The novel virus has a predilection for multi-organ involvement in addition to the respiratory manifestations. It also affects the endocrine system due to the close interplay between immunological and endocrine responses at multiple levels. The activation of inflammatory mediators and immune-mediated glandular damage via the formation of antibodies or cell-mediated damage to the thyroid gland resulting in subacute thyroiditis has also been reported in COVID-19 positive patients. We aimed to explore derangements of biochemical markers and thyroid function tests among patients suffering from COVID-19 infection at our center via a retrospective study conducted on 54 patients with no previous history of thyroid disease. They had a mean age of 53.29 ± 15.59 years, with the majority of them being females (61%). There was a major difference in serum TSH observed among severe/critical COVID-19 patients (p<0.001). Free T3 and T4 levels in the blood were not found to be linked with disease severity. Low serum TSH (<0.996 uIU/mL) was found to be statistically significant with disease severity, Cox proportional hazard model showed a significantly higher risk of disease severity with low TSH levels [HR: 3.303 (95% CI, 1.124-9.705); p=0.03]. The receiver operating characteristic analysis, at a TSH cut-off value of <0.996 uIU/mL, exhibited a sensitivity of 85.7% and specificity of 72.7%, indicating disease severity (AUC=0.779; p=0.001). Patients with low TSH levels (0.996 uIU/mL) had a higher cumulative survival proportion. (Chi-square: 12.650, p<0.001). This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.