Endocrine Abstracts

Background: The relationships between thyroid hormones (TH) and platelets (PLT) have not been fully established. Physiological concentrations of L-thyroxine (T4) activate human PLT resulting in ATP release and aggregation. On the other hand, subclinical hypothyroidism has been frequently associated with hypercoagulability, in particular mean platelet volume (MPV), a marker of platelet activation, has been found higher in patients with subclinical hypothyroidism. A possible prothrombotic action of TSH has also been hypothesized. COVID-19 is a pleiotropic virus known to exert its effects in many endocrine glands, including the thyroid. In fact, both direct and indirect mechanisms of Sars-CoV2 infection can render the thyroid dysfunctional. In COVID-19 patients hyperactivated platelets, with an increased MPV, and a low T3 syndrome have been described.

Aim: The aim of this study is to evaluate the relationships among TSH, FT3, FT4 and FT3/FT4 ratio and the MPV in 104 patients affected by COVID-19 on admission to the emergency room.

Methods: 104 patients (46 males, 58 females) with real-time polymerase chain reaction testing-confirmed COVID-19 admitted to the Policlinico Umberto I hospital of Rome were included in the analysis. Patients without a history of thyroid disease who had a thyroid function test at admission, before starting any treatment, were enrolled.

Results: The mean age of the patients was 75.2 ± 11.6 years. The mean MPV was 9.03±1.36 fL. The mean levels of TSH, FT3 and FT4 were, respectively 1.69±1.14 μU/ml; 2.48±0.64 pg/ml; 1.43±0.53 ng/ml. FT3 showed a trend of negative correlation with MPV (r=-,1195P=0.351), not statistically significant. FT4 was positively correlated with MPV (r=.2951, P=0.019). Both TSH and FT3/FT4 ratio had a statistically significant inverse correlation with MPV (respectively, r=-,3848;P=,001 for TSH, r=-,2437, P=,05 for FT3/FT4). All the linear regression were adjusted for age, sex and BMI.

Discussion: In this cohort of COVID-19 patients the relationship between TSH and MPV showed an opposite behavior with respect to that reported in non-sick subjects, suggesting that different mechanisms of interaction of TH with PLT may exist in the setting of acute COVID-19 infection that may be protective against platelet activation.