Thyroid Dysfunction among the Patients with Critical COVID-19

Abstract

Objective: Since the angiotensin-converting enzyme (ACE) is the functional receptor for SARS-CoV-2, predominantly expressed by the alveoli, SARS-CoV-2 primarily involves the lungs. Aside from the lungs, ACE is expressed in other organs, including the thyroid gland. This study aimed to evaluate the incidence of thyroid dysfunction (TD) in patients admit ted to the intensive care unit (ICU) with critical COVID-19, with inflammatory markers and disease severity, compared to patients with normal thyroid function. Materials and Methods: This retrospective study included 52 patients admitted to the ICU with PCR-confirmed critical COVID-19 between April 2020 and September 2021. Thyroid function tests were obtained within the first three days after ICU admission. TD was defined as the detection of any abnormal level in thyroid-stimulating hormone (TSH), free thyrox ine hormone (FT4), and free triiodothyronine hormone (FT3). None of the patients had a prior history of thyroid disease or received medications related to thyroid diseases. Results: TD was detected in 34 patients (65.4%). The majority of patients (67%) required ex tracorporeal membrane oxygenation (ECMO), with a higher frequency in patients with TD (74%). Patients with and without TD were similar concerning age, gender, and the need for ECMO. Patients with TD had significantly decreased levels of TSH, FT3, and FT4 (p=0.002, <0.001, =0.005, respectively); a significantly greater acute physiology and chronic health evaluation II (APACHE-II) score (p=0.048); a significantly higher white blood cell count (p=0.031) and elevated levels of procalcitonin (p=0.003), C-reactive protein (p=0.049) and cardiac troponin T (p=0.025). Other parameters, such as ICU stay, sequential organ fail ure assessment [SOFA] score, and mortality, did not differ significantly (p=0.449, p=0.315, p=0.142, respectively). Conclusion: Our findings suggest that patients admitted to the ICU with critical COVID-19 are at an increased risk for the development of TD, which should also be taken into account in relation to inflammatory markers, cardiac troponin T levels, and APACHE-II scores.