Final Height in Patients With CH Diagnosed by the Screening

Congenital Hypothyroidism

Final Height, Neonatal 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

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Egypt