Clinical meaning
Hashimoto thyroiditis is a chronic autoimmune inflammation of the thyroid gland and the most common cause of hypothyroidism in iodine-sufficient regions. It is characterised by lymphocytic infiltration and progressive destruction of thyroid follicular cells, leading to gradual decline in thyroid hormone production. The autoimmune process involves both cellular and humoral immunity. CD4+ T-helper cells activate CD8+ cytotoxic T lymphocytes that directly destroy thyroid follicular cells. Simultaneously, B lymphocytes produce autoantibodies, most importantly anti-thyroid peroxidase (anti-TPO) antibodies (present in >90% of cases) and anti-thyroglobulin antibodies (present in 60-70%). While these antibodies are primarily disease markers, anti-TPO antibodies can fix complement and contribute to thyroid cell destruction. Antibody-dependent cell-mediated cytotoxicity (ADCC) via natural killer cells also contributes. Genetic susceptibility involves HLA-DR3 and HLA-DR5 associations, CTLA-4 polymorphisms, and PTPN22 gene variants. Environmental triggers include high iodine intake (iodine excess enhances thyroid cell immunogenicity), selenium deficiency, infections (molecular mimicry), pregnancy (postpartum immune rebound), and certain medications (lithium, amiodarone, interferon-alpha, immune checkpoint inhibitors). As thyroid tissue is progressively destroyed, thyroid hormone production falls. The pituitary responds by increasing TSH secretion (negative feedback loop), which initially...