Final Height in Patients With CH Diagnosed by the Screening
Final Height in Patients With CH Diagnosed by the Screening
The aim of this study is to evaluate longitudinal growth and final height in patients with
 Congenital Hypothyroidism detected by neonatal screening and factors affecting it.
Linear growth and final height are reported as rather normal in patients with CH diagnosed
 through the screening and the target height is the most important factor determining linear
 growth. Data on final height in patients with CH suggest that adult height is significantly
 correlated with parental height and the mean L-Thyroxine daily dose administered over the
 first 6 months of treatment. The lowest recommended dose during this period is 8.5μg/kg/day.
 Periodical adjustments of L-Thyroxine daily dose should be guided by clinical observation and
 serum free T4 levels.

 To our knowledge this is the first study from our center to assess final height in patients
 with congenital hypothyroidism diagnosed through the Egyptian neonatal screening program.

 A complex network of endocrine signals stimulates the process of longitudinal growth
 including growth hormone, insulin-like growth factor-1, glucocorticoids, thyroid hormone,
 estrogen, androgens, vitamin D and leptin.

 Thyroid hormones are essential for development and normal bone growth. Biochemical studies
 have shown that thyroid hormones can affect the expression of various bone markers in the
 serum, reflecting changes in bone remodeling which involves both osteoblastic and
 osteoclastic activities.

 Thyroid hormones act through chondrocytes bearing thyroid hormone receptors (TRs) to modulate
 growth plate proliferation, differentiation and vascular invasion. Several mechanisms mediate
 these functions including direct action on the chondrocytes, osteoblasts and mast cells. It
 also works through interaction with other hormones and growth factors acting in endocrine,
 paracrine and autocrine fashions.

 Overall, T3 acts via TRα in chondrocytes and osteoblasts to regulate intramembranous and
 endochondral ossification and control the rate of linear growth, bone maturation and
 mineralization,T4 induces the expression of both type II and X collagen and chondrocyte
 hypertrophy.

 Hypothyroidism in children causes growth arrest, delayed bone maturation, and epiphyseal
 dysgenesis that can result in short stature and delayed closure of the epiphyses.

 In severe undiagnosed cases, complete post-natal growth arrest and skeletal dysplasia occurs
 with characteristic X-ray features including stippled epiphyses reflecting epiphyseal
 dysgenesis, congenital hip dislocation, vertebral immaturity, scoliosis, patent fontanelles
 and sutures and delayed eruption of teeth.

 Prompt treatment of patients suffering from CH with thyroid hormone replacement induces a
 period of rapid catch-up growth in which skeletal maturation and bone age are also
 accelerated. Ultimately, normal adult height can be expected.

 It is controversial whether factors as the degree of hypothyroidism at diagnosis, the timing
 of the onset of treatment and the doses of replacement L-thyroxine (L-T4) affect linear
 growth in children with congenital hypothyroidism, detected by screening and treated from
 early infancy
Inclusion Criteria:

 -  Patients having a documented history of CH diagnosed by Egyptian neonatal screening
 program.

 -  Patients receiving L-thyroxine (L-T4) since the diagnosis is established.

 Exclusion Criteria:

 -  Patients who are non-compliant on L-thyroxine (L-T4) and failed to follow up at the
 clinic on regular basis.

 -  Patients who were missed from diagnosis by neonatal screening.

 -  Patients with associated hormonal disorders affecting same parameters concerned in the
 study.