Arnie Pye
Senior Member (Voting Rights)
Preprint, not peer reviewed : https://papers.ssrn.com/sol3/papers.cfm?abstract_id=4332223
Autoantibodies to Selenoprotein P in Patients with Chronic Fatigue Syndrome suggest Selenium Transport Impairment and Acquired Resistance to Thyroid Hormone
Qian Sun1,2,†, Elisa Oltra3,†, D. A. Janneke Dijck-Brouwer4,†, Thilo Samson Chillon1,†,
Petra Seemann2, Sabrina Asaad1, Kamil Demircan1, José Andrés Espejo-Oltra3,
Teresa Sánchez-Fito3, Eva Martín-Martínez5, Waldemar B Minich1, Frits A. J. Muskiet4,
Lutz Schomburg1,*
Highlights
Comprehensive analysis of Se and thyroid hormone in chronic fatigue syndrome
Biomarkers of Se status, i.e., total Se, GPx3 and SELENOP correlate linearly
Autoantibodies to SELENOP are relatively frequent in chronic fatigue syndrome
SELENOP-aAb are associated with dysregulated GPx3 and DIO activities
Strongly reduced urinary iodine reflects DIO suppression by SELENOP-aA
Abstract
Chronic Fatigue Syndrome (CFS) presents with symptoms similar to hypothyroidism, including mental and physical fatigue, poor sleep, depression, and anxiety. However, the typical thyroid hormone (TH) profile of elevated thyrotropin (TSH) and low thyroxine (T4) is not observed. Recently, autoantibodies to the selenium transporter SELENOP (SELENOP-aAb) have been identified in Hashimoto’s thyroiditis and shown to impair selenium transport and selenoprotein expression.
We hypothesized that SELENOP-aAb are prevalent in CFS and impair TH metabolism.Selenium status in CFS (n=167) was compared to that of healthy controls (n=545). Two additional small groups were included, namely patients with fibromyalgia (FM; n=39), a disease often comorbid with CFS, and patients with post-COVID condition (n=24).
The serum/plasma Se biomarkers total Se, glutathione peroxidase (GPx3) and SELENOP levels showed linear correlations without reaching saturation, indicative of Se deficiency. TSH and total T4 levels fitted within normal ranges, but relative total T3 (%TT3) was low, and relative rT3 (%rT3) was elevated in CFS. SELENOP-aAb prevalence was 9.6-15.6% in CFS versus 0.9-2.0% in controls, depending on cut-off for positivity. An impairment of Se transport in SELENOP-aAb positive CFS patients is suggested by the lack of correlation between total Se and GPx3 activity. The same patients present with disturbed TH parameters, including low deiodinase (DIO) activity (SPINA-GD index) and particularly low urinary iodine as compared to controls (43.2 (16.0) vs. 89.0 (54.9) µg/L, P<0.001), indicating that SELENOP-aAb affect TH deiodination and iodine excretion.
We conclude that a considerable subset of CFS patients express SELENOP-aAb that disturb Se transport and cause low GPx3 and DIO activities. Hereby, TH deiodination decreases as an acquired condition that is not readily reflected by TSH or T4 in blood. This hypothesis opens new explanations and therapeutic options for SELENOP-aAb positive CFS and, perhaps, post-COVID condition patients, but requires additional clinical evidence from intervention trials.
Autoantibodies to Selenoprotein P in Patients with Chronic Fatigue Syndrome suggest Selenium Transport Impairment and Acquired Resistance to Thyroid Hormone
Qian Sun1,2,†, Elisa Oltra3,†, D. A. Janneke Dijck-Brouwer4,†, Thilo Samson Chillon1,†,
Petra Seemann2, Sabrina Asaad1, Kamil Demircan1, José Andrés Espejo-Oltra3,
Teresa Sánchez-Fito3, Eva Martín-Martínez5, Waldemar B Minich1, Frits A. J. Muskiet4,
Lutz Schomburg1,*
Highlights
Comprehensive analysis of Se and thyroid hormone in chronic fatigue syndrome
Biomarkers of Se status, i.e., total Se, GPx3 and SELENOP correlate linearly
Autoantibodies to SELENOP are relatively frequent in chronic fatigue syndrome
SELENOP-aAb are associated with dysregulated GPx3 and DIO activities
Strongly reduced urinary iodine reflects DIO suppression by SELENOP-aA
Abstract
Chronic Fatigue Syndrome (CFS) presents with symptoms similar to hypothyroidism, including mental and physical fatigue, poor sleep, depression, and anxiety. However, the typical thyroid hormone (TH) profile of elevated thyrotropin (TSH) and low thyroxine (T4) is not observed. Recently, autoantibodies to the selenium transporter SELENOP (SELENOP-aAb) have been identified in Hashimoto’s thyroiditis and shown to impair selenium transport and selenoprotein expression.
We hypothesized that SELENOP-aAb are prevalent in CFS and impair TH metabolism.Selenium status in CFS (n=167) was compared to that of healthy controls (n=545). Two additional small groups were included, namely patients with fibromyalgia (FM; n=39), a disease often comorbid with CFS, and patients with post-COVID condition (n=24).
The serum/plasma Se biomarkers total Se, glutathione peroxidase (GPx3) and SELENOP levels showed linear correlations without reaching saturation, indicative of Se deficiency. TSH and total T4 levels fitted within normal ranges, but relative total T3 (%TT3) was low, and relative rT3 (%rT3) was elevated in CFS. SELENOP-aAb prevalence was 9.6-15.6% in CFS versus 0.9-2.0% in controls, depending on cut-off for positivity. An impairment of Se transport in SELENOP-aAb positive CFS patients is suggested by the lack of correlation between total Se and GPx3 activity. The same patients present with disturbed TH parameters, including low deiodinase (DIO) activity (SPINA-GD index) and particularly low urinary iodine as compared to controls (43.2 (16.0) vs. 89.0 (54.9) µg/L, P<0.001), indicating that SELENOP-aAb affect TH deiodination and iodine excretion.
We conclude that a considerable subset of CFS patients express SELENOP-aAb that disturb Se transport and cause low GPx3 and DIO activities. Hereby, TH deiodination decreases as an acquired condition that is not readily reflected by TSH or T4 in blood. This hypothesis opens new explanations and therapeutic options for SELENOP-aAb positive CFS and, perhaps, post-COVID condition patients, but requires additional clinical evidence from intervention trials.
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