pediatrics
Hyperthyroidism in Infants and Children
Etiology
 hyperthyroidism is rare but potentially life-threatening. It develops in fetuses of women with current or prior Graves disease . In Graves disease, maternal autoantibodies against the thyroid receptor for thyroid-stimulating hormone (TSH) overstimulate thyroid hormone production by binding to TSH receptors in the thyroid gland. These antibodies cross the placenta and cause thyroid hyperfunction in the fetus (intrauterine Graves disease), which can result in fetal death or preterm birth due to fetal hyperactivity or tachycardia. Because infants clear the antibodies after birth, neonatal Graves disease is usually transient. However, because the clearance rate varies, duration of neonatal Graves disease varies. Graves disease is the cause of hyperthyroidism in > 90% of cases. There is an increased incidence of Graves disease during puberty, with 80% of cases occurring after 11 years of age. The primary mechanism is stimulating antibodies for the TSH receptor. Other antibodies block the TSH receptor, and the balance between stimulating and blocking determines the severity of Graves disease. Many children with Graves disease have a family history of autoimmune thyroid disease or other autoimmune conditions. Children with Down Syndrome (Trisomy 21) are at increased risk of Graves disease. Less common causes of hyperthyroidism in children and adolescents include autonomously functioning toxic nodules, transient hyperthyroidism during the early phase of Hashimoto Thyroiditis followed by eventual hypothyroidism (hashitoxicosis), or adverse drug effects (eg, 