EndoCovid: Thyroid and adrenal hormonal alterations in a cohort of critically ill patients with COVID-19. A preliminary analysis

Coronavirus disease 2019 (COVID-19) infection was primarily described as atypical pneumonia with severe respiratory disorders1, although the reported evidence revealed a condition of multisystemic impact over time. It maintains a variable respiratory severity that significantly affects other organs and systems, such as the vascular endothelium, the central nervous system, the heart, and many endocrine glands such as the thyroid, the adrenals, and the pancreas2. The impact of SARS-Cov-2 on the endocrine system is so frequent that specialists have coined the term "EndoCovid" to refer to the endocrinological disorders that occur during this disease and require special attention in post-COVID patients. 193. The universal distribution of the angiotensin 2 receptor (ACE-2), which is the proven gateway for the virus to enter our cells, makes the viral presence in glandular tissue possible and causes damage by three fundamental mechanisms: direct damage immunological mechanism and functional alteration4,5. Specifically, it has already been demonstrated with SARS-Cov-1 and currently with SARS-Cov-2, damage at the pituitary level6, with hypophysitis reported in autopsies7. This alteration leads to secondary hypopituitarism that must be considered for its diagnosis and treatment, emphasizing cortisol deficiency, which often debuts hyponatremia, a condition associated with a poor prognosis6. The virus can also cause direct damage to the thyroid (COVID-19-associated thyroiditis and post-COVID-19 or post-vaccination autoimmune thyroid pathology) and the adrenal glands, which is associated with severe forms of the disease although the impact of this disorder in outcomes such as mortality is not clear8. Several of the critically ill patients that we attended with a diagnosis of severe COVID-19 infection, who had overcome the hypoxemia, were noticed to worsen and died after day 10 of hospitalization. A non-pharmacological distributive shock with negative bacterial cultures was determined as their cause of death. Under this premise, we requested the adrenal and thyroid hormones dosage, observing a significant hormonal deficit. The subsequent compensation of the endocrine disorder meant a significant clinical improvement and even survival of patients whose clinical characteristics and severity scales pointed to a high probability of death. We present a series of 66 patients with severe COVID-19 infection, where 28 (42.4%) died, and 38 (57.6%) survived; the patient's average age was 47.74 years, with differences being observed when comparing by discharge condition (p-value 0.024, 51.79 years in non-survivors vs. 44.76 years in survivors); male predominance was observed 81.82%. (Table 1)