Immunogenetics
	A possible role for major histocompatibility complex (MHC) antigens in the pathology of AITD, and PPT in particular, has been postulated for some time. Initially, no association between HLA- A or -B phenotypes and PPT could be found. However, Tachi et al(49) reported a higher incidence of HLA-A26, -BW46 and -BW67 together with a significantly lower frequency of HLA-BW62 and -CW7 in women with postpartum hypothyroidism. Later, an increased incidence of HLA-A1 and -B8 in women with this condition was reported(50). An association between certain HLA class II antigens and PPT ( HLA-DR3, DR4 and DR5) has been suggested(51-56). It has also been postulated that PPT may be an early manifestation of Hashimoto's thyroiditis(57); this is consistent with the association of Hashimoto's thyroiditis with an increased frequency of HLA-DR3, DR4 and/or DR5, HLA-DQ7 and a negative association with HLA-DR2(51,58-61) as well as our own data(24). The class III area of the MHC contains the coding for several proteins which are important in the pathogenesis of the autoimmune diseases (viz. tumor necrosis factor, heat shock protein 70, complement). We have measured the allotype frequency of three complement proteins Bf, C4A and C4B and found that there were significant differences in their overall frequency distribution in women with PPT(56). These findings are similar to those reported by Ratana-chaiavong et al(62) in Graves' disease , an autoimmune thyroid disease which is also associ-ated with an increased frequency of HLA-DR3. This may indicate linkage disequilibrium with candidate genes in the class III region but could equally be interpreted on a functional basis as the pathogenesis of PPT is known to be linked to activation of the complement system(40,41).