Graves' disease in childhood

Abstract

The vast majority of thyrotoxicosis cases in children are caused by Graves' disease (GD) and these account for 10-15% of all childhood thyroid diseases. The major clinical features of thyrotoxicosis in children are, in general, similar to those in adults. As in adults, the three conventional methods of treatment are antithyroid drugs (ATD), thyroidectomy and ablative radioiodine (131I). Although ATD are associated with side effects and a high relapse rate even after prolonged therapy, they still seem to be chosen as the first line of therapy for GD in childhood by most pediatric endocrinologists, although some have started using 131I as their first therapeutic modality. However, when ATD therapy has to be discontinued, or after relapse which may occur during or following ATD therapy, a definitive mode of therapy has to be chosen. Since thyroidectomy has the disadvantages of hospitalization and surgical complications, there is now an increasing tendency to advocate radioiodine as a choice of treatment in children older than five years old who achieve a high rate of remission. It should be kept in mind that with both thyroidectomy and radioiodine treatment, permanent hypothyroidism is very common and requires lifelong replacement therapy. According to the long-term follow-up data which have been published, radioiodine treatment in older children and adolescents seems to be safe and effective. Although studies of children with GD treated with ablative doses of radioiodine have not revealed an apparent increased risk of thyroid malignancy, a long-term study of larger populations is needed in order to define the true incidence of thyroid neoplasia, and other possible side effects, in children treated with radioiodine. Although the relatively low risks, low cost and practicability of radioiodine treatment has favored this therapy for children, as it has for adults, in the United States, it is still less attractive for European physicians. Progress in the immunological understanding of GD and of its genetic background will hopefully elucidate the pathways leading to GD, as well as the factors determining who is at high risk of developing GD, and may thus ultimately promote novel strategies for a more successful and safe therapy.