Thyroid function in COVID-19 and the association with cytokine levels and mortality

The hypothalamic-pituitary-thyroid hormone axis might be affected in COVID-19, but existing studies have shown varying results. It has been hypothesized that hyperinflammation, as reflected by the secretion of cytokines, mi ght induce thyroid dysfunction among patients with COVID-19. We explored thyroid h ormone involvement in the acute phase of symptomatic COVID-19 and its possible associ ations with cytokine levels and mortality risk. This was a single- center study of 11 6 consecutive patients hospitalized for moderate-to-severe COVID-19 disease. Serum concentrations of thyroidstimulating hormone (TSH), free thyroxine (T-4), and 45 cytokines/chemokines were measured in all patients within 3 days of admission. Data were extracted retrospectively through a manual review of health records. At admission, 95 (81.9%) were euthyroid; while 21 (18.1%) had biochemically thyroid dysfunction includin g subclinical thyrotoxicosis (n = 11), overt thyrotoxicosis (n = 2), hypothyroidism (n = 1), non-thyroidal illness (n = 2), and normal TSH but high free T-4 (n = 5). TSH levels were inversely correlated with IL-8 (r(s) = -0.248), IL-10 (r(s) = -0.253), IL-15 (r(s) = -0.213), IP-10 (r(s) = -0.334), and GM-CSF (r(s) = - 0.254). Moreover, IL-8 levels, IP-10, and GM-CSF were signific antly higher in patients with serum TSH < 0.4 mIU/L. Lastly, a two-fold increment of IL-8 and IL-10 was associated with significantly higher odds of having TSH < 0.4 mIU/L (odds r atio 1.86 (1.11-3.10) and 1.78 (1.03-3.06)). Serum TSH was not associated with 30- or 90-day mortality. In conclusion, this study suggests that fluctuations of TSH levels in patients with COVID-19 may be influenced by circulating IL-8, IL-10, IL-15, IP-10, and GM- CSF as previously described in autoimmune thyroid diseases.