To the Editor Although recent evidence suggests that COVID-19 can affect practically all organs, data on the impact of SARS-CoV-2 on the thyroid gland are very scarce. Two patients with Graves' disease (GD) and COVID-19 have been recently published [1], and we would like to provide more evidence with two more cases. Patient 1 was a 45-year-old woman with a 12-year medical history of GD. She had 2 previous episodes of hyperthyroidism that were treated with antithyroid drugs (ATD), first in 2008 after diagnosis (ATD for 22 months) and then at a relapse in 2015 (ATD for 25 months). She also had Graves' ophthalmopathy that was treated with corticosteroids for 3 months in 2018. At the beginning of March 2020, her thyroid function was normal, with free thyroxine levels (FT4) of 1.36 ng/dL (normal range, 0.93-1.7 ng/dL) and serum thyroid-stimulating hormone levels (TSH) of 0.75 µIU/ mL (normal range, 0.27-4.2 µIU/mL), although anti-TSH receptor antibodies (anti-TSHR-Ab) were slightly elevated (1.9 mIU/mL; normal range < 1.5 mIU/mL). In May 2020, she developed bilateral pneumonia and was diagnosed with SARS-CoV-2 infection. This patient also presented palpitations and nervousness. Her blood test results showed a TSH of < 0.005 µIU/mL, a FT4 of > 7.7 ng/dL and an anti-TSHR-Ab of 28.7 mIU/mL. Thyroid ultrasound showed hypervascularization. She started methimazole (MMI) at a daily dose of 40 mg, which resulted in a rapid normalization of her thyroid function. No deterioration of her ophthalmopathy was observed. The MMI dosage of 40 mg/day was reduced to 5 mg/day during follow-up and she shows improvement in her condition after 3 months of treatment.