Our patient is a twenty-four-year-old female with a sixteen-year history of HT-related hypothyroidism on oral levothyroxine 100 mcg once daily. She complained of occasional palpitations, nervousness, weight loss, and irregular menses. Thyrotoxicosis was confirmed with a thyroid function test, and levothyroxine dose was reduced. However, the patient continued to exhibit thyrotoxic symptoms even after completely stopping levothyroxine. On examination, the patient was calm but tachycardic and afebrile, and her blood pressure was 116/90 mmHg, weight was 58 kg, and BMI was 21.8. She was noted to have peripheral tremors. Her thyroid exam revealed the presence of diffuse nontender goiter, with no palpable nodules. Eye examination was only remarkable for mild exophthalmos, and there was no evidence of dermopathy.\nThyroid function revealed depressed TSH <0.01 mIU/L (0.3–4.2) and high T4 26.4 pmol/L (11.6–21.9) (). Based on the persistence of symptoms despite stopping thyroid hormone supplementations and the presence of ophthalmopathy elements, the rare shift to GD was suspected. Autoimmune workup revealed a strong positive Anti-TSH Receptor (Anti-TSHR) titer, in addition to persistent positivity of previously positive thyroid peroxidase antibody (TPO Ab) and an increasing titer of Antithyroglobulin Ab (). Thyroid ultrasound revealed slight enlargement of the right lobe and increased vascularity in both lobes. Radioactive iodine uptake scan (RAIU) showed diffuse radiotracer uptake more prominent in the right thyroid lobe (). Those findings kept with the shift to GD.\nThe patient received suppressive therapy with oral carbimazole 20 mg once daily and propranolol. A subsequent follow-up three months later showed normalization of thyroid function and improvement in clinical status.
A 32-year-old female presented with symptoms of low energy level, weight gain, cold intolerance, increased bowel movements, flaking, and itchy scalp in the year 2014. On examination, she was found to have a palpable goiter. Her family history was significant for thyroid disease affecting her sibling. Neck ultrasound demonstrated diffusely enlarged thyroid with mild heterogeneous echotexture and left hypoechoic solid nodule measuring 0.75 cm []. Thyroid function test (TFT) was within the normal limits (TSH: 3.4 μIU/mL and FT4: 1.1 ng/dL; normal laboratory values of TSH 0.350–4.940 uIU/mL and FT4: 0.7–1.5 ng/dL respectively) however, antithyroid peroxidase (1446.0 IU/ml; reference range 0.0–5.6 IU/ml) and Tg antibodies (95.4 IU/ml; reference range 0.0–4.1 IU/ml) were high. A diagnosis of euthyroid Hashimoto's disease was made, and the patient was followed up on ultrasound and TFT.\nIn the year 2016, the patient presented with irritability and anxiety. Repeat ultrasound showed status quo. However, there was a surge in thyroid antibodies and an increase in TSH levels (7.2 μIU/mL). The clinical impression was consistent with Hashimoto's thyroiditis and the patient was started on low-dose thyroxine, which she tolerated well for 3 years. On yearly follow-up, there was a downtrend in thyroid antibodies, TSH returned to normal range, and findings on ultrasound remained stable.\nIn October 2019, the patient presented with syncopal episode. Evaluation of TFT demonstrated low TSH of 0.003 μIU/mL and raised FT4 of 2.4 ng/dL. The patient was asked to stop thyroxine tablets and to repeat TFTs in 4 weeks. Repeat TSH was <0.002 μIU/mL and FT4 of 2.6 ng/dL. I-123 thyroid uptake and the scan was performed, which demonstrated findings consistent with Graves' disease [] with 24 h uptake of 63.6% (normal range 10%–25%). The patient was subsequently treated with 15.9 mCi of radioiodine (I-131). Follow-up in 6 weeks of radioiodine therapy, the patient was clinically stable.