Browsing by Author "Nogueira, Celia Regina"
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- Editorial: New insights in thyroid and Covid-19Publication . Sgarbi, Jose Augusto; Nogueira, Celia Regina; Brenta, Gabriela; Campinho, Marco AntónioThe Coronaviruses Disease 2019 (Covid-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is perhaps the most dramatic threat to human health since the Spanish flu in 1918. Almost 700 million cases and more than 6 million deaths have been reported worldwide by November 20, 2022 (1). The lung is the main affected organ, and the most critical clinical presentation has been characterized by interstitial pneumonia, acute respiratory distress syndrome, multiple organ failure, and death (2). Multiple endocrine organs, such as the pituitary, pancreas, adrenal, gonads, and thyroid gland, have also been affected (3). Detrimental effects on thyroid function have been reported in patients with and without pre-existing thyroid disease. Nonthyroidal illness syndrome (NTIS), subacute thyroiditis (SAT), Hashimoto’s thyroiditis, and Graves’ disease have been the most frequent thyroid dysfunctions associated with Covid-19 (4). Two major pathophysiological models have been implicated, a direct effect by virus attack causing follicular cells damage and an indirect effect caused by an immune-inflammatory abnormal response to the virus (5). Most recently, thyroid autoimmune diseases have also been reported following Covid-19 vaccination (6).
- Editorial: the thyroid and Covid-19, volume IIPublication . Jiménez, Javier; Campinho, Marco António; Nogueira, Celia Regina; Sgarbi, JoseCoronaviruses are enveloped RNA viruses of wide distribution in humans associated with mild respiratory disease. By contrast, severe acute respiratory syndrome coronavirus (SARS-CoV) is one of those coronaviruses that can cause fatal illness. In late December 2019, an outburst of pneumonia of unknown cause in Wuhan, China, was identified as the early stage of the coronavirus disease (COVID-19) pandemic outbreak, and the SARS-CoV-2 was found responsible (1). Two main proteins expressed by SARS-CoV-2 are essential for the manifestations of COVID-19. The first is the transmembrane protease serine 2 (TMPRSS2), which acts on the transcription and replication of the virus. The second is the Spike protein found on the surface of viral particles, which binds to angiotensin-converting enzyme 2 (ACE2) in tissue cells and is a determinant for transmitting infection. Therefore, SARS-CoV-2 infection depends on two steps: ACE2 receptor recognition via Spike protein and cell membrane fusion via transmembrane protease (2). ACE2 is expressed in different tissues, and the thyroid is no exception (3). It has been shown that the thyroid gland has high expression levels of ACE2, which may explain the direct effects on the thyroid parenchyma, making it more susceptible to viral attack (3). SARS-CoV-2 infection can lead to thyroid diseases by severely destroying parafollicular and follicular epithelial cells, leading to follicle rupture. As a result, SARS-CoV-2 virus infections are associated with inflammatory thyroid diseases such as subacute thyroiditis, Graves’ disease, thyrotoxicosis, Hashimoto’s thyroiditis, and euthyroid patient syndrome (4). As regards thyroid cancer, the COVID-19 pandemic has also affected its traditional management, and the consequences of this strategic change are largely unknown. Furthermore, it is intriguing that if the virus attacks the thyroid gland, it can also modulate thyroid cancer behavior (5).