Cell-mediated immunity and postpartum thyroid dysfunction : A possibility for the prediction of disease?

• Published in: The journal of clinical endocrinology and metabolism 1998-06, Vol.83 (6), p.1959-1966
• Main Authors: KUIJPENS, J. L, DE HAAN-MEULMAN, M, VADER, H. L, POP, V. J, WIERSINGA, W. M, DREXHAGE, H. A
• Format: Article
• Language: English
• Subjects: Autoantibodies - blood; Biological and medical sciences; Dendritic Cells - immunology; Diseases of mother, fetus and pregnancy; Female; Gynecology. Andrology. Obstetrics; Humans; Immunity, Cellular; Iodide Peroxidase - immunology; Killer Cells, Natural; Lymphocyte Count; Medical sciences; Monocytes - immunology; Pregnancy; Pregnancy. Fetus. Placenta; Prospective Studies; Puerperal Disorders - immunology; T-Lymphocytes - immunology; Thyroid Diseases - immunology; Thyrotropin - blood; Thyroxine - blood
• ISSN: 0021-972X; 1945-7197
• DOI: 10.1210/jc.83.6.1959

Postpartum (pp) thyroid dysfunction (PPTD) is thought to be caused by an autoimmune (AI) destruction of thyroid follicles during the pp period. The chronic thyroid AI process [already present in pregnancy, as shown by the positivity for thyroid peroxidase antibodies (TPO-Ab)] becomes overt disease in the pp period, and one assumes that this exacerbation represents a rebound phenomenon after a general immunosuppression during pregnancy. The presence of TPO-Ab in pregnancy has been suggested as a predictor for later PPTD development. Apart from B cells, e.g. production of autoantibodies, various functions of the cell-mediated immune (CMI) system, including those of peripheral T cells, monocytes, and dendritic cells (DC), are also disturbed in AI states. The objectives of the present study were: determining alterations in various CMI parameters in pregnancies followed by PPTD vs. those not followed by PPTD; and determining the usefulness of these parameters in the prediction of PPTD. In a prospective study (region: Kempenland, southeast Netherlands), a random sample of 291 women were tested at 12 and 32 weeks gestation and 4 weeks pp for TPO-Ab. Women were followed until 9 months pp, for developing PPTD. PPTD was defined as both: an abnormal TSH, and fT4 pp women developing PPTD and/or being positive for TPO-Ab (n = 26); and thyroidological uneventful control women of the same cohort, matched for age and parity (n = 21), were tested for thyroid-stimulating antibodies, percentages of peripheral blood lymphocyte subsets using fluorescence-activated cell sorter analysis (CD3, CD4, CD8, CD16, CD56, major histocompatibility complex-class II), for monocyte polarization, and for cluster capability of monocyte-derived DC. Results were: 1) 31 women (10.7%) were positive for TPO-Ab (TPO-Ab+) in gestation (12 and/or 32 weeks); 2) 15 women (5.2%) developed PPTD, of whom 10 were TPO-Ab+ in gestation; 3) pregnancy-related CMI alterations consisted of low percentages of CD16+CD56+ natural killer (NK), cells and a low DC cluster capability at 12 weeks gestation (these functions were normalized at 32 weeks gestation); 4) the TPO-Ab+ PPTD+ women (4 hyper, 5 hypo, and 1 hyper/hypo) were characterized by a persistently low percentage of NK cells, a lowered monocyte polarization, and a raised percentage of major histocompatibility complex-class II+CD3+ T cells; 5) the TPO-Ab- PPTD+ women (all 5 hyper) had neither thyroid-stimulating antibodies nor CMI alterations, apart from thos