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Studies on antibody functional affinity(35) and IgG subclass distribution(34)
in PPT suggest that, as in other autoimmune diseases, activation of the
complement system may have a role in pathogenesis.
The interaction of the complement system with thyroid antigen/autoantibody
complexes has been quantitated by the use of two assay tech-niques, one
based on the haemolysis of sheep erythrocytes in the presence of excess
complement(37) and, the other, an ELISA for the quantitation of complement
C3b immobilised as a result of classical complement pathway activation(38).
It has been shown that not only is there activation of the complement system
by thyroid directed autoantibodies(39), but that complement activation
is related to the extent of the thyroiditis(40) and correlates with the
severity of the thyroid dysfunction(41). (Fig. 5).
In other forms of autoimmune thyroid disease (AITD), where complement
activation has been suspected, it has been possible to measure elevated
levels of the C5-C9 membrane attack complex (MAC) in the patients serum(42).
However, despite an exhaustive search we have been unable to detect elevated
MAC levels in serum samples from postpartum women who subsequently developed
PPT(43).
Figure 5:
Mean serum bioactive TPO antibody in TPO positive postpartum women. [square] - 75 women -
euthyroid for whole period; [arrow up] - 44 women - transient thyroid dysfunction during the year;
[arrow down] - 29 women - persistent thyroid dysfunction;
- - - - titre in transient group significantly higher (p <0.05 or greater) than euthyroid group.
Persistent group significantly higher titre than transient group, at all time points (Adapted from
Parkes et al41 with permission).
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