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Postpartum Thyroiditis Is Associated with Fluctuations in Transforming Growth Factor-ß1 Serum Levels

Metabolism and Pathological Biochemistry Laboratory (A.O., S.D.A., E.G., V.C., M.S.), Immunology Laboratory (V.V., M.B.), and Epidemiology and Biostatistic Laboratory (M.A.S., R.C.), Italian National Institute of Health, 00161 Rome Italy; and Obstetric and Gynecologic Department, Tor Vergata University (H.V., F.M.), 00186 Rome, Italy

Address all correspondence and requests for reprints to: Dr. Antonella Olivieri, Laboratorio di Metabolismo e Biochimica Patologica, Istituto Superiore di Sanità, V.le Regina Elena 299, 00161 Rome, Italy. E-mail: olivieri{at}iss.it.

Postpartum thyroiditis (PPT) is characterized by a rapid evolution and recovery of euthyroidism. Therefore, it can represent a good model to study early cytokine fluctuations in autoimmune thyroid diseases. TGFß1 is an immunosuppressive cytokine, as it inhibits T and B cell proliferation, natural killer cell cytotoxic activity, and the generation of T cell cytotoxicity.

The aim of this study was to assess serum concentrations of TGFß1 during pregnancy and to study possible serum fluctuations of this cytokine during the different phases of PPT. Thyroid biochemical pattern, antithyroid autoantibodies (ATA), and total and active TGFß1 (aTGFß1) serum concentrations were evaluated in 63 pregnant women. Thirty-four of them were ATA⁺, and 29 were ATA^-. Twenty of the 34 ATA⁺ women were followed in the postpartum year. Nine of these 20 women developed PPT; 11 remained euthyroid. All of the PPT women became euthyroid during the follow-up. Our results showed 1) detectable serum levels of aTGFß1 in 50% of ATA⁺ pregnant women, suggesting that the presence of autoantibodies may characterize a favorable condition for TGFß1 activation; and 2) decreased total TGFß1 and increased aTGFß1 serum levels during the active phase of PPT in ATA⁺ women. This seems to suggest that inflammation may be responsible for TGFß1 activation and autoantibody increase because of antigen release. Although further studies of women with persistent hypothyroidism after the postpartum year are needed, the possibility that the enhanced activation of TGFß1 may contribute to resolution of thyroid inflammation postpartum cannot be excluded.

This work was supported by Health Ministry Project 1999 99/F (Inflammatory Bowel Diseases and Autoimmune Diseases–Mucosal Immunoregulation in Pathogenesis and Prevention).

Abbreviations: ATA, Antithyroid autoantibodies; aTGFß1, active TGFß1; FT₃, free T₃; FT₄, free T₄; PPT, postpartum thyroiditis; LAP, latency-associated peptide; TgAb, thyroglobulin autoantibodies; TPOAb, thyroid peroxidase autoantibodies; tTGFß1, total TGFß1.

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