This paper compares the vital signs of patients with COVID sick syndrome and controls. Of the parameters measured, FT4 and (F)T3, and inflammation markers CRP and ESR changed significantly between the two groups. FT4 and FT3 declined significantly, and CRP and ESR rose significantly. TSH did not change significantly. Therefore COVID disease is a form of nonthyroidal illness, but TSH is not altered. Another incidence of thyroid hormones being the most significant indicators.
There have been a number of studies showing non-thyroidal illness (NTI) in COVID-19 patients. This study restricted the diagnosis of Euthyroid Sick Syndrome (now called NTI or 'low T3 syndrome') to hospitalised patients with an fT3 < 2.3 pg/ml (no reference interval was given in the paper). Patients with NTI and an fT3 above 2.3 pg/ml are omitted from the study.
Other studies have adopted the 'reflex' thyroid testing strategy (an abomination). This is where fT3 and fT4 are tested only if TSH falls below its lower limit. This strategy fails to identify the majority of NTI cases, patients with a lowered fT3 and low normal TSH.
A further complication is that a minority of COVID-19 patients develop subaccute thyroiditis, they become thyrotoxic for a short period. This confounds the results, especially fT4 due to thyroxine's long half life.
I'm lobbying for a study of NTI in athyroetic COVID-19 patients receiving levothyroxine monotherapy. If the patients don't have a thyroid the results won't be distorted by COVID-19 effects on the thyroid. It would also be beneficial to measure TSH isoforms in these patients and compare with controls. This might give a clue as to which forms of TSH affect deiodinase. It gives a unique opportunity to explain why some patients have poor T4 to T3 conversion.
I will ask the American Thyroid Association (ATA) to support this research as the USA has high COVID-19 infection rates. There's no harm in asking!
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