Abstract

Thyroid disorders have witnessed a surge in prevalence over the last two decades, ranking as the most prevalent endocrine disorders after metabolic syndrome. These encompass hyperthyroidism, hypothyroidism, thyroiditis, and the presence of potentially benign or malignant thyroid nodules. Thyroid hormone, crucial for normal development, growth, and metabolic regulation, undergoes activation from thyroxine to triiodothyronine, influencing a myriad of genes. The cellular signaling pathway is intricately regulated, involving thyroid hormone transporters, receptor isoforms, and interactions with corepressors and coactivators. Non-genomic actions of thyroid hormone have also come to light. The hypothalamic-pituitary-thyroid axis primarily governs thyroid function and hormone levels, complemented by other feedback loops. Thyroid function tests (TFTs) encompass thyrotropin (TSH), free thyroxine (FT4), and free triiodothyronine (FT3) levels. Evolving evidence suggests that optimal thyroid hormone levels may vary within the normal range, influencing clinical outcomes. There is no universally established optimum, but mid-range levels may best signify euthyroidism. In hypothyroidism, elevated TSH levels and low FT4 and FT3 levels are indicative, while hyperthyroidism manifests with low TSH levels and elevated FT4 and/or FT3 levels. Recent research proposes a paradigm shift towards evaluating and treating hypothyroidism based on thyroxinemia rather than relying solely on TSH levels. Furthermore, metabolic syndrome, characterized by interconnected metabolic abnormalities, exhibits a heightened risk in individuals with thyroid dysfunction, particularly hypothyroidism. Insulin resistance, attributed to thyroid dysfunction, potentially underlies metabolic syndrome. Understanding these intricacies paves the way for more effective clinical management.

Description