To investigate the maternal autoimmune status of patients with molar pregnancies. The study was conducted at Yuzuncu Yil University, Department of Obstetrics and Gynecology between January 2012 and June 2016. The medical records of patients who were diagnosed and followed for complete and partial molar pregnancies were reviewed retrospectively. The data of patients who were studied for maternal thyroid auto-antibodies including AntiThyroid peroxidase (TPO) and Anti-Tyroglobulin (Tg) were included in the study. The mean maternal age of complete molar pregnancies were significantly higher than partial molar pregnancies (p=0.010). There were no significant differences between two groups in terms of beta-hCG, TSH, and free T4 (p=0.815, p=0.204, and p=0.072, respectively). None of the patients were anti-TPO positive in the study. There was no significant difference in anti-thyroglobulin positivity between the two groups (p=0.950). Maternal thyroid autoantibody status did not show any difference between the partial and complete molar pregnancies. Thyroid dysfunction seen in molar pregnancies seems to be due to the stimulation of follicular cell receptors with hCG rather than auto-antibodies against thyroid gland.
___
1. Yoshimura M, Pekary AE, Pang XP, et al. Thyrotropic activity of basic isoelectric forms of human chorionic gonadotropin extracted from hydatidiform mole tissues. Journal of Clinical Endocrinology and Metabolism 1994; 78: 862- 864.
2. Palmer JR. Advances in the epidemiology of gestational trophoblastic disease. The Journal of Reproductive Medicine 1994; 39: 155-162.
3. Hershman JM. Physiological and pathological aspects of the effect of human chorionic gonadotropin on the thyroid. Best Pract Res Clin Endocrinol Metab 2004; 18: 249-265.
4. Talbot JA, Lambert A, Anobile CJ, et al. The nature of human chorionic gonadotrophin glycoforms in gestational thyrotoxicosis. Clinical Endocrinology (Oxford) 2001; 55: 33-39.
5. Ashoor G, Maiz N, Rotas M, Jawdat F, Nicolaides KH. Maternal thyroid function at 11-13 weeks of gestation and spontaneous preterm delivery. Obstetrics and Gynecology 2011; 117: 293-298.
6. Ruf J, Carayon P. Structural and functional aspects of thyroid peroxidase. Arch. Biochem. Biophy 2006; 445: 269-277.
7. Carayanniotis G. The cryptic self in thyroid autoimmunity: the paradigm of thyroglobulin. Autoimmunity 2003; 36: 423-428.
8. Prummel MF, Wiersinga WM. Thyroid peroxidase autoantibodies in euthyroid subjects. Best Pract. Res. Clin. Endocrinol. Metab 2005; 19: 1-15 . 9. Panesar NS, Li CY, Rogers MS. Reference intervals for thyroid hormones in pregnant Chinese women. Ann Clin Biochem 2001; 38: 329-332.
10. Smith HO. Gestational trophoblastic disease epidemiology and trends. Clin Obstet Gynecol 2003; 46: 541-556.
11. Tomer Y, Huber GK, Davies TF. Human chorionic gonadotropin (hCG) interacts directly with recombinant human TSH receptors. J Clin Endocrinol Metab 1992; 74: 1477-1479.
12. Stagnaro-Green A, Pearce E. Thyroid disorders in pregnancy. Nat Rev Endocrinol 2012; 8: 650- 658.
13. Lata K, Dutta P, Sridhar S, et al. Thyroid autoimmunity and obstetric outcomes in women with recurrent miscarriage: a casecontrol study. Endocr Connect 2013; 2: 118-124.
14. Negro R, Mestman JH. Thyroid disease in pregnancy. Best Pract Res Clin Endocrinol Metab 2011; 25: 927-943.
15. Banerjee S. Thyroid disorders in pregnancy. Journal of the Association of Physicians of India 2011; 59: 32-34.
16. Shaarawy M, Sheiba M. Diagnostic and prognostic significance of circulating tumor suppressor gene p53 autoantibodies in patients with gestational trophoblastic tumors. Acta Oncol 2004; 43: 43-48.