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People who experience inflammation of the thyroid gland during acute COVID-19 disease may still have subacute thyroiditis months later, even if thyroid function has returned to normal, according to new research.
In addition, thyroiditis appears to be different from thyroid inflammation caused by other viruses, said Ilaria Muller, MD, PhD, when she presented her findings March 21 at the ENDO 2021 virtual meeting.
“SARS-CoV-2 appears to have a multifactorial action on thyroid function,” said Muller, of the University of Milan, Fundazione IRCCS Ca ‘Granda Ospedale Maggiore Policlinico, Italy.
In July 2020, Muller and colleagues described patients hospitalized at their institution with severe COVID-19, 15% of whom had thyrotoxicosis due to atypical subacute thyroiditis, compared with only 1% of a comparison group hospitalized in the same intensive care units during the spring. of 2019, as reported Medscape Medical News.
“Atypical” thyroiditis that occurred in patients with COVID-19 was not associated with neck pain and affected more men than women. In addition, it was associated with low levels of TSH and free triiodothyronine (T3) and normal or high levels of free thyroxine (T4), which is a very different presentation to the classic non-thyroid disease syndrome (NTIS) that is commonly seen. in critically ill patients, she explained.
Although transient elevations of T4 may occur in acute diseases, this phenomenon is not associated with low TSH. This recently described scenario appears to be a combination of thyrotoxicosis and NTIS, according to Muller and colleagues speculated last summer.
Follow patients with COVID-19 and thyroid dysfunction for one year
Now, in an evaluation of 51 patients 3 months after moderate to severe COVID-19 hospitalization, reported by Muller in ENDO 2021, inflammatory markers and thyroid function had normalized, although with imaging, a one-third of patients still had focal hypoeconomic areas. suggestive of thyroiditis.
Of these, two-thirds had reduced uptake of thyroid scintigraphy, but few had antithyroid autoantibodies.
“COVID-19-induced thyroid dysfunction does not appear to be mediated by autoimmunity. It is important to continue following these patients, as they could develop thyroid dysfunction in the following months,” Muller stressed.
When asked to comment, he told session moderator Robert W. Lash, MD, chief of professionals and clinical affairs of the Endocrine Society. Medscape Medical News: “When you’re sick of the ICU, it’s not uncommon to do weird thyroid tests. Some viruses also cause thyroid problems … What makes it different is that although a lot of thyroid inflammation is caused by antibodies, this no . “
“It seems like it was [SARS-CoV-2] causing damage to the thyroid gland, which is interesting, “he said, adding that the thyroid gland expresses high levels of angiotensin-converting enzyme 2 (ACE2) and serine transmembrane protease 2 (TMPRSS2), which can infect SARS- CoV-2 human cells.
“That’s probably part of that same story,” Lash said.
For patients who had thyroid abnormalities during acute COVID-19 disease or who have symptoms that could be related to the thyroid later, he advises: “You should monitor thyroid tests. It only raises your awareness … You can check- ne thyroid tests every 6 months for a year “.
Signs of focal thyroiditis despite normalized thyroid function
The 51 patients (33 men and 18 women) hospitalized with moderate to severe COVID-19 had no history of thyroid disease and had not been taking thyroid, amiodarone, or steroid medications before baseline TSH.
From baseline to 3 months, TSH increased from 1.2 to 1.6 mIU / L, while serum C-reactive protein concentrations of T4, T3, C, and complete blood counts had normalized. (all Pg <0.01 vs. baseline).
Thyroid ultrasound at 3 months in 49 patients showed signs of focal thyroiditis in 16 (33%).
Among the 14 patients who underwent thyroid uptake scans of 99mTc or I123, four (29%) were normal, eight (57%) had reduced focal uptake, and two (14%) had reduced uptake.
Of the 16 patients with focal thyroiditis, only three were positive for autoantibodies to thyroglobulin (TgAb) or thyroid peroxidase (TPOAb). All were negative for TSH receptor autoantibodies.
“It’s important to note that of the two with a diffusely reduced uptake, only one was positive for TPOAb or TgAb,” noted Muller, who added, “SARS-CoV-2 disease appears to trigger some dysfunction that probably has complex and multifactorial mechanisms “.
In response to a question about a possible role for thyroid biopsies and cytology, Muller replied, “Without a doubt, this is the key … So far we are only guessing, so the key will be cytological studies or histological data to see what is really going on in the thyroid. “
“What we know is this [unlike] classic thyroiditis that has been described after viral diseases, including SARS-CoV-2, these patients have a different scenario … There is probably something in the thyroid with a different mechanism, so we certainly need studies of cytology and histology “. she concluded.
The study was funded by the Fondazione IRCCS Ca ‘Granda Ospedale Maggiore Policlinico, Milan, Italy, and by a COVID-19 research grant from the European Society of Endocrinology. Muller and Lash have not reported any relevant financial relationships.
ENDO 2021. Summary OR23-2. Filed March 21, 2021.
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