lymphocytic infiltration and inﬂammation are found and anti-TPO antibodies are often present (419,420). The following are criteria for the diagnosis of postpartum thyroiditis: (i) no history of thyroid hormonal abnormalities either before or during pregnancy, (ii) documented abnormal TSH level (either depressed or elevated) during the first year postpartum, and (iii) absence of a positive TSH-receptor antibody titer (Graves disease) or a toxic nodule. A number of studies describe clinical and biochemical evidence of postpartum thyroid dysfunction in 5% to 10% of new mothers (421,422).
Postpartum thyroiditis usually begins with a transient hyperthyroid phase between 6 weeks and 6 months postpartum followed by a hypothyroid phase. Only one-fourth of the cases follow this classic clinical picture, and more than one-third have either hyperthyroidism or hypothyroidism alone. Individuals with type 1 diabetes have a threefold increased risk of developing postpartum thyroiditis. Women with a history of postpartum thyroiditis in a previous pregnancy have nearly a 70% chance of recurrence in a subsequent pregnancy. Although psychotic episodes are rare, postpartum thyroid dysfunction should be considered in all women with postpartum psychosis. The thyrotoxic phase may be subclinical and overlooked, particularly in areas where iodine intake is low (423). Unlike patients with Graves disease, those with the hyperthyroidism caused by postpartum thyroiditis have a low level of radioactive isotope uptake. Women with a history of postpartum thyroiditis should be followed closely as they have a 20% risk of permanent hypothyroidism immediately following the onset of thyroiditis, up to a 60% risk of permanent
Antithyroid Antibodies and Disorders of Reproduction hypothyroidism over the next 5 to 10 years, and up to a 70% risk of postpartum thyroiditis in future pregnancies (424,425).
The absence of thyroid tenderness, pain, fever, elevated sedimentation rate, and leukocytosis helps to rule out subacute thyroiditis (de Quervain thyroiditis). Evaluation of TSH, T4,T3,T3 resin uptake, and antimicrosomal antibody titer confirms the diagnosis.
Most patients are diagnosed during the hypothyroid phase and require 6 to 12 months of thyroxine replacement if they are symptomatic (370). Because approximately 60% of women develop permanent hypothyroidism, TSH should be evaluated following discontinuation of replacement therapy.
Rarely, patients are diagnosed during the hyperthyroid phase (426). Antithyroid medications are not routinely used for these women. Propranolol may be used for relief of symptoms but should be used with appropriate counseling in nursing mothers.
Women who have antithyroid autoantibodies before and after conception appear to be at an increased risk for spontaneous abortion (427,428). Nonorgan-specific antibody production and pregnancy loss are documented in cases of antiphospholipid abnormalities (429). The concurrent presence of organ-specific thyroid antibodies and nonorgan-specific autoantibody production is not uncommon (429–431). In cases of recurrent pregnancy loss, thyroid autoantibodies may serve as peripheral markers of abnormal T-cell function and further implicate an immune component as the cause of reproductive failure. The clinical implications of these findings in the management of patients with recurrent pregnancy loss are not known. Recurrent pregnancy loss is covered in Chapter 33.