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Amino et al(2) first documented the association of postpartum thyroiditis
with high titres of antithyroid antibodies and the dramatic rise of antimicrosomal
antibody (now identified as TPO antibody) titre after delivery was clearly
shown in the study of Fung et al(11) (Fig. 4). Furthermore, gestation and
the postpartum period are characterised by fluctuations in the immune response
and the postpartum increase appears to be a reflection of a general enhancement
of immunoglobulin synthesis. Interestingly, the pattern of transient antibody
increase in microsomal antibody levels was observed also for serum total
IgG and IgG subclass levels but not for IgM, IgA, or IgE, or indeed against
viral and bacterial antigens(31). Analysis of the IgG subclass distribution
in postpartum thyroiditis has shown that microsomal antibodies were associated
with variable IgG subclasses eg. increased IgG-1 and IgG-4, increased IgG-2
and 3, increased IgG-1 or no variation at all(32-35). Clearly the application
of varying methodologies to the measurement of IgG subclass distribution
has contributed to these results. The rapid perturbation of the immune
system in the postpartum year contrasts with the relatively stable situation
seen in chronic Hashimoto's thyroiditis.
Figure 4:
Using a technique of epitopic profiling of the polyclonal thyroid peroxidase autoantibodies (epitopic fingerprinting), fingerprint constancy occurred regardless of fluctuations in TPO autoantibody levels(36). Thus, despite marked variations in TPO epitopic profiles among different individuals the temporal constancy suggests inheritance of the fingerprint of this antibody. Although the antibody response is dramatic its precise role in the immunopathogenesis of the condition remains to be determined. Probably, the antibody titre is merely a marker of disease and the immunological damage is mediated by lymphocyte and complement associated mechanisms (vide infra). |
