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Departments of Medicine (A.A.K., A.B.P., L.D.K.E.P., J.H.L.) and Medical Biochemistry (R.J.), University of Wales College of Medicine, Cardiff CF14 4XN, Wales, United Kingdom
Address all correspondence and requests for reprints to: Prof. J. H. Lazarus, Department of Medicine, University Hospital of Wales, Heath Park, Cardiff CF14 4XN, Wales, United Kingdom.
Postpartum thyroid dysfunction (PPTD) develops during the first 9 months in up to 50% of women who have thyroid peroxidase antibodies (anti-TPOAb +ve). Humoral immunity in PPTD has been well documented, but the cellular immunological events accompanying the Th2 to Th1 state postpartum are less clear. Peripheral blood lymphocyte cytokine secretion was examined in 48 TPOAb +ve and 33 TPOAb -ve women at 36 wk gestation and at 6, 12, and 24 wk postpartum. Eighteen women with PPTD had significantly greater secretion of interferon
and IL-4 than euthyroid women at 36 wk gestation with no significant differences in cytokine secretion at other time points. Also, at 36 wk gestation, the median plasma cortisol concentration in the PPTD group was significantly lower than the euthyroid group (442 nmol/liter vs. 567 nmol/liter, P < 0.02). There were no differences between the groups in levels of prolactin, progesterone, or estradiol. These data suggest that there may be less immunological suppression at 36 wk in TPOAb +ve women destined to develop PPTD possibly because of lower levels of cortisol. Thus, the immunological determinants of PPTD may in part occur antenatally, although the mechanism(s) for this is still unclear.
This work was supported by a grant from Saudi Arabia (to A.A.K.).
Abbreviations: CV, Coefficient of variation; FACS, fluorescence-activated cell sorter; FT3, free T3; FT4, free T4; IFN, interferon; PPT, postpartum thyroiditis; PPTD, postpartum thyroid dysfunction; PPTE, euthyroid postpartum; TPOAb, thyroid peroxidase autoantibodies; TPOAb +ve, antithyroid peroxidase antibody positive.
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