INCREASE IN ANTIMICROSOMAL ANTIBODY-RELATED IGG1 AND IGG4, AND TITERS OF ANTITHYROID PEROXIDASE ANTIBODIES, BUT NOT ANTIBODY DEPENDENT CELL-MEDIATED CYTOTOXICITY IN POSTPARTUM THYROIDITIS WITH TRANSIENT HYPERTHYROIDISM

To evaluate possible immunological mechanisms involved in the development of postpartum thyroiditis with transient hyperthyroidism followed by transient hypothyroidism (PPT), antithyroid peroxidase antibodies (anti-TPO), antimicrosomal antibody (AMA) related immunoglobin G subclass and antibody-dependent cell-mediated cytotoxicity (ADCC) were studied in 43 post-partum (PP) women who were euthyroid at delivery and completed a subsequent 1 year follow up. Among the 25 mothers who developed PPT, 14 had positive AMA (PPT:AMA+) and 11 negative AMA (PPT:AMA-) at delivery. Among the 18 mothers who remained euthyroid (E) up to one year post-partum and were used as controls, 8 were AMA positive(E:AMA+) and 10 AMA negative (E:AMA-) at delivery. AMA measured by a hemag-glutination method correlated well with anti-TPO antibodies measured by RIA in the PP mothers studied. When AMA-related IgG subclass activity was analysed comparing PPT women with appropriate euthyroid controls at the different time intervals studied, it was seen that PPT:AMA+ when compared to E:AMA+ women have significantly increased activity of AMA related lgG1 at all PP time intervals studied (p < 0.001), but IgG4 was only increased at 5-7 months PP (p < 0.05). PPT:AMA-when when compared to E:AMA- have significantly increased IgG4 at 2-4 (p < 0.001), 5-7 and 10-12 (p < 0.05) months PP, but IgG1 is only increased at 5-7 months PP (p < 0.05). The development of PPT coincides with an increase in activity in AMA related IgG1 and IgG4 in all groups with a lesser increase in AMA related IgG2 for PPT:AMA+, thereby documenting a variable polyclonal IgG subclass antibody response in those women who develop PPT. The studies in ADCC failed to demonstrate any differences in women with PPT compared to euthyroid PP controls. In conclusion, these observations appear to indicate that AMA and anti-TPO are more likely markers rather than etiological factors for the development of PPT. As well, they suggest that the destructive hyperthyroidism of PPT may not be mediated by ADCC but may involve different as yet unidentified cytotoxic mechanisms.