The exact pathogenesis of postpartum thyroiditis (PPT)  is not completely understood. However, studies have shown that PPT is an autoimmune disorder in which thyroid tissue antigens are recognized as non-self-antigens. The immune cells mediate inflammatory response to thyroid gland leading to its destruction. This destruction is followed by sudden release of stored thyroid hormone in blood and the appearance of clinical as well as laboratory picture of hyperthyroidism  transiently. This is followed by recovery to euthyroid or hypothyroid state depending on the extent of destruction of thyroid gland, persistence of inflammatory state, and recovery strength of gland. Pregnancy is understood to be associated with reduced immunity to protect fetus from unwanted exposure to maternal immune system. At the end of pregnancy the suppressed immunity is suddenly escalated, leading to the slow evolution of autoimmune response to thyroid auto-antigens, resulting in thyroiditis. The search of exact auto-antibody and auto-antigens triggering an autoimmune response, which correlates with a clinical and pathological picture of postpartum thyroiditis, is still ongoing. Thyroid peroxidase (TPO) auto-antibody is significantly associated with the pathogenesis of postpartum thyroiditis.
Postpartum thyroiditis pathophysiology
Silent thyroiditis pathophysiology
De Quervain's thyroiditis pathophysiology
Hashimoto's thyroiditis pathophysiology
Thyroid adenoma pathophysiology
Pituitary adenoma pathophysiology
Struma ovarii pathophysiology
Postpartum thyroiditis epidemiology and demographics