Case 2. A 14-year-old male presented with a 2-month history of palpations, jitteriness, insomnia, heat intolerance, and 10 lb weight loss. Initial examination revealed a nontender, firm goiter, tongue fasciculations, peripheral tremor, increased deep tendon reflexes, tachycardia, and hypertension. He was diagnosed with thyrotoxicosis due to GD based on wFT4 of 5.6 ng/dL and TSH of <0.01 mIU/mL and positive TBII at 34% (<=16) and TSIG at 130% (<=125); anti-TPO Ab and anti-TG Ab were positive at 107 IU/mL (<35) and 90 IU/mL (<20), respectively. He was treated with MMI therapy, which was then discontinued after 24 months, after which he remained clinically and biochemically euthyroid for a 12-month period.
Although asymptomatic, follow-up testing revealed biochemical thyrotoxicosis (peak FT4 of 3.9 ng/dL and TSH of 0.01 mIU/mL), with anti-TPO and anti-TG Ab levels at 308 IU/mL and 147 IU/mL, respectively, and negative TBII and TSIG antibody levels. I123 thyroid uptake and scan demonstrated low 4-hour uptake of 3% and 24-hour uptake of 5%. Hashitoxicosis was then diagnosed but did not require treatment. However, subsequent clinical and biochemical monitoring revealed increasing FT4 levels with associated development of clinical thyrotoxicosis. Repeat I123 thyroid uptake and scan demonstrated elevated 4-hour and 24-hour uptakes at 70% and 82%, respectively. He underwent RAI with development of hypothyroidism within 1 month for which he has been on thyroxine replacement therapy.
 Case 3. The fraternal twin sister of Case 1 presented at 17 years of age to our emergency room with jitteriness, anxiety, tongue fasciculations, peripheral tremor, and hypertension and tachycardia. Testing showed extremely elevated FT4 at >7.77 ng/dL (0.9-1.8) with TSH suppressed at 0.01 mIU/mL (0.35-5.5); TSIG was positive at 432% (<140) and TBII at 83.2% (<=16), with positive anti-TPO Ab at 606 IU/mL (<35); anti-TG Ab was negative. She was diagnosed with thyrotoxicosis due to GD for which she was started on MMI therapy. After therapy for 18 months and with negative TSIG and TBII antibodies, a trial off MMI was initiated. She remained clinically and biochemically euthyroid off MMI for a period of 12 months at which time biochemical thyrotoxicosis developed. FT4 peaked at 3.0 ng/dL with TSH suppressed at 0.002 mIU/mL. Anti-TPO Ab remained positive at 612 IU/mL with TSIG and TBII levels still negative. She remained asymptomatic. I123 thyroid uptake and scan revealed low 4-hour uptake of 2.9% (5-15) and low 24-hour uptake of 4.7% (10-35), suggestive of Hashitoxicosis. Subsequently, she developed clinical signs of thyrotoxicosis with peak FT4 of 7.4 ng/dL and suppressed TSH at 0.001 mIU/mL. TSIG and TBII were now positive at 506% and 78.3%, respectively, with anti-TPO Ab positive at >900 IU/mL. MMI was restarted for recurrence of thyrotoxicosis due to GD followed by RAI after her repeat I123 thyroid uptake and scan revealed elevated 4-hour and 24-hour uptakes of 66 and 68%, respectively. Subsequent to RAI, she developed primary hypothyroidism that was treated with thyroxine replacement therapy.