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Source: COVID-19-Thyroid Gland   Mar 22, 2021  2 years, 6 months, 1 week, 4 days, 1 hour, 47 minutes ago

Italian Study Presented At Endocrine Society's 2021 Annual Meeting Shows That SARS-CoV-2 Causes A Unique Thyroid Inflammation In Some Patients.

Italian Study Presented At Endocrine Society's 2021 Annual Meeting Shows That SARS-CoV-2 Causes A Unique Thyroid Inflammation In Some Patients.
Source: COVID-19-Thyroid Gland   Mar 22, 2021  2 years, 6 months, 1 week, 4 days, 1 hour, 47 minutes ago
A new study presented in the last 24 hours at the Endocrine Society's 2021 Annual Meeting (ENDO 2021) by researchers from Fondazione IRCCS Ca' Granda Policlinico Hospital of Milan and the University of Milan in Italy has indicated that certain patients with moderate to severe COVID-19 disease seem to experience inflammation of the thyroid gland that is different from thyroid inflammation caused by other viruses.

Alarmingly one-third of the study participants still had signs of thyroid inflammation after three months, even though their thyroid function had normalized.
The research team is also following patients to determine whether this inflammation will trigger permanent thyroid dysfunction.
It was found that in spring 2020, 15 percent of the COVID-19 patients hospitalized in acute medicine units at Fondazione IRCCS Ca' Granda Policlinico Hospital of Milan in Italy had thyroid hormone alterations due to multi-factorial causes, including thyroid inflammation. In comparison, only 1 percent of hospitalized patients during the same period in 2019 prior to the pandemic had thyroid hormone alterations.
Lead researcher Dr Ilaria Muller, M.D., Ph.D. from the University of Milan in Italy told Thailand Medical News, “Typically individuals with thyroiditis, or inflammation of the thyroid gland, triggered by other viruses usually recover thyroid function in the short term. However, there is a long-term increased risk of permanently reduced thyroid function, caused by late-onset effects of viral infection, or by the immune system attacking the thyroid gland.”
Dr Muller wanted to find out whether the thyroiditis associated with SARS-CoV-2, the virus that causes COVID-19 disease, follows the same pattern as thyroid inflammation caused by other viruses.
The study team started a surveillance program to monitor the thyroid function of patients every three months after being hospitalized for moderate to severe COVID-19 disease. The patients undergo routine blood and ultrasound testing to monitor their thyroid function and signs of inflammation.

Dr Muller found the thyroiditis in people with moderate to severe COVID-19 disease differs from typical thyroiditis in several ways. These include the absence of neck pain, the presence of mild thyroid dysfunction, higher frequency among men and the association with severe COVID-19 disease.
To date all 53 patients have completed the evaluation at three months. All had normal thyroid function.
Dr Muller added, "After three months, patients' thyroid function has normalized, but signs of inflammation were still present in about one-third of patients. We are continuing to monitor these patients to see what happens during the following months. It is important to know whether SARS-CoV-2 virus has late-onset negative effects on the thyroid gland, in order to promptly diagnose, and eventually treat, the condition."
She further added, “SARS-CoV-2 seems to have multifactorial action on thyroid function.”
It was observed that the "atypical" thyroiditis that occurred in the patients with COVID-19 was not associated with neck pain and affected more men than women. Moreover, it was associated with low TSH and free-triiodothyronine (T3) levels, and normal or elevated levels of free thyroxine (T4), which is a very different presentation to classic nonthyroidal illness syndrome (NTIS) usually seen in critically ill patients.
Though transient T4 elevations can occur in acute illness, that phenomenon is not associated with low TSH. This newly described scenario appears to be a combination of thyrotoxicosis and NTIS.
In the detailed assessment of 51 patients 3 months after hospitalization for moderate-to-severe COVID-19 reported by Muller at ENDO 2021, both inflammatory markers and thyroid function had normalized, yet on imaging, a third of patients still exhibited focal hypoechoic areas suggestive of thyroiditis.
Also two thirds of these patients had reduced uptake on thyroid scintigraphy, but few had antithyroid autoantibodies.
Dr Muller added, "The thyroid dysfunction induced by COVID-19 seems not mediated by autoimmunity. It is important to continue to follow these patients since they might develop thyroid dysfunction during the following months.”
To certain experts, it looks like this was SARS-CoV-2 causing damage to the thyroid gland.
It should be noted that that the thyroid gland expresses high levels of angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2), which allow SARS-CoV-2 to infect human cells.
Dr Muller advises that for patients who had thyroid abnormalities during acute COVID-19 illness or develop symptoms that might be thyroid-related afterward, they should insists on doing regular thyroid tests during the first few months a and if possible also check their thyroid tests every 6 months for a year.
The study found that 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 medications, amiodarone, or steroids before baseline TSH was measured.
Also from baseline to 3 months, TSH rose from 1.2 to 1.6 mIU/L, while serum concentrations of T4, T3, C-reactive protein, and full blood counts had all normalized (all P < 0.01 vs baseline).
Interestingly Thyroid ultrasound at 3 months in 49 patients showed signs of focal thyroiditis in 16 (33%).
However among 14 patients of those who further underwent thyroid 99mTc or I123 uptake scans, four (29%) were normal, eight (57%) had focally reduced uptake, and two (14%) had diffusely reduced uptake.
It was also found that 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 autoantibodies.
"Significantly, of the two with diffusely reduced uptake, only one was positive for TPOAb or TgAb," Dr Muller noted, adding, "SARS-CoV-2 disease seems to trigger some dysfunction which very likely has complex and multifactorial mechanisms."
When questioned about the possible role for biopsies and thyroid cytology, Dr Muller replied: "That's definitely the key...So far we're just making guesses, so the key will be cytological or histological studies to see what is really going on in the thyroid."
She added, "What we know is that [unlike] classical thyroiditis after viral diseases, these patients have a different scenario...Probably something is going on within the thyroid with a different mechanism, so surely cytology and histology studies are what we need."
Thailand Medical News has brought up alerts about the SARS-CoV-2 coronavirus ability to affect the thyroid glands as early as May 2020.
For more on COVID-19-Thyroid Gland Issues, keep on logging to Thailand Medical News.


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