Congenital Hypothyroidism

The hypothalamic-pituitary-thyroid axis is active by midgestation and mature by birth. Prior to midges-tation, fetal development relies on maternal thyroid hormones (Greenspan and Gardner 2004). Congenital hypothyroidism occurs in approximately 1 of 4,000 live births and is usually due to thyroid dysgenesis or deficits in thyroid hormone production. Congenital hypothyroidism is one of the most common causes of mental retardation; however, because maternal thyroid hormones transfer across the placenta, early diagnosis and treatment with L-thyrox-ine can result in normal cognitive development of affected children (New England Congenital Hypothyroidism Collaborative 1990). Maternal hypothy-roidism alone, or in conjunction with fetal hypothy-roidism, leads to cognitive impairment in children despite postnatal therapy. This observation illustrates the importance of thyroid hormone exposure during early fetal development for subsequent cognitive function (Haddow et al. 1999; Morreale de Escobar et al. 2000; Vermiglio et al. 2004). A two-to-one incidence of congenital hypothyroidism exists for females compared to males, and the inci-

Figure 19-1. Hypothalamic-pituitary' thyroid axis.

Thyrotropin-releasing hormone (TRH) secreted by the hypothalamus stimulates the anterior pituitary to secrete thyroid-stimulating hormone (TSH). TSH then stimulates the thyroid gland to produce thyroid hormones thy-roxine (T4) and triiodothyronine (T3). Thyroid hormones exert negative feedback to the hypothalamus and anterior pituitary to maintain homeostatic regulation of this axis.

dence of congenital hypothyroidism is higher in people with Down syndrome than in the overall population (American Academy of Pediatrics et al. 2006; LaFranchi 1999). Newborn screening for congenital hypothyroidism was instituted in the 1970s and is now ubiquitous throughout North America and other areas of the world. In North America alone, approximately 1,400 cases of congenital hypothyroidism are identified annually (American Academy of Pediatrics et al. 2006).

Prior to newborn screening, individuals with untreated congenital hypothyroidism had poor performance on IQ testing, increased participation in special education programs, and impaired fine motor control. Daily dosages of 10-15 M-g/kg levothyroxine (Fisher and Foley 1989) initiated early (within the first 2 weeks of life) to normalize T4 are associated with normal cognition and social behavior in toddlers (Dubuis et al. 1996) and young school children (Simone-Roy et al. 2004). Regardless of these positive outcomes in young individuals, HRQOL and self-esteem in young adults affected by congenital hypothyroidism lag behind their unaffected counterparts despite recommended T4 treatment (van der Sluijs et al. 2008). Additionally, young adults with congenital hypothyroidism who received lower than recommended doses of T4 replacement during development exhibited lower IQ and lower secondary school completion rates, as well as poorer motor function, than their unaffected siblings (Oerbeck et al. 2003). Despite improved detection and treatment of congenital hypothyroidism in newborns and children, increased attention is needed to improve the mental health outcomes in older children and adults.

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