Journal of pediatric endocrinology & metabolism : JPEM · 2018
In iodine-induced thyrotoxicosis, steroid therapy today could keep the surgical knife at bay.
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Henry Rohan K, Chaudhari Monika
Аннотация
BACKGROUND: Amiodarone-induced thyrotoxicosis (AIT) type 2, characterized as a destructive thyroiditis, is well described in the medical literature; however, iodine-induced thyrotoxicosis (IIT) is not, though the latter has similar features and can be managed similarly.
CASE PRESENTATION: We present a 17-year-old female who presented with a history of an intermittent goiter with thyroid function tests (TFTs): thyroid-stimulating hormone (TSH)<0.015 (0.4-4 μU/mL), free thyroxine (T4)≥6 (0.7-2.1 ng/dL) and total triiodothyronine (T3) 651 (50-200 mg/dL). Thyroid antibodies were all negative. Despite methimazole therapy for 6 weeks, hyperthyroidism proved refractory to medical management. 123I scan uptake was suppressed. With hyperthyroidism being recalcitrant to therapy, a nutritional history revealed consumption of an iodine supplement containing at least 7 times the recommended daily allowance (RDA) for 5 years, contributing to the Jod-Basedow phenomenon. Urinary spot and 24-hour urinary iodine were both elevated. Though a surgical consult was obtained, surgery was cancelled once TFTs improved and then normalized with steroid therapy. The TFTs and urinary iodine levels remained normal post steroid therapy.
CONCLUSIONS: We suggest that in addition to the need for a thorough nutritional history, a trial of corticosteroids should be utilized in the management of IIT which can present with findings similar to AIT type 2 which is recalcitrant to thionamide therapy. If successful, corticosteroids may delay or prevent surgical management thus avoiding possible complications with the latter approach.
CASE PRESENTATION: We present a 17-year-old female who presented with a history of an intermittent goiter with thyroid function tests (TFTs): thyroid-stimulating hormone (TSH)<0.015 (0.4-4 μU/mL), free thyroxine (T4)≥6 (0.7-2.1 ng/dL) and total triiodothyronine (T3) 651 (50-200 mg/dL). Thyroid antibodies were all negative. Despite methimazole therapy for 6 weeks, hyperthyroidism proved refractory to medical management. 123I scan uptake was suppressed. With hyperthyroidism being recalcitrant to therapy, a nutritional history revealed consumption of an iodine supplement containing at least 7 times the recommended daily allowance (RDA) for 5 years, contributing to the Jod-Basedow phenomenon. Urinary spot and 24-hour urinary iodine were both elevated. Though a surgical consult was obtained, surgery was cancelled once TFTs improved and then normalized with steroid therapy. The TFTs and urinary iodine levels remained normal post steroid therapy.
CONCLUSIONS: We suggest that in addition to the need for a thorough nutritional history, a trial of corticosteroids should be utilized in the management of IIT which can present with findings similar to AIT type 2 which is recalcitrant to thionamide therapy. If successful, corticosteroids may delay or prevent surgical management thus avoiding possible complications with the latter approach.