Globally, it affects between 0.2% and 1.3% of the population.[7] It results from excessive synthesis and release of thyroid hormones, commonly due to autoimmune or inflammatory etiologies.[8] During early pregnancy, rising levels of human chorionic gonadotropin suppress thyroid-stimulating hormone, potentially delaying the recognition of subclinical thyroid dysfunction.[9] In the postpartum period, immune reactivation can precipitate thyroiditis, particularly in genetically predisposed individuals. This evidence concerns the gene TG and thyroiditis.