The Association Between FT3 With the Outcome and Inflammation/Coagulopathy/Fibrinolysis of COVID-19

Abstract

BackgroundThe coronavirus disease 2019 (COVID-19) pandemic has caused substantial threats to people’s physical health and lives, claiming the lives of over 5 million people worldwide. It is imperative to identify the disease severity and intervene with effective therapy as early as possible. Previous studies have shown that low free triiodothyronine (FT3) may possess the predictive value on COVID-19 prognosis.MethodsIn this retrospective cohort study, 15-day clinical and laboratory data of 186 hospitalized patients of COVID-19 after admission were analyzed. Groups were based on the disease severity of COVID-19, survival or non-survival, and presence or absence of euthyroid sick syndrome (ESS). Categorical variables were compared with the chi-square test or Fisher’s exact test. Continuous variables were tested by Wilcoxon rank-sum test for the non-normal distribution. Spearman correlations were used to assess the correlations between FT3 with clinic parameters of multiple time points.ResultsThe non-survival patients had significant lower levels of FT3 (3.24 ± 0.42 vs. 4.19 ± 0.08 pmol/L, p < 0.05) and thyroid-stimulating hormone (TSH) (0.69 ± 0.19 vs. 2.32 ± 0.2 uIU/ml, p < 0.05), and the FT3 of severe patients was significantly lower than that of non-severe patients (3.67 ± 0.14 vs. 4.33 ± 0.09 pmol/L, p < 0.05). Fifty-nine cases of COVID-19 patients were diagnosed with ESS. Compared with non-ESS patients, those with ESS were older and had higher proportions of fever, shortness of breath, hypertension, diabetes, severe disease, and mortality. In addition, the correlation analysis between FT3 and clinical parameters showed that FT3 were positively related to the lymphocyte count and albumin and negatively correlated with C-reactive protein, erythrocyte sedimentation rate, and D-dimer at all time points in the first 15 days after admission.ConclusionLow FT3 had a significant predictive value on the prognosis of COVID-19 patients, and FT3 was significantly related with clinic parameters of inflammation/coagulopathy/fibrinolysis.

The differences in virus shedding time between the Delta variant and original SARS-CoV-2 infected patients

“…In addition, we observed relatively higher levels of ALB and HDL, along with lower levels of TBil and LDL in patients infected with the Delta variant compared to those infected with the original SARS-CoV-2. Our previous research has shown that low HDL level and high TBil level may be correlated with a poor prognosis in patients with original COVID-19 ( 25 , 26 ). Given the large-scale vaccination program that was already underway in China When the Delta variant emerged in 2021, the above changes of hematological parameters may be explained by the protective effect of vaccines ( 27 ).…”

The use of triiodothyronine during critical illness

“…As with most other diseases, low T3 syndrome occurs in patients with COVID-19. This was first described in patients admitted to hospital with COVID-19 in Wuhan (China) in 2020, who were found to have serum T3 concentrations lower than normal, the extent of decline proportional to severity of disease, and independently associated with mortality [2][3][4]. A systematic review subsequently identified 163 studies of thyroid hormone and COVID, with seven specifically reporting the association in ICU patients.…”

Evaluating the potential mediating role of ADAMTS13 activity in the relationship between obesity and the severity of COVID-19: A retrospective cohort study

“…The high prevalence of coagulopathy in patients infected with the coronavirus 2019 (COVID-19) pandemic and its well-documented association with the substantial elevation in mortality rates and unmet clinical outcomes have prompted many researchers to investigate coagulopathy-relevant abnormalities, such as elevated D-dimer levels, fibrin degradation product, and prolonged prothrombin time in this patient population. [1–4] Complete autopsies of deceased COVID-19 patients, including postmortem computed tomography, supported by a plethora of studies in critically ill patients, have identified deep venous thrombosis and subsequent pulmonary embolism as hallmarks of pandemic-related deaths. [5–7] Furthermore, patients with COVID-19 frequently have pulmonary and extrapulmonary microthrombotic and thromboembolic indicators as well as significant pulmonary angiogenesis.…”