Thyroid function in COVID-19 and the association to 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 secretion of cytokines, might induce thyroid dysfunction among patients with COVID-19. We explored thyroid hormone involvement in the acute phase of symptomatic COVID-19, and its possible associations with cytokine levels and mortality risk. This was a single-center study of 116 consecutive patients hospitalized for moderate‐to‐severe COVID-19 disease. Serum concentrations of thyroid‐stimulating hormone (TSH), free thyroxine (T4) and 45 cytokines/chemokines were measured in all patients within 3 days of admission. Data were extracted retrospectively through manual review of health records. At admission, 95 (81.9%) were euthyroid, while 21 (18.1%) had a biochemical thyroid dysfunction. This included subclinical thyrotoxicosis (n=11), overt thyrotoxicosis (n=2), hypothyroidism (n=1), non-thyroidal illness (n=2), and normal TSH but high free T4 (n=5). TSH levels were inversely correlated with IL-8 (r = -0.248), IL-10 (r = -0.253), IL-15 (r = -0.213), IP-10 (r = -0.334) and GM-CSF (r = -0.254). Moreover, IL-8 levels, IP-10, and GM-CSF were significantly higher in patients with serum TSH <0.4 mIU/L. Lastly, a twofold increment of IL-8 and IL-10 was associated with significantly higher odds of having TSH <0.4 mIU/L (odds ratio 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.