Postpartum thyroiditis (PPT) is characterized by the development of postpartum thyroid dysfunction (PPTD), which may occur up to 12 months after delivery. Usually the syndrome presents as transient hyperthyroidism (median time of onset, 13 wk) followed by transient hypothyroidism (median time of onset, 19 wk). Clinically, women are relatively asymptomatic during the hyperthyroid phase, although some may notice palpitations requiring treatment with -adrenergic blocking agents. In contrast, patients experience persistent and troublesome symptoms related to the hypothyroid period, which usually must be treated with levothyroxine, normally for up to 1 yr (1, 2). Several studies from different countries have shown that about 12–61% of women who develop postpartum hypothyroidism go on to a permanent hypothyroid state when assessed 1 yr or more after delivery (2–4); these women then require lifelong levothyroxine replacement therapy. In those women who do not develop permanent hypothyroidism, the chance of experiencing a recurrence of PPTD after a previous episode is around 70% (5). The incidence of PPTD has been the subject of much debate. Although most reviews cite a range from 4–9% (6), there is considerable variation in these figures due to sample bias, frequency of blood sampling, and definition of the syndrome. For example, an incidence of 16.7% quoted by Fung et al. (2) was later shown to be erroneous due to the inclusion of the large denominator of thyroid peroxidase (TPO) antibody-negative persons used in the calculation. Nevertheless, the wider incidence has ranges from 1.1 to 21.1%. PPTD is an immunological disorder occurring more frequently in women with certain human leukocyte antigen haplotypes and being usually characterized by the presence of circulating TPO antibodies (7). Indeed, the condition occurs in up to 50% of women found to be TPO antibody positive at the end of the first trimester of gestation (i.e. before the titers start to decline during pregnancy). The other 50% of TPO antibody-positive women who have no thyroid dysfunction are considered to have PPT but not PPTD. Furthermore, there is evidence that the TPO antibody titer at 16 wk gestation is related to the severity of the PPTD (8). The prospective study of PPT by Stagnaro-Green et al. (9) is an important contribution to the epidemiology of postpartum thyroid disease and adds to the debate in several ways. They took advantage of a previously reported study of screening for thyroid function in pregnancy that examined 4562 pregnant women from southern Italy (Puglia) in the first trimester (10). In that study, women were randomly assigned to a universal screening group or a case-finding group. In addition, women in both groups were grouped as high risk if they had one of the following: family history of autoimmune thyroid disease, presence of goiter, signs and symptoms suggestive for thyroid dysfunction, personal history for type 1 diabetes or other autoimmune disease, and history of neck irradiation, previous miscarriages, or preterm deliveries. A total of 4384 women were tested at 6 and 12 months postpartum for thyroid function (TSH and TPO antibodies), with free T4 being measured if hyperthyroidism was suspected. They were also screened in the first trimester, and those with thyroid dysfunction at that time were not studied further for this analysis. PPTD was defined by the usual criteria (2). The incidence of PPT was low at 3.9%. This figure should be compared with two studies from northern Italy that reported incidences of 8.7 and 18%, respectively (11, 12). However the base population in both studies did not exceed 400. Although women who were TPO antibody positive or women in the high-risk groups reported by Stagnaro-Green et al. (9) were significantly more likely to