Prevention and treatment of postpartum Graves' disease

Abstract

Postpartum Graves' disease requires differentiation from postpartum thyroiditis and subacute thyroiditis in addition to other causes of hyperthyroidism. This may be done by assessing thyrotropin receptor antibody and radioiodine uptake together with clinical examination and thyroid scanning. The effect of pregnancy on thyroid function causes changes in iodine metabolism, thyroid hormone transport proteins and thyroid gland size. Amelioration of autoimmune disease such as Graves' disease, systemic lupus erythematosus and rheumatoid arthritis is often observed during pregnancy followed by postpartum exacerbation. The immunological effects of pregnancy involve placental factors as well as a transient diversion from T helper (Th) 1 to Th2 T-cell cytokine profile in addition to a change in B-cell lymphopoiesis. Prevention of postpartum Graves' disease by immune strategies which have been experimentally performed to reduce expression of diabetes in the non-obese diabetic mouse are attractive but not currently feasible in humans. Treatment of Graves' disease prior to pregnancy or postpartum with ¹³¹I is effective. Therapy with anti-thyroid drugs with or without thyroxine is variably effective.