MON-411 Effects Of Selenium Supplementation In A Patient With Hashimoto’S Thyroiditis And Autoimmunity: A Case Report

Abstract Disclosure: I. Murta: None. J. Bicca: None. N. Cardoso: None. Background: Hashimoto’s thyroiditis (HT) is the most prevalent cause of hypothyroidism in iodine-sufficient regions. It is more susceptible in women, affecting approximately 160 million people worldwide. HT is characterized by anti-thyroid peroxidase (anti-TPO) antibodies and/or typical ultrasound patterns. The current standard of care is thyroid hormone replacement therapy with levothyroxine. Thyroid homeostasis is dependent on selenium (Se), an essential trace element involved in the synthesis of selenoproteins such as glutathione peroxidase (GPx) and deiodinases (DIOs). Recent studies have explored the potential impact of Se supplementation on HT, though its exact benefit and underlying immunologic mechanisms remain unclear. Clinical Case: We report the case of a 28-year-old woman, SF, BMI 31 kg/m² (70 kg, 150 cm), with a 10-year history of anti-TPO positivity and maternal history of HT. She presented with fatigue, xerosis, fissured hands and feet, mood fluctuations, regular menstrual cycles, and had been attempting to conceive for one year. Laboratory evaluation revealed TSH 30 mIU/L, free T4 0.04 ng/dL, LDL 200 mg/dL, hemoglobin 11 g/dL, ferritin 50 ng/mL, transferrin saturation 50%, with normal MCV and MCH. We confirmed these findings on repeat testing and anti-TPO >1300 IU/mL. Levothyroxine 100 mcg/day was initiated, with follow-up in 3 months. At reassessment, the patient reported regular cycles and improvement in xerosis; however, fatigue and memory complaints persisted. Exams showed TSH 2.3 mIU/L, LDL 101 mg/dL, anti-TPO >1300 IU/mL, and anti-thyroglobulin (anti-TG) 160 IU/mL. Tirzepatide 5 mg was initiated and escalated to 15 mg, along with selenomethionine 300 mcg/day. After 6 months, she had lost 15 kg, anti-TPO titers had decreased to 650 IU/mL, and fatigue and cognitive symptoms had improved. Se supplementation was continued for an additional year, reducing anti-TPO titers to 250 IU/mL. Conclusion: Se deficiency may challenge the negative feedback regulation of the hypothalamic-pituitary-thyroid-peripheral axis by reducing GPx and DIO activity, leading to increased oxidative stress, apoptosis, and impaired conversion of T3 to T4 factors that may contribute to thyroid autoimmunity. Therapeutic Se supplementation may reduce anti-TPO and anti-TG antibody titers, lower TSH levels, and improve patient quality of life. These effects are likely mediated by Se antioxidant properties, inhibition of HLA-DR expression induced by IFN-γ, and prevention of follicular cell apoptosis via TNF antagonism. The reduced anti-TPO titers observed in our patient may be explained by weight loss and Se supplementation. Current scientific evidence does not support Se supplementation as a public health policy. More accurate diagnostic tools for Se deficiency and robust clinical trials are needed to confirm its therapeutic utility. Presentation: Monday, July 14, 2025