Recent epidemiological studies in Japan and Sweden have disclosed a high prevalence of transient thyroid dysfunction in women following delivery. These changes seem to reflect an immunoregulatory "rebound" following pregnancy-induced immunosuppression. Thyroid microsomal antibody titers characteristically decrease during pregnancy and increase again after delivery to maximum levels around six months postpartum. At this time some microsomal antibody-positive women develop goitrous hypothyroidism. Subsequently, the microsomal antibody titers fall, reaching the early pregnancy values one year postpartum by which time hypothyroidism subsides. The severity of hypothyroidism is closely related to the titer of microsomal antibody, especially the immunoglobulin G1 subclass of microsomal antibody, and partly predictable from the titer in early pregnancy. The HLA-DR4 antigen was observed in 58% of microsomal antibody-positive Swedish women as compared to 33.7% in the general population (relative risk = 2.71). This association was even stronger in microsomal antibody-positive women who developed postpartum hypothyroidism (69%; relative risk = 4.36). Finally, postpartum thyrotoxicosis with a high radioiodine uptake may occur in women with latent Graves' disease. In these cases changes of TSH-receptor-stimulating antibodies analogous to microsomal antibodies seem to occur.