There is a paucity of studies regarding oxidative balance and selenium (Se) status in congenital hypothyroidism. Recently, more attention has been given to the use of Se supplementation as a new treat ...

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There is a paucity of studies regarding oxidative balance and selenium (Se) status in congenital hypothyroidism. Recently, more attention has been given to the use of Se supplementation as a new treatment for thyroid disorders. Oxidative stress increases in different thyroid disorders and causes many pathological outcomes. The present study aimed to determine the serum prooxidant-anti - oxidant balance (PAB), Se, thyroid stimulating hormone (TSH) and free thyroxine (FT4) concentration in congenital hypothyroidism patients and the association of their probable change with hematological indices.
Although there was no correlation between PAB and also Se with hematologic and biochemical markers in congenital hypothyroidism patients, changes in these two factors might be considered as a potential risk factor due to the other known effects of high PAB values and low Se concentrations (1).

Selenium plays a role in antioxidant status and, together with iodine, in thyroid function. Iodine deficiency exists in New Zealand during pregnancy and lactation, and selenium deficiency may further affect thyroid function. This study investigated selenium intakes of pregnant and lactating women, in Palmerston North, in the North Island of New Zealand. Dietary intake was estimated using three repeated 24-h dietary recalls. Dietary intake in pregnancy was also estimated from 24-h urinary excretion of selenium. Selenium concentrations were determined in urine and breastmilk using inductively-coupled plasma mass spectrometry. Median selenium intakes based on dietary data were 51 (39, 65) μg/day in pregnancy and 51 (36, 80) μg/day in lactation, with 61% and 68% below estimated average requirement (EAR). Median daily selenium intake in pregnancy based on urinary excretion was 49 (40, 60) µg/day, with 59% below EAR. Median selenium concentration in breastmilk was 11 (10, 13) µg/L and estimated median selenium intake for infants was 9 (8, 10) µg/day, with 91% below the Adequate Intake of 12 μg/day. These pregnant and breastfeeding women were at risk of dietary selenium inadequacy. Further research is required to assess selenium status in relation to thyroid function and health in this group (2).

Low selenium status is associated with increased risk of Graves' disease (GD). While several trials have discussed the efficacy of selenium supplementation for thyroid function, in GD patients, the effectiveness of selenium intake as adjuvant therapy remains unclear. In this systematic review and meta-analysis, we aimed to determine the efficacy of selenium supplementation on thyroid function in GD patients. Two reviewers searched PubMed, Web of Science, the Cochrane Central Register of Controlled Trials, and four Chinese databases for studies published up to October 31, 2017. RCTs comparing the effect of selenium supplementation on thyroid hyperfunction in GD patients on antithyroid medication to placebo were included. Serum free thyroxine (FT4), free triiodothyronine (FT3), thyrotrophic hormone receptor antibody (TRAb), and thyroid-stimulating hormone (TSH) levels were assessed. Ten trials involving 796 patients were included. Random-effects meta-analyses in weighted mean difference (WMD) were performed for 3, 6, and 9 months of supplementation and compared to placebo administration. Selenium supplementation significantly decreased FT4 (WMD=-0.86 [confidence interval (CI)-1.20 to -0.53]; p=0.756; I2=0.0%) and FT3 (WMD=-0.34 [CI-0.66 to -0.02]; p=0.719; I2=0.0%) levels at 3 months, compared to placebo administration; these findings were consistent at 6 but not 9 months. TSH levels were more elevated in the group of patients taking selenium than in the control group at 3 and 6, but not 9 months. TRAb levels decreased at 6 but not 9 months. At 6 months, patients on selenium supplementation were more likely than controls to show improved thyroid function; however, the effect disappeared at 9 months. Whether these effects correlate with clinically relevant measures remains to be demonstrated (3).

Graves' orbitopathy is a debilitating disorder which occurs in patients with autoimmune thyroid disease, mainly Graves' disease, and adds layers of complexity to management of both conditions. We conducted a comprehensive review of literature for publications relating to established and new management options for Graves' orbitopathy and have summarized key articles in this review. Initial evaluation of patients with Graves' disease should also include clinical evaluation for orbitopathy. If eye disease is present, patients are best managed by a multi-specialty team including an endocrinologist and ophthalmologist. All patients with Graves' orbitopathy benefit from risk factor modification and normalization of thyroid function tests. Patients with active, mild disease generally benefit from local therapies and selenium, while patients with moderate-to-severe disease usually require the addition of intravenous glucocorticoid therapy. If there is an inadequate response to glucocorticoid therapy, several second-line therapies have been investigated for use, including orbital radiotherapy (with additional glucocorticoids), rituximab, cyclosporine, mycophenolate mofetil, and methotrexate. Use of new biologic agents, mainly teprotumumab and tocilizumab, have demonstrated impressive reductions in disease activity and severity. If these results are confirmed, the treatment paradigm is likely to change in the future. Finally, there are several novel immunotherapies being investigated for Graves' disease, which may have treatment implications for Graves' orbitopathy as well. Overall, there are many encouraging advances in the therapy of Graves' orbitopathy that are making the future more promising for patients suffering from this disease (4).

References____________________________

(1) Alteration in Prooxidant-antioxidant Balance Associated with Selenium Concentration in Patients with Congenital Hypothyroidism.
Rostami S, Fathollahpour A, Abdi M, Naderi K.
J Med Biochem. 2018 Jul 1;37(3):355-363. doi: 10.1515/jomb-2017-0052. eCollection 2018 Jul.

(2) Selenium Intake in Iodine-Deficient Pregnant and Breastfeeding Women in New Zealand.
Jin Y, Coad J, Weber JL, Thomson JS, Brough L.
Nutrients. 2019 Jan 1;11(1). pii: E69. doi: 10.3390/nu11010069.

(3) Effects of Selenium Supplementation on Graves' Disease: A Systematic Review and Meta-Analysis.
Zheng H, Wei J, Wang L, Wang Q, Zhao J, Chen S, Wei F.
Evid Based Complement Alternat Med. 2018 Sep 26;2018:3763565. doi: 10.1155/2018/3763565. eCollection 2018. Review.

(4) Current and Emerging Treatment Strategies for Graves' Orbitopathy.
Genere N, Stan MN.
Drugs. 2019 Feb;79(2):109-124. doi: 10.1007/s40265-018-1045-9. Review.

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