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Objective: We have previously observed thyroid dysfunction, i.e. atypical thyroiditis (painless thyrotoxicosis associated to non-thyroidal illness syndrome), in patients with severe-acute-respiratory-syndrome-coronavirus-2 disease (Covid-19). This study aimed to analyse the evolution of thyroid dysfunction over time. Methods: 183 consecutive patients hospitalised for severe Covid-19 without known thyroid history were studied at hospital admission (baseline). Survivors were offered 12-month longitudinal follow-up including assessment of thyroid function, autoantibodies and ultrasound scan (US). Patients showing US focal hypoechoic areas suggestive of thyroiditis (focal-hypoechogenicity) also underwent thyroid 99mTc or 123I uptake scan. Results: At baseline, after excluding from TSH analysis 63 out of 183 (34%) Covid-19 patients commenced on steroids before hospitalisation, 12 (10%) showed atypical thyroiditis. Follow-up of 75 patients showed normalisation of thyroid function and inflammatory markers, and no increased prevalence of detectable thyroid autoantibodies. Baseline US (available in 65 patients) showed focal-hypoechogenicity in 28% patients, of whom 82% had reduced thyroid 99mTc/123I uptake. The presence of focal-hypoechogenicity was associated with baseline low TSH (p=0.034), high FT4 (p=0.018) and high IL-6 (p=0.016). Focal-hypoechogenicity persisted after 6 and 12 months in 87% and 50% patients, respectively, but reduced in size. After 9 months thyroid 99mTc/123I uptake partially recovered from baseline (+28%), but was still reduced in 67% patients. Conclusions: Severe Covid-19 induces mild transient thyroid dysfunction correlating with disease severity. Focal-hypoechogenicity, associated with baseline high FT4, IL-6 and low TSH, does not seem to be related to thyroid autoimmunity and may persist after one year although decreasing in size. Long-term consequences seem unlikely.

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