The Common Vein Copyright 2010
Postpartum Thyroiditis is a subacute inflammatory process that can affect women in their first postpartum year. The disease is thought to be caused by autoimmune thyroiditis that presents itself during the postpartum immunologic rebound period.
Structural changes of the thyroid include inflammatory cell infiltration and thyroid follicle destruction. Functionally, gland destruction can lead to increased release of preformed thyroid hormone from colloid stores. Follicle cell destruction can then lead to inability of the thyroid gland to produce appropriate levels of thyroid hormone.
The classic clinical presentation is initial hyperthyroidism after release of stored thyroid hormone, followed by insidious development of hypothyroidism. Studies have shown that this classic picture only occurs in ¼ of patients. In most cases the hypothyroidism is the presenting complaint with symptoms of increased fatigue, cold intolerance, and depression.
Imaging of postpartum thyroiditis includes thyroid scintigraphy which shows a decreased radioiodine uptake, even during hyperthyroid phase. This distinguishes subacute thyroiditis induced hyperthyroidism from graves hyperthyroidism which has increased iodine uptake. Ultrasound may reveal some non-specific inflammatory changes, but is not helpful in the diagnosis. The best way to diagnose postpartum thyroiditis is clinically and with laboratory tests showing either hyper or hypothyroidism. Because symptoms are often temporary, treatment is focused on the presenting complaints. Symptoms of hyperthyroidism are often treated with Beta-blockers, such as propanolol. Hypothyroid symptoms may be treated with temporary synthetic thyroxine replacement.