Hearing Loss Clinical Trial
Congenital hypothyroidism (CH) occurs in 1:4000 live births. Neurological disturbances like
speech delay, motor delay and lower IQ were reported in children with CH. Evidence from
animal experiments indicate that CH is associated with high frequency of deafness.
Morphological changes of the external and internal cholera hairs were reported in mutagenic
mice with CH. Anatomical changes of the internal ear and low hearing threshold were reported
in mice bearing Dual oxidase 2 (Duox2) gene mutations, which is responsible of oxidation of
iodide. Knockout of Pax8 gene in mice resulted in both agenesis of thyroid gland and
deafness. Early L-thyroxin therapy prevented the development of deafness in those mice. The
expression of thyroid receptor α (TRα) in the external and internal cholera hairs in mice
indicates that the thyroid hormones have an important role in the development of the
internal ear.
The etiology of deafness in human is both genetic and environmental. The prevalence of
deafness in live births is 1:1000 and among them 60% is genetic. Connexin 26 gene mutations
are the most common cause of inherited deafness and account for about 40% of the genetic
cases. In two conditions in human the coexistence of hypothyroidism and deafness were
reported; Pendred syndrome and thyroid hormone resistance syndrome.
The prevalence of hearing loss in human with CH was explored in only few studies and the
results are contrary.
The aim of the current study is to study the prevalence of hearing loss among children with
CH and to compare the clinical, biochemical and genetic characteristics between subjects
with hearing loss to those without hearing loss.
n/a
Observational Model: Case Control, Time Perspective: Prospective
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