rT3 and Inflammation in Hashimoto's Thyroiditis

Hashimoto's thyroiditis (HT) is characterized by an enlarged thyroid gland infiltrated with lymphocytes. The incidence of HT is estimated to be 0.3-1.5 cases per 1000 people, with a female/male predominance of 7-10:1. It has a strong association with other autoimmune diseases. The autoimmune presentation of HT relies on the interaction between environmental factors and genetic background such as human leukocyte antigen (HLA), T lymphocyte-associated 4 (CTLA-4), protein tyrosine phosphatase, non-receptor type 22 (PTPN22) genes, and X chromosome inactivation patterns, leading to an imbalance between self-tolerance mechanisms maintained by regulatory T and B lymphocytes. Furthermore, genetic polymorphisms in self antigens, cytokines and their receptors (e.g., interleukin 2 receptor IL2R), estrogen receptors, adhesion molecules (CD14, CD40), the promoter region of selenoprotein S, and apoptosis-related gene products have been associated with thyroid autoimmunity. Genetic factors account for 70-80% of the risk in the development of Hashimoto's disease, while environmental factors account for 20-30%. HT is diagnosed based on clinical symptoms, antithyroid antibodies, and histological features. Ultrasound imaging of the thyroid gland can aid in differential diagnosis, especially in patients with thyroid peroxidase antibody (TPOAb) negative HT. Ultrasound features of HT include decreased echogenicity, heterogeneity, hypervascularity, and the presence of small cysts. Hashimoto's disease can have stages presenting with hyperthyroidism, euthyroidism, and hypothyroidism. In diagnosis, hyperthyroidism, euthyroidism, and hypothyroidism are determined based on measurements of thyroid-stimulating hormone (TSH), free T4 (sT4), and free T3 (sT3), which are biochemical parameters used. Hashimoto's thyroiditis is an inflammatory condition affecting the thyroid gland, and patients develop clinical thyroid dysfunction depending on the duration of the disease. HT causes atrophy of the th