Over the many months, we have seen many thoughts about Covid and thyroid issues.
It is good, therefore, to see a review paper, especially one from the UK, expressly considering Covid and the endocrine system.
The thyroid section does seem rather limited but at least it exists.
This is not intended to start a discussion about all the other, non-thyroid/non-endocrine issues of Covid. It is far too large a subject. Let's try to keep responses focussed on the actual paper and issues.
Interplay between endocrinology, metabolism and COVID-19 infection
There are more than 170 million confirmed cases of COVID-19 worldwide, yet its effects on the endocrine system remain under-reported due to lack of awareness by the public, primary care givers and specialists. This is a narrative review using up-to-date literature discussing the consequences that infection with SARS-CoV-2 can have on diabetes and the endocrine glands including the adrenals, thyroid and pituitary, as well as hyponatremia and hypogonadism. Endocrinologists, internists and primary care physicians need to be aware of the involvement of the endocrine organs when dealing with people recovering from COVID-19 and actively manage any complications to reduce mortality and improve the quality of life of those affected.
From the 'thyroid' section ( 20.2 % seems highly significant , so no wonder they've noticed "the thyroid " )
"Hypothyroidism was present in 5.2% of 287 hospitalised COVID-19 non-intensive care unit (ICU) patients in a single-centre retrospective study, with the majority of them being subclinical rather than overtly hypothyroid.35 The same study found 20.2% of patients with thyrotoxicosis .... "
Fifty-eight patients (20.2%) were found with thyrotoxicosis (overt in 31 cases),
"..... SUBJECTS and METHODS
"In our hospital, measurement of TSH was included in the routine biochemical evaluation of hospitalized patients with COVID-19. In patients with serum TSH values either below or above the reference range, free-thyroxine (FT4) and free-triiodothyronine (FT3) were measured for a comprehensive evaluation of thyroid function. In some patients with overt thyrotoxicosis, thyroid ultrasound and measurements of TSH receptor antibodies (TRAb), thyroglobulin antibodies (TgAb) and thyroperoxidase antibodies (TPOAb) were performed. Thyroid function was evaluated on the first day of hospitalization with blood samples drawn in the fasting condition......//
...Serum TSH, FT4, FT3 and IL-6 were measured at 08:00 h ........ Overt thyrotoxicosis was defined by low TSH values and serum FT3 and/or FT4 above the reference ranges. Overt hypothyroidism was defined by high TSH values and serum FT4 and/or FT3 below the reference ranges. Subclinical thyroid dysfunction was defined when TSH was either low or high accompanied by FT4 and FT3 in the reference ranges......//
.....DISCUSSION
A remarkable number of our hospitalized patients had suppressed TSH values and this finding was very likely expression of thyrotoxicosis rather than NTI. In fact, none of these patients had low FT3 values and in more than one-half of them, FT4 values were above the reference range.
Nevertheless, we cannot exclude that a possible coexistent NTI may have influenced the biochemical presentation of thyrotoxicosis, since serum FT3 increased less than FT4, no significant difference in FT3 values was found between overt and subclinical thyroid dysfunction and the recovery of thyrotoxicosis (i.e. in the few patients in whom longitudinal measurements of thyroid hormones were performed) was apparently faster than that observed in non-hospitalized patients.
In this context, the role of IL-6 may be hypothesized. In cell cultures, IL-6 was shown to decrease T3 secretion possibly contributing to the normal levels of FT3 in our thyrotoxicotic patients (10).
Thyrotoxicosis was found in about 20% of our patients and several others showed serum TSH in the lower part of the reference range. These findings suggest that COVID-19 may favor the development of thyrotoxicosis at a higher incidence than that expected in the general population (17).
Although our study was not designed to clarify the mechanisms responsible for thyroid dysfunction in patients with COVID-19, it is reasonable to hypothesize that thyrotoxicosis was caused by destructive thyroiditis. This hypothesis was supported by the findings that thyrotoxicosis was often mild and improved spontaneously during follow-up .
A further finding supporting the diagnosis of destructive thyroiditis was the negativity for TRAb in the few patients in whom these antibodies were evaluated, although the absence of circulating TRAb cannot exclude Graves-like mild hyperthyroidism in all cases (18).
The close relationship between thyrotoxicosis and higher serum IL-6 in our patients suggests that thyroid gland inflammation might be triggered and sustained by the cytokine storm associated with COVID-19, mimicking thyroid disorders developing during the course of immunotherapies (19, 20).
An alternative hypothesis is the possible direct action of SARS-CoV-2 on thyroid gland (12), based on the evidence that several tissues and organs may be directly damaged by the virus during COVID-19 (21). Indeed, there is evidence that thyroid tissue highly expresses the angiotensin-converting enzyme 2 (22), which is the protein used by SARS-CoV-2 for invading human cells (23).
Besides the pathophysiological aspects, this study highlights some specific clinical concerning the clinical relevance and management of thyrotoxicosis in patients of COVID-19.
Sixteen percent of patients with overt thyrotoxicosis developed thromboembolic events, a rate being more than two times higher than that recently reported in COVID-19 patients hospitalized in non-intensive care units (24).
This finding along with the high prevalence of atrial fibrillation and the close relationship between suppressed TSH and high mortality rate and longer hospitalization suggest that thyrotoxicosis may be clinically relevant in COVID-19 patients."
I wonder how often they routinely run a TSH [+fT4 [+fT3] ] for 'other illnesses' .. TSH isn't even part of an FBC is it. So it wouldn't surprise me if there isn't much recorded date to use as control.
Still i'm glad they've got interested in thyroid for Covid . Having decent data for TSH /fT4 /fT3/antibodies all together will all help towards better thyroid knowledge in the long run.
Forgive me for not fully understanding all but I seem to think they measured TSH as low but then measured T4 and T3 not over range . Something we commonly read here. They didn’t record as HYPER . Do you think this knowledge and conclusion will filter down to GPs at last ? One thing that might help some of us !
the study they referred to (the one that i quoted from) differentiated between 'thyrotoxicosis' and 'overt thyrotoxicosis' (these writers are using those terms to mean 'subclinical hyper' , and 'hyper')"Fifty-eight patients (20.2%) were found with thyrotoxicosis (overt in 31 cases),"
"Overt thyrotoxicosis was defined by low TSH values and serum FT3 and/or FT4 above the reference ranges."
So it wasn't the full 20.2 % (58) that we would agree were thyrotoxic/hyperthyroid , but the 31 WERE over range on T3 and /or T4 . which is still a significant %, and higher that they would expect.
(None of these patients were on any thyroid medication or had any other prior thyroid issue.. Once taking thyroid hormone replacement , people have a different relationship between their TSH and fT3/4 levels. which is why we often see low TSH on here when T3 /4 are in range )
So in the study above, out of 237 people in hospital (but not in ICU)with Covid ,
31 had hyperthyroid results (TSH under and fT3 or 4 over), while 27 had just a below range TSH.
(I'm not sure i've understood what you asked though )
What I am trying to say is this. The doctors only read TSH snd decide that you are on too much thyroxine . Which here we what them to check T4 and T3 to be guided of dose we need .
I thought the study did include all 3 tests and I hoped it would be better treatment dosage readings g the more telling thyroid hormones .
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