Since the late 1960s, many studies have focused on post-partum thyroiditis (PPT) and 295 papers whose titles mention PPT were recorded on MEDLINE as of August 2001. We refer briefly to some excellent reviews and some original articles in order to update our knowledge on PPT.
European Journal of Endocrinology 146 275-279Definition Post-partum thyroiditis (PPT) is an autoimmune disorder characterized by lymphocytic infiltration of the thyroid gland and by transient thyrotoxicosis followed by hypothyroidism or by one or the other occurring in the first year after parturition. It has been the subject of several excellent reviews (1 -8). Thyroid function abnormalities are not due to the presence of thyrotrophin (TSH) receptor antibodies (TRAb) either with stimulating or inhibiting thyroid activity or to a toxic adenoma.
PathogenesisSeveral findings strongly suggest that PPT is an autoimmune disease.PPT has been reported more frequently in women with HLA-DR3, DR4 or DR5 phenotypes. These results are similar to those seen in women with Hashimoto's thyroiditis. PPT has been observed also in patients with Graves' disease and primary autoimmune hypothyroidism.In general, PPT occurs in women with positive antithyroid peroxidase antibodies (TPOAb) in early pregnancy. During pregnancy TPOAb titres decline, whereas in the post-partum period they markedly and rapidly increase, similar to all immunoglobulin G. The fact that TPOAb in the post-partum period retain their specificity in recognizing epitopes suggests that PPT is not related to thyroid antigen specific changes but to a non-specific immune phenomenon.TPOAb are often able to fix the complement, thus inducing the initial cell destruction. The role of complement in the development of PPT is confirmed by the observation that positive TPOAb women who develop PPT have higher complement activation than positive TPOAb women without PPT. Lymphocytic infiltration of the thyroid is the most evident pathologic feature of PPT. However, in peripheral blood there is no variation in the ratio of T to B lymphocytes. An increased CD4 + /CD8+ ratio and an increased activation of T lymphocytes has been reported in PPT women. Some authors suggested a possible role of thyroid cell specific T-cell clone with cytolytic activity. It is probable that T-cell clones reactive to thyroglobulin (Tg), TPO and TSH receptor are expanded within the thyroid during the early phase of PPT.All these possible mechanisms, able to induce the development of PPT, are only temporary since in the vast majority of women the disease does not chronicize and normal thyroid function is resumed. Thus, the immune system has to recover normal tolerance by unknown mechanisms.
PrevalencePrevalence of PPT is variable, ranging from 1.1% in Thailand to 16.7% of parturient women in Great Britain (Table 1) (5,(9)(10)(11)(12)(13)(14). The variability of PPT prevalence may be due to different or inappropriate screening procedures or to different genetic and environment risk factors. In three different studies it has been ...