Derangements of biochemical markers and thyroid function analysis among COVID-19-positive patients: A developing country single-center experience.

Coronavirus disease‐19 (COVID‐19) was initially reported in the Hubei Province of China in December 2019 and eventually declared a Public Health Emergency of International Concern by the World Health Organization (WHO) on January 30, 2020. The severe acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2) has affected nearly 153 million and resulted in greater than 3.21 million deaths as of May 4, 2021. The virus poses a major threat to us today, making COVID‐19 one of the deadliest pandemics in history.1 The novel virus has a predilection for multiorgan involvement in addition to the respiratory manifestations due to the widespread presence of angiotensin‐converting enzyme 2 (ACE‐2) receptors. The virus also affects the endocrine system due to the close interplay between immunological and endocrine responses at multiple levels.2 The thyroid gland expresses the ACE‐2 receptor, which is necessary for the virus to dock and enter the cell. It also has a possible role in viral replication inside the cell. 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.2 Furthermore, thyroid hormone dysfunction has also been linked to increased mortality in critically ill patients with acute respiratory distress syndrome, which is a leading complication in COVID‐19.3 Although there are postulates contemplating hypothalamic–pituitary–adrenal axis disruption or pituitary dysfunction as a sequela to the SARS‐CoV‐2 infection, the role of the thyroid hormone is critical in assessing the outcome of critically ill individuals. Hence, we aimed to explore derangements of biochemical markers and thyroid function tests among patients suffering from COVID‐19 infection.