Early and aggressive thyroxine replacement is critical for newborns with congenital hypothyroidism. Still, some neonates identified by screening programs who were treated promptly will exhibit cognitive deicits into adolescence (Song, 2001). herefore, in addition to timing of treatment, the severity of congenital hypothyroidism is an important factor in long-term cognitive outcomes. Olivieri and colleagues (2002) reported that 8 percent of 1420 newborns with congenital hypothyroidism also had other major congenital malformations.
Transient autoimmune thyroiditis is consistently found in approximately 5 to 10 percent of women during the first year after childbirth (Nathan, 2014; Stagnaro-Green, 2011b, 2012a). Postpartum thyroid dysfunction with an onset within 12 months includes hyperthyroidism, hypothyroidism, or both. The propensity for thyroiditis antedates pregnancy and is directly related to increasing serum levels of thyroid autoantibodies. Up to 50 percent of women who are thyroid-antibody positive in the irst trimester will develop postpartum thyroiditis (Stagnaro-Green, 2012a). In a Dutch study of 82 women with type 1 diabetes, postpartum thyroiditis developed in 16 percent and was threefold higher than in the general population (Gallas, 2002). Importantly, 46 percent of those identified with overt postpartum thyroiditis had TPO antibodies in the first trimester.
In clinical practice, postpartum thyroiditis is diagnosed infre quently because it typically develops months after delivery and causes vague and nonspeciic symptoms (Stagnaro-Green, 2004). he clinical presentation varies, and classically two clinical phases that may develop in succession are recognized.
The first and earliest is destruction-induced thyrotoxicosis with symptoms from excessive release of hormone from glandular disruption. The onset is abrupt, and a small, painless goiter is common. Although there may be many symptoms, only fatigue and palpitations are more frequent in thyrotoxic women com pared with normal controls. This thyrotoxic phase usually lasts only a few months. hionamides are inefective, and if symp toms are severe, a 3-blocking agent may be given. he second and usually later phase between 4 and 8 months postpartum is hypothyroidism from thyroiditis. hyromegaly and other symp toms are common and more prominent than during the thyro toxic phase. hyroxine replacement at doses of25 to 75 �g/d is typically given for 6 to 12 months.
Stagnaro-Green and associates (20 11 b) reported postpartum surveillance results in 4562 Italian gravidas who had been screened for thyroid disease in pregnancy. Serum TSH and anti-TPO antibody levels were measured again at 6 and 12 months. Overall, two thirds of 169 women (3.9 percent) with postpartum thyroiditis were identiied to have hypothyroidism only. The other third were diagnosed with hyperthyroidism. Only 14 percent of all women demonstrated the "classic" biphasic progression described above. These indings are consistent with data compiled from 20 other studies between 1982 and 2008 (Stagnaro-Green, 2012a).
Importantly, women who experience either type of postpartum thyroiditis have a 20-to 30-percent risk of eventually developing permanent hypothyroidism, and the annual progression rate is 3.6 percent (Nathan, 2014). Women at greater risk for developing hypothyroidism are those with higher titers of thyroid antibodies and higher TSH levels during the initial hypothyroid phase. Others may develop subclinical disease, but half of those with thyroiditis who are positive for TPO antibodies develop permanent hypothyroidism by 6 to 7 years (Stagnaro-Green,r2012a).