Endocrine Abstracts

Introduction: Congenital hypothyroidism (CH) with in situ thyroid gland (GIS) and non-autoimmune subclinical hypothyroidism (NASI) are functional defects of thyroid gland occurring at birth and after birth, respectively. In recent years, a higher incidence of these disorders has been documented. The etiology remains unclear, with only an almost 50% of cases attributable to mutations in known dyshormonogenesis-associated or TSH-receptor genes. Although replacement therapy with levothyroxine (L-T4) is the treatment of choice for hypothyroidism, previous studies have reported an improvement/normalization of thyroid function in some cases of dyshormonogenetic CH after iodine administration.

Objective: The objective of this study was to evaluate the effect of treatment with physiological doses of iodine in a group of children with CH and GIS and NASI.

Patients and Methods: 34 children, 17 with CH and GIS (mean age 10.22±3.15 years) and 17 with NASI (mean age 10.70±4.36 years) were given iodine for 9 months, after stopping for 4 weeks L-T4, when taken. 3 children with CH and 1 with NASI had mutations of DUOX2, whereas the etiology was unknown in the remaining children. Iodine treatment was initiated with a daily dose of 50 µg, increasing to a maximal 150 µg/d. At the beginning of the study, all patients presented serum TSH between 4 and 12 µU/ml, free thyroid hormones within the normal range, undetectable anti-TG and anti-TPO antibodies and a thyroid of normal size and normoechogenic pattern at ultrasound. The same parameters were evaluated every 3 months for 12 months.

Results: Treatment with iodine failed to normalize TSH. Under the lowest dose of iodine, TSH did not change as compared to the baseline in both groups. After increasing the daily dose, there was a progressive increase in serum TSH in both groups, that became statistically significant (P = 0.038) when basal TSH values of whole group of patients were compared with those after 150 mg/d of iodine. Other parameters of thyroid function did not change after treatment in both groups. None of children developed serum and ultrasound markers of thyroid autoimmunity.

Conclusions: This study shows a failure of treatment with physiological iodine doses to correct CH with GIS and NASI. These results, which are apparently in contrast with the data reported in the literature, are probably due to the lower doses used in our study. Moreover, the increase of serum TSH levels observed during treatment may reflect the spontaneous course of the disease rather than a detrimental effect of iodine.