Higher Prevalence of “Low #T3 Syndrome” in Patients With Chronic #Fatigue Syndrome: A Case–Control Study
https://www.frontiersin.org/articles/10.3389/fendo.2018.00097/full
We measured parameters of thyroid function, (metabolic) inflammation, gut wall integrity and nutrients influencing thyroid function and/or inflammation. Most remarkably, CFS patients exhibited similar thyrotropin, but lower free triiodothyronine (FT3) (difference of medians 0.1%), total thyroxine (TT4) (11.9%), total triiodothyronine (TT3) (12.5%), %TT3 (4.7%), sum activity of deiodinases (14.4%), secretory capacity of the thyroid gland (14.9%), 24-h urinary iodine (27.6%), and higher % reverse T3 (rT3) (13.3%). FT3 below the reference range, consistent with the “low T3 syndrome,” was found in 16/98 CFS patients vs. 7/99 controls (OR 2.56; 95% confidence interval = 1.00–6.54). Most observations persisted in two sensitivity analyses with more stringent cutoff values for body mass index, high-sensitive C-reactive protein (hsCRP), and WBC. We found possible evidence of (chronic) low-grade metabolic inflammation (ferritin and HDL-C). FT3, TT3, TT4, and rT3 correlated positively with hsCRP in CFS patients and all subjects. TT3 and TT4 were positively related to hsCRP in controls. Low circulating T3 and the apparent shift from T3 to rT3 may reflect more severely depressed tissue T3 levels. The present findings might be in line with recent metabolomic studies pointing at a hypometabolic state. They resemble a mild form of “non-thyroidal illness syndrome” and “low T3 syndrome” experienced by a subgroup of hypothyroid patients receiving T4 monotherapy. Our study needs confirmation and extension by others. If confirmed, trials with, e.g., T3 and iodide supplements might be indicated
https://www.frontiersin.org/articles/10.3389/fendo.2018.00097/full
We measured parameters of thyroid function, (metabolic) inflammation, gut wall integrity and nutrients influencing thyroid function and/or inflammation. Most remarkably, CFS patients exhibited similar thyrotropin, but lower free triiodothyronine (FT3) (difference of medians 0.1%), total thyroxine (TT4) (11.9%), total triiodothyronine (TT3) (12.5%), %TT3 (4.7%), sum activity of deiodinases (14.4%), secretory capacity of the thyroid gland (14.9%), 24-h urinary iodine (27.6%), and higher % reverse T3 (rT3) (13.3%). FT3 below the reference range, consistent with the “low T3 syndrome,” was found in 16/98 CFS patients vs. 7/99 controls (OR 2.56; 95% confidence interval = 1.00–6.54). Most observations persisted in two sensitivity analyses with more stringent cutoff values for body mass index, high-sensitive C-reactive protein (hsCRP), and WBC. We found possible evidence of (chronic) low-grade metabolic inflammation (ferritin and HDL-C). FT3, TT3, TT4, and rT3 correlated positively with hsCRP in CFS patients and all subjects. TT3 and TT4 were positively related to hsCRP in controls. Low circulating T3 and the apparent shift from T3 to rT3 may reflect more severely depressed tissue T3 levels. The present findings might be in line with recent metabolomic studies pointing at a hypometabolic state. They resemble a mild form of “non-thyroidal illness syndrome” and “low T3 syndrome” experienced by a subgroup of hypothyroid patients receiving T4 monotherapy. Our study needs confirmation and extension by others. If confirmed, trials with, e.g., T3 and iodide supplements might be indicated
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Persistent #fatigue induced by #interferon-alpha: a novel, inflammation-based, proxy model of chronic fatigue syndrome
https://www.sciencedirect.com/science/article/pii/S0306453018301963
Highlights
•Baseline fatigue is not associated with the development of persistent fatigue after IFN-α.
•IFN-α-induced persistent fatigue is associated with increased baseline IL-10.
•Patients who develop persistent fatigue experience greater increases in IL-6 and 10 in response to IFN-α.
•Persistently fatigued patients recover at a similar rate, but from a more severe acute response to the initial trigger.
•Once established, neither the persistent fatigue phenotype, nor CFS, are associated with peripheral immune activation.
Persistent #fatigue induced by #interferon-alpha: a novel, inflammation-based, proxy model of chronic fatigue syndrome
https://www.sciencedirect.com/science/article/pii/S0306453018301963
Highlights
•Baseline fatigue is not associated with the development of persistent fatigue after IFN-α.
•IFN-α-induced persistent fatigue is associated with increased baseline IL-10.
•Patients who develop persistent fatigue experience greater increases in IL-6 and 10 in response to IFN-α.
•Persistently fatigued patients recover at a similar rate, but from a more severe acute response to the initial trigger.
•Once established, neither the persistent fatigue phenotype, nor CFS, are associated with peripheral immune activation.
Sciencedirect
Persistent fatigue induced by interferon-alpha: a novel, inflammation-based, proxy model of chronic fatigue syndrome
The role of immune or infective triggers in the pathogenesis of Chronic Fatigue Syndrome (CFS) is not yet fully understood. Barriers to obtaining immu…