or
without this condition. Furthermore, there are a number of other
syndromes that have overlapping features with PWS.
Early in life many children with PWS
have significant hypotonia and in some cases have feeding problems
associated with failure to thrive during the first year of life.
It usually isn't until 18 to 24 months of age that one may begin
to see the voracious appetite and subsequent weight gain that one
typically associates with this condition. Unlike other children
with obesity where height tends to be equal to or greater than the
90th%ile when weight is above the 95th%ile, children with PWS often
have heights at or below the 50th%ile despite significant weight
gain. Also this height vs. weight discrepancy may become more pronounced
over time.
Some features that might be seen more
often in children with PWS include: bitemporal narrowing, almond-shaped
eyes, lighter pigmentation than unaffected family members, small
hands and feet, hypogonadism, cryptorchidism, and hypoplastic enamel
leading to early, severe caries.
Diagnostic testing can be done as a
two-pronged approach using both cytogenetic and molecular technologies.
FISH cytogenetic studies looking for a submicroscopic deletion on
chromosome 15 in the 15q11-13 region will pick up about 65% of children
with PWS; molecular testing will detect an additional 30% of affected
patients whose PWS is due to maternal uniparental disomy. For a
more detailed laboratory discussion you may wish to refer to our
website at http://www.genesatwork.org under Genetic Lab Testing
Facts, subheading Molecular, Prader-Willi syndrome and Angelman
syndrome.
Other syndromic causes of obesity
and mental retardation include: Bardet-Biedl syndrome with additional
features of polydactyly and retinitis pigmentosa as well as Cohen
syndrome with down-slanting palpebrae, a prominent nose, and long,
thin fingers and toes. Fragile X syndrome, although not typically
associated with obesity, can have this as a prominent feature and
may be missed if not considered in the differential diagnosis. Overgrowth
syndromes such as Sotos syndrome would generally have a more proportionate
overgrowth picture with macrocephaly and advanced bone age as well
as a rather muscular build.
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