Case 1. A 15-year-old female was diagnosed with thyrotoxicosis based on elevated free T4 (FT4) of 2.4 ng/dL (0.9-1.4) and suppressed TSH of 0.02 mIU/L (0.5-4.3) identified in work-up for irregular menses. Additional testing demonstrated elevated anti-TPO Ab at 180 IU/mL (0-35) and anti-TG Ab at 136 IU/mL (0-20); TBII were elevated at 22% (<=16), with TSIG within the normal range at 119% (<=125). Physical examination revealed a firm, nontender goiter only. I123 thyroid uptake and scan revealed increased 4-hour uptake at 34% (5-15%) and 24-hour uptake at 62% (15-35%).
Thyrotoxicosis due to GD was diagnosed but not treated due to absence of significant symptoms. After 6 months, worsening biochemical thyrotoxicosis associated with palpitations, insomnia, loss of weight, tongue fasciculations, peripheral tremor, tachycardia, and hypertension developed. Testing showed peak FT4 of 10.4 ng/dL and suppressed TSH of 0.01 mIU/L. TBII antibodies had increased to 49% with TSIG positive at 158%. Methimazole (MMI) therapy was started, with biochemical and clinical resolution of thyrotoxicosis within 2 months. After 18 months on therapy, with GD antibodies negative, MMI was discontinued to assess spontaneous resolution. She remained biochemically and clinically euthyroid for 4 months off MMI. Biochemical thyrotoxicosis without clinical symptoms developed after 4 months (peak FT4 of 2.4 ng/dL and TSH of 0.01 mIU/mL) with repeat anti-TPO and TG antibody levels at >1000 IU/mL and 147 IU/mL, respectively, and TBII and TSIG remaining negative. Repeat I123 thyroid uptake and scan revealed low 4-hour uptake of 2.5% and low 24-hour I123 uptake of 2.3%. This presentation was consistent with Hashitoxicosis, and because of mild nature and anticipation of its transient course antithyroid therapy was not initiated.
After 6 weeks, primary hypothyroidism actually developed (FT4 of 0.6 ng/dL and TSH of 25.66 mIU/mL) for which thyroxine replacement therapy was started. However, within 3 months, clinical and biochemical thyrotoxicosis was diagnosed which, despite discontinuation of therapy, deteriorated (peak FT4 of 3.9 ng/dL and TSH of 0.01 mIU/mL). Repeat I123 thyroid uptake and scan revealed elevated 4-hour and 24-hour uptake at 34% and 62%, respectively. 131I radioiodine ablation (RAI) was successfully performed with development of primary hypothyroidism within 2 months when thyroxine replacement therapy was restarted.