Tag: TSH

Impact of Covid-19 disease on thyroid function: longitudinal study

Abstract:

Background: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic disease (Covid-19) affects thyroid function with different mechanisms: non-thyroidal illness syndrome (NTIS), direct infection of thyroid gland and cytokine storm. We provided the first description of painless atypical thyroiditis coexisting with NTIS in patients hospitalised for moderate-to-severe Covid-19 disease. We aimed to: 1) correlate thyroid dysfunction with Covid-19 disease severity; 2) follow the evolution of thyroid function over time.

Methods: Baseline (at hospital admittance) and longitudinal study of patients hospitalised for moderate-to-severe Covid-19 disease, without known history of thyroid disfunction, assessing serum thyroid function and autoantibodies, inflammatory markers and thyroid ultrasound scan (US). Patients showing at US focal hypoechoic areas suggestive for thyroiditis (thyroiditis-areas) also underwent thyroid 99mTc or I123 uptake scan.

Results: 183 Covid-19 patients were studied baseline, of whom 63 (34%) were already on steroid treatment before hospital admission, thus were not considered for TSH analysis. Decreased serum TSH positively correlated with albumin (P=0.02) and lymphocyte count (P<0.01) but not with C-reactive-protein (P=0.12) and interleukin-6 (P=0.10); TSH also progressively and inversely correlated to the need of oxygen support (P=0.02). Serum FT3 correlated positively with albumin (P<0.01) and inversely with D-dimer (P=0.02). Baseline thyroid US scan showed thyroiditis-areas in 18/65 (28%) patients, associated with reduced thyroid uptake at 99mTc/I123 scintigraphy in 14/17 (82%) cases. Thyroiditis-areas were more frequent among patients with baseline low TSH (6/10, 60%) compared with those with normal TSH (10/40, 25%, P=0.034). The patients with thyroiditis-areas also had higher baseline FT4 (P=0.018) and IL-6 (P=0.016) compared with those with normal thyroid US. Follow-up analysis was conducted in 75/183 (41%) patients; thyroid function and inflammatory markers normalized at all time-points in nearly all cases and no increase of thyroid autoantibodies positivity was observed. The thyroiditis-areas, even if often reduced in size, were still present after 6 and 12 months in 13/15 (87%) and 6/12 (50%) patients, respectively. After 9 months the thyroid uptake at 99mTc/I123 scintigraphy was still reduced in 4/6 (67%) patients, even if partially recovered (mean +28%) compared with baseline.

Conclusions: Thyroid dysfunction during moderate-to-severe Covid-19 disease is mild and transient, and thyroid hormones correlate with disease severity. Thyroiditis-areas at US occur frequently and may persist after one year, even if reduced in size; long-term consequences are unknown. The association of thyroiditis-areas with low TSH and high FT4 and IL-6 serum concentrations support the hypothesis of direct thyroid gland involvement in SARS-CoV-2 infection.

Source: Ilaria Muller, Matteo Varallo, Anita Daturi, Tiziana E Re, Davide Dazzi, Virgilio Longari, Andrea Gori, Giovanna Mantovani , Maura Arosio & Mario Salvi. Impact of Covid-19 disease on thyroid function: longitudinal study. Endocrine Abstracts (2022) 81 RC11.1 | DOI: 10.1530/endoabs.81.RC11.1 https://www.endocrine-abstracts.org/ea/0081/ea0081rc11.1

Autoantibodies to Selenoprotein P in Patients with Chronic Fatigue Syndrome Suggest Selenium Transport Impairment and Acquired Resistance to Thyroid Hormone

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.

Source: Sun, Qian and Oltra, Elisa and Dijck-Brouwer, D. A. Janneke and Chillon, Thilo Samson and Seemann, Petra and Asaad, Sabrina and Demircan, Kamil and Espejo-Oltra, José Andrés and Sánchez-Fito, Teresa and Martin-Martinez, Eva and Minich, Waldemar B. and Muskiet, Frits A. J. and Schomburg, Lutz, Autoantibodies to Selenoprotein P in Patients with Chronic Fatigue Syndrome Suggest Selenium Transport Impairment and Acquired Resistance to Thyroid Hormone. Available at SSRN: https://ssrn.com/abstract=4332223 or http://dx.doi.org/10.2139/ssrn.4332223 (Full text available as PDF file)

The Link Between Empty Sella Syndrome, Fibromyalgia, and Chronic Fatigue Syndrome: The Role of Increased Cerebrospinal Fluid Pressure

Abstract:

The etiopathogenesis of fibromyalgia (FM) and chronic fatigue syndrome (CFS) is not yet elucidated. Hypothalamo-pituitary-adrenal (HPA) axis dysfunction is reflected in the hormonal disturbances found in FM and CFS. Some study groups have introduced a novel hypothesis that moderate or intermittent intracranial hypertension may be involved in the etiopathogenesis of FM and CFS.

In these conditions, hormonal disturbances may be caused by the mechanical effect of increased cerebrospinal fluid pressure, which hampers blood flow in the pituitary gland. Severe intracranial pressure may compress the pituitary gland, resulting in primary empty sella (ES), potentially leading to pituitary hormone deficiencies.

The aim of this narrative review was to explore whether similar hormonal changes and symptoms exist between primary ES and FM or CFS and to link them to cerebrospinal fluid pressure dysregulation. A thorough search of the PubMed and Web of Science databases and the reference lists of the included studies revealed that several clinical characteristics were more prevalent in primary ES, FM or CFS patients than in controls, including increased cerebrospinal fluid pressure, obesity, female sex, headaches and migraine, fatigue, visual disturbances (visual acuity and eye motility abnormalities), vestibulocochlear disturbances (vertigo and neurosensorial hearing loss), and bodily pain (radicular pain and small-fiber neuropathy).

Furthermore, challenge tests of the pituitary gland showed similar abnormalities in all three conditions: blunted adrenocorticotropic hormone, cortisol, growth hormone, luteinizing hormone, and thyroid stimulating hormone responses and an increased prolactin response. The findings of this narrative review provide further support for the hypothesis that moderately or intermittently increased cerebrospinal fluid pressure is involved in the pathogenesis of FM and CFS and should stimulate further research into the etiopathogenesis of these conditions.

Source: Hulens M, Dankaerts W, Rasschaert R, Bruyninckx F, De Mulder P, Bervoets C. The Link Between Empty Sella Syndrome, Fibromyalgia, and Chronic Fatigue Syndrome: The Role of Increased Cerebrospinal Fluid Pressure. J Pain Res. 2023;16:205-219
https://doi.org/10.2147/JPR.S394321 https://www.dovepress.com/the-link-between-empty-sella-syndrome-fibromyalgia-and-chronic-fatigue-peer-reviewed-fulltext-article-JPR (Full text)

Systemic exertion intolerance disease associated to neuroendocrine dysfunction and cortical atrophy: a case report

Abstract:

Background: Scarce evidence about the organic and functional abnormalities of systemic exertion intolerance disease (SEID) is found in literature and the pathophysiology is still unclear.

Methods: Following the CARE Guidelines, this case report describes a patient with a 5-year history of nonspecific symptoms, lately recognized as SEID.

Results: Low serum thyroid- and adrenocorticotropic stimulating hormone levels, and 24-h urinary cortisol excretion almost twice the upper limit were detected. Computed tomography scan found significant cortical atrophy. Low-dose modafinil improved the clinical outcome, added to nonpharmacologic approach.

Conclusion: To ascertain an accurate SEID diagnosis and treatment are a challenge in daily clinical practice, that must be engaged based in clear methods and good practice recommendations. Thus, family practitioners should be aware of this diagnosis.

Source: López-Amador N. Systemic exertion intolerance disease associated to neuroendocrine dysfunction and cortical atrophy: a case report. Fam Pract. 2022 May 28:cmac060. doi: 10.1093/fampra/cmac060. Epub ahead of print. PMID: 35640045. https://pubmed.ncbi.nlm.nih.gov/35640045/

Characterization of pituitary function with emphasis on GH secretion in the chronic fatigue syndrome

Abstract:

OBJECTIVE: Previous studies have revealed that hormonal disturbances may accompany the chronic fatigue syndrome (CFS). Changes in the secretion of the pituitary-adrenal axis have been demonstrated, as well as abnormalities in the GH-IGF-I axis. However, data have not always been well characterized and were sometimes conflicting. The small number of CFS patients investigated in earlier studies may have played a role in the interpretation of the results.

SUBJECTS AND DESIGN: Hormonal testing was performed in 73 nonobese CFS patients and nonobese 21 age-and gender-matched healthy controls. We investigated GH, ACTH and cortisol responses to insulin-induced hypoglycaemia. In a subgroup of patients arginine and clonidine stimulation for GH was also performed. Nocturnal secretion of GH, ACTH and cortisol were determined. Serum levels of IGF-I, prolactin, TSH, and free thyroxine were also measured. Visceral fat mass was assessed by CT scanning.

RESULTS: GH response to insulin induced hypoglycaemia assessed by peak value (17.0 +/- 13.1 microg/l vs. 22. 1 +/- 9.8 microg/l; P = 0.01) and by AUC (450.0 +/- 361.3 microg/l vs. 672.3 +/- 393.0 microg/l; P = 0.002) was significantly decreased in CFS patients vs. controls. Nocturnal GH secretion assessed by GH peak value (5.4 +/- 3.7 vs. 9.0 +/- 5.1 microg/l; P = 0.44) and by AUC (34.4 +/- 20.2 vs. 67.4 +/- 43.1; P = 0.045) was also significantly impaired in CFS patients. Arginine and clonidine administration showed no differences in GH secretion between CFS patients and controls. In the CFS group, GH peak values were significantly higher after ITT than after arginine (P = 0.017) or clonidine (P = 0.001). No differences in serum IGF-I levels were found between CFS patients and controls. Except for a significantly lower nocturnal cortisol peak value, no differences were found in ACTH and cortisol secretion between CFS patients and controls. Significantly higher serum prolactin levels (7.4 +/- 4.7 microg/l vs. 4.4 +/- 1.3 microg/l; P = 0.004) and significantly higher serum TSH levels (1.6 +/- 1.0 mU/l vs. 1.0 +/- 0.4 mU/l; P = 0.011) were found in CFS patients. Serum free thyroxine was comparable in both groups. Visceral fat mass was significantly higher in CFS patients (86.6 +/- 34.9 cm2 vs. 51.5 +/- 15.7 cm2; P < 0.001).

CONCLUSIONS: We observed a significant impairment of GH response during insulin-induced hypoglycaemia and a low nocturnal GH secretion in CFS patients. These changes did, however, not lead to different concentrations in serum IGF-I. The clinical expression of this inadequate GH secretion can thus be questioned, although the alteration in body composition may be related to this relative GH deficiency. Significantly increased prolactin and TSH levels were found when compared to controls. These findings give support to the hypothesis of a decreased dopaminergic tone in CFS. Further investigations are required in order to identify specific adaptations within the neurotransmitter system in CFS and to determine the clinical importance of the impaired GH homeostasis.

 

Source: Moorkens G, Berwaerts J, Wynants H, Abs R. Characterization of pituitary function with emphasis on GH secretion in the chronic fatigue syndrome. Clin Endocrinol (Oxf). 2000 Jul;53(1):99-106.http://www.ncbi.nlm.nih.gov/pubmed/10931086