Endocrine Abstracts

Background

In the 2002 outbreak of severe acute respiratory syndrome (SARS) a number of patients presented abnormalities in the thyroid functioning, neuroendocrine and calcium homeostasis. It was detected in autopsies from SARS Coronavirus (SARS-CoV) patients that the thyroid gland was significantly affected by the disease, with extensive injury and death of follicular and parafollicular cells. In the present SARS-CoV-2 pandemic some studies start to report acute thyroiditis and alterations in the levels of thyroid hormones [(triiodothyronine (T3), thyroxine (T4), thyroid stimulating hormone (TSH)]. Thyroid cells present high levels of mRNA expression of angiotensin-converting enzyme 2 (ACE2), the host receptor for SARS-CoV-2. It remains poorly studied the thyroid expression of proteins that predispose to SARS-CoV-2 infection and if thyroid cells can be a direct or indirect target of SARS-CoV-2 infection.

Aims

We aim to establish the expression of ACE-2, Furin and TMPRSS2 in thyroid from infected and uninfected patients. We aim also to investigate if thyroid cells can be directly infected by the SARS-CoV-2 and which are the putative consequences of this infection in the gland morphology.

Material and methods

In collaboration with Centro Hospitalar Universitário de São João and Universidade São Paulo, Brazil, we have access to autopsy thyroid samples (n = 15) and clinical data from patients infected with SARS-CoV-2. We evaluated the expression, in the autopsy thyroid samples and in a series of other thyroid lesions (normal, thyroiditis and tumors; n = 40), of the ACE2, Furin and TMPRSS2. We analyzed the autopsy thyroid samples for cleaved caspase 3 (apoptosis) and the IHC for viral proteins (spike and nucleocapsid).

Results/conclusions

Our results show positivity for cleaved Caspase 3 and extensive morphologic alterations in the necropsy thyroid samples. ACE2 expression was more intense and frequent in thyroid samples from infected individuals than in the control series. We detected signs of acute inflammation, just vasodilatation and no increased number of neutrophils. We are still evaluating the putative correlation of the inflammation with histologic features using digital pathology and immunohistochemistry. The autopsy thyroid samples will be studied with RNAscope for validation of SARS-CoV-2 RNA expression and other parameters: histological features, proliferation and immune response. We expect to disclose the (direct or indirect) effects of SARS-CoV-2 infection in thyroid gland and eventual consequences in thyroid function of recovered COVID-19 patients.