Do Changes In Serum Leptin Influence The Outcome Of Postpartum Thyroid Dysfunction?
G Mazziotti1, FF Casanueva2, M Lage2, LDKE Premawardhana1, AB Parkes1 & JH Lazarus1
Experimental evidence suggests that leptin plays an important role in modulation of cell-mediated immunity in organ-specific autoimmune diseases. This longitudinal study evaluates changes in serum leptin values in relation to development and outcome of postpartum thyroiditis (PPT). Materials and Methods: Fifty postpartum (6 week) euthyroid women with elevated thyroglobulin (TgAb) and/or thyro-peroxidase (TPOAb) antibodies were investigated. Body mass index (BMI), serum leptin values, thyroid function (serum TSH, FT4, FT3) and autoimmunity (TgAb, TPOAb) were longitudinally evaluated at 6, 12, 16, 20, and 24 weeks postpartum. Results: At study entry the median BMI and serum leptin were 25.2 (range: 17.2-38.5) and 8.2 ng/ml (range: 1.3-44.6), respectively. The two parameters were significantly correlated (r=0.65; p<0.001). During follow-up, neither the median serum leptin concentration nor the median BMI changed significantly. However, in some patients the leptin values increased (+8.6% to +337.5%), whilst in others they decreased (-2.4% to -66.7%). Patients were grouped according to the percentage change in leptin level. Whilst there was no difference in the number of women developing postpartum thyroid dysfunction (PPTD) in the 1st tertile (leptin variation from -66.7% to -16.8%; 12/17) and the 3rd tertile (leptin variation from +26.6% to +337.5%; 10/16 - Chi sq. 0.243; ns) groups, PPTD was transient in 9 of 12 of the 1st tertile group was but persistent in 8 of 10 women in the 3rd tertile group (Chi Sq. 6.6; p = 0.010). Changes in leptin values did not correlate with thyroid hormone levels. Conclusions: This longitudinal study suggests that, whilst leptin is not important for the development of thyroid dysfunction in PPT women, it may play a critical role in determining the long term outcome of disease, probably as consequence of its known effects on the Th1 immune response.