Abstract
Selenium (Se) deficiency has been implicated in the pathogenesis of Hashimoto’s thyroiditis (HT), although the available evidence is limited. The present study aimed to explore the interrelationships between serum Se status with measures of thyroid function and antioxidant defense in new cases of HT patients with hypoechogenic thyroid. HT patients (n = 49) and matched controls (n = 50) were recruited. Selenium, thyroid hormone panel, thyroid volume (TVol), glutathione (GSH), glutathione peroxidase3 (GPx3) activity, urinary iodine concentration (UIC), and urinary creatinine (Cr) were assessed. HT patients exhibited lower Se levels compared to controls (p < 0.001) with the rates of Se-deficient (<0.85 µmol/L) participants being 58.8% and 34%, respectively. Se-deficient patients exhibited higher thyroid stimulating hormone (TSH), Thyroid volume (TVol), thyroglobulin, antibody-titers, GPx3 activity and UIC/Cr compared to Se-sufficient patients (all p < 0.001). In the Se-deficient patients, inverse correlations were seen between Se-levels with TSH, TVol, and Thyroid peroxidase antibody (TPO-Ab) (all p < 0.001). This study is the first to uncover that coexisting Se-deficiency and elevated iodine in HT may enhance autoimmune reactions and accelerate the deterioration of thyroid function through oxidative stress. Our study also highlights the importance of optimal Se status in this disease, thus providing a rationale for the execution of intervention trials for the evaluation of the clinical benefits of antioxidant-status improvement in HT.
Highlights
Functions are controlled through an intricate interplay between the nervous and hormonal systems
The current study aimed to investigate the interrelationships between serum Se levels and indices of thyroid function, antibody titers, glutathione peroxidase3 (GPx3) activity, reduced glutathione (GSH) and urinary iodine excretion (UIC) in new cases with Hashimoto’s thyroiditis (HT) who were found to have a hypoechogenic thyroid on ultrasound evaluation
We found that the frequency of Se-deficiency in HT patients and healthy controls was 58.8% and 34%
Summary
Functions are controlled through an intricate interplay between the nervous and hormonal systems. A key player in the regulation of metabolism is the thyroid gland. Located in the anterior neck, the gland may exhibit both hypo- and hyperactivity arising from myriad etiologies ranging from viral infections to dietary insufficiencies. Hashimoto’s thyroiditis (HT) is the most prevalent cause of chronic hypothyroidism in iodine sufficient regions, which stems from an autoimmune response against thyroid peroxidase (TPO) and/or thyroglobulin (Tg) [1,2,3]. The reported regional prevalence of HT is variable, mainly due to the application of different diagnostic criteria, laboratory testing methods and global localization [4]. The complex etiology of HT involves the partially understood interplay between the immune system, oxidative stress and trace element imbalance [1,5,6,7]
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