Euthyroid Sick Syndrome (Functional Hypothyroidism) in Patients With COVID-19
Runmei Zou,1,†Chenfang Wu,2,†Siye Zhang,2Guyi Wang,2Quan Zhang,3Bo Yu,2Ying Wu,2Haiyun Dong,2Guobao Wu,2Shangjie Wu,4 and Yanjun Zhong2,* https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7575767/ Published online 2020 Oct 7. doi: 10.3389/fendo.2020.566439PMCID: PMC7575767PMID: 33117282
“Euthyroid Sick Syndrome” (ESS) is Functional Hypothyroidism (see my post on thyroid). It is the physiologic adaptation and pathologic response to stress, particularly to the stress of acute disease. It can be defined as a state in which T3 and T4 are low, without increased TSH.
In the pathophysiological process of ESS, type III deiodinase is activated and type I is suppressed, so there is preferential conversion of T4 to rT3 instead of T3 (9), conversion of free T3 to (inactive) T2 and reduced importation of T4 into the cells.
In addition, there is increased binding of thyroid hormone to plasma protein.
For these reasons, Free T3 plummets.
ESS occurs in infection, trauma, myocardial infarction, malignancy and virtually all other severe diseases (10). Previous studies have suggested that low levels of free T3 (FT3) are associated with severe disease and poor prognosis in critical illness (11, 12).
For example, a study consisting of 503 patients diagnosed with community-acquired pneumonia reported that ESS is an independent risk factor for mortality (19).
Also, in a previous study of 48 SARS patients, 93.7% patients had low T3 (8), high ESR and procalcitonin, but lower lymphocyte count than those without ESS (in this study, Cortisol and rT3 levels unknown).
Herein, Zou et al report studying 149 COVID-19 patients: 41 (27.52%) had ESS (9). 14 of the 41 (34.15%) were male and 65.85, female.
The median age was 58 (IQR: 50–66Yr).
The COVID-19 patients with ESS had stronger inflammatory responses, with higher CRP, ESR and Procalcitonin, but lower lymphocyte count than those without ESS (the levels of Cortisol and rT3 were unknown). ESS patients had more fever [39 (95.12%)], fatigue [18 (43.90%)], cough [36 (87.80%)], shortness of breath [25 (60.98%)], expectoration [20 (48.78%)], and anorexia [21 (51.22%)] than patients without ESS. Hypertension [10 (24.39%)] and diabetes [7 (17.07%)] were the common comorbidities.
Patients with ESS had significantly lower T4 and free T4 (FT4) than non-ESS patients, but the TSH did not differ.
WHY IS THIS IMPORTANT?
The authors have neatly proven that over 25% of their Covid patients had ESS (Functional Hypothyroidism, “FH”) but evidently they are not familiar with the condition and have not made the obvious connection: the symptoms of “long covid” and ESS/FH are indistinguishable.
In my opinion (please remember that since I am no longer licensed, my opinion does not constitute medical advice or instruction), long covid can be equated with ESS/FH and as such, can be expected to respond to administration of oral Triiodothyronine (dose supervised by a physician and titrated according to response of serum T3, rT3, ESR, CRP & TSH), along with support of other hormones, vitamins and minerals, as necessary.
- References: (NOTE that these references are from the paper by Zou et al. They are not the product of my research).
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