|Year : 2017 | Volume
| Issue : 2 | Page : 86-88
A rare presentation of autoimmune thyroid disease in mother and neonate postpartum
Department of Endocrinology, Andhra Medical College, Visakhapatnam, Andhra Pradesh, India
|Date of Web Publication||26-May-2017|
7-5-123, Plot 78, Mythreyi Nagar, Pandurangapuram, Visakhapatnam - 530 003, Andhra Pradesh
Source of Support: None, Conflict of Interest: None
This is a case of long-standing hypothyroidism on levothyroxine (LT4) replacement developing Graves' disease postpartum and the newborn presenting with transient congenital hypothyroidism. The clinical and laboratory data of the case are reported along with a brief literature review. A 27-year-old female who has hypothyroidism for the past 3 years and gestational diabetes mellitus delivered uneventfully. The thyroid function tests (TFTs) of the newborn showed congenital hypothyroidism which was transient and resolved by 3 months' age. An ultrasound of thyroid showed gland in situ. The diagnosis of the newborn is transient congenital hypothyroidism probably due to thyroid-stimulating hormone receptor-blocking antibodies (TBAbs). The mother who has hypothyroidism for the past 3 years was stable with euthyroidism and was on LT4 100 ug daily. Seven months postpartum, she had lid lag and proptosis of her left eye. Her TFTs revealed thyrotoxicosis and was advised to stop LT4. Magnetic resonance imaging orbits were normal and her TBAbs are elevated at 4.65 IU/L (<1.22). Antimicrosomal antibodies and antithyroid peroxidase antibodies were negative. The orbitopathy resolved over 6 weeks and the mother remains euthyroid without LT4 on a follow-up period of 8 months. Close monitoring of autoimmune thyroid disease (AITD) in pregnancy and postpartum is necessary due to the immune switching in this period and may obviate the need for LT4 therapy. The suspicion of transient congenital hypothyroidism due to TBAb should be high in neonates born to mothers with AITD.
Keywords: Autoimmune thyroid disease, postpartum, pregnancy, thyroid-blocking antibodies, thyroid-stimulating antibodies, thyrotropin receptor antibody
|How to cite this article:|
Ayyagari M. A rare presentation of autoimmune thyroid disease in mother and neonate postpartum. Thyroid Res Pract 2017;14:86-8
|How to cite this URL:|
Ayyagari M. A rare presentation of autoimmune thyroid disease in mother and neonate postpartum. Thyroid Res Pract [serial online] 2017 [cited 2020 Jun 3];14:86-8. Available from: http://www.thetrp.net/text.asp?2017/14/2/86/207129
| Introduction|| |
Autoimmune thyroid disease (AITD) is a spectrum ranging from Hashimoto's thyroiditis to Graves' disease (GD). Pregnancy and postpartum are known to alter the severity of AITD. The increased demand for thyroid hormones in pregnancy leads to an increase in levothyroxine (LT4) dose in hypothyroidism, and the immunotolerant state of pregnancy leads to remission of GD in pregnancy. Hypothyroidism reverts to the prepregnancy LT4 dose and GD exacerbates in the postpartum period. This is a case of long-standing hypothyroidism on LT4 developing GD postpartum and the newborn presenting with transient congenital hypothyroidism. This interesting case exemplifies how the expression of AITD may be altered during pregnancy and postpartum.
| Case Report|| |
A 27-year-old female who has hypothyroidism for the past 3 years and gestational diabetes mellitus delivered on December 25, 2015. She was on 100 mcg of LT4 during her pregnancy and maintained TSH in normal range. Her pregnancy was uneventful and the newborn was healthy with birth weight of 3 kg and normal APGAR score. The newborn underwent thyroid function testing (TFT) at 2 weeks' age which revealed primary congenital hypothyroidism [Table 1]. The infant was started on LT4 50 ug daily and the follow-up showed normalization of thyroid function in 6 weeks. An ultrasound of thyroid showed gland in situ. [Table 1] illustrates the follow-up of the infant for 1 year which showed normalization of thyroid function. The diagnosis of the newborn is transient congenital hypothyroidism probably due to thyroid-stimulating hormone receptor-blocking antibodies (TBAbs).
The mother who has hypothyroidism for the past 3 years was stable with euthyroidism, using LT4 100 ug daily. Seven months postpartum, she had lid lag and proptosis of her left eye. Her TFT [Table 2] revealed thyrotoxicosis and was advised to stop LT4. Magnetic resonance imaging orbits were normal and her TRAbs are elevated at 4.65 IU/L (<1.22). Antimicrosomal antibodies and antithyroid peroxidase antibodies were negative. [Table 2] highlights the 8-month follow-up TFT of the mother. LT4 was stopped and she was prescribed selenium 100 ug daily for orbitopathy. The orbitopathy resolved over 6 weeks and the mother remains euthyroid without LT4 on a follow-up period of 8 months' postpartum.
| Discussion|| |
This case illustrates the profound effect of pregnancy and postpartum on AITD. Two types of thyrotropin receptor (TRAb) autoantibodies are responsible for two distinct clinical syndromes. Thyroid-stimulating antibodies (TSAbs) cause GD while TBAbs cause hypothyroidism. This case is an example of TRAb behaving as TSAb in the mother postpartum producing GD and the newborn having transient CH probably due to TBAb. GD may precede or follow chronic autoimmune thyroiditis in the same patient, presumably related to the similar autoimmune process in the two disorders. GD usually flares up postpartum and Hashimoto's thyroiditis may also exacerbate postpartum. Transient GD during pregnancy has been reported in patients with hypothyroidism due to fluctuating immune status. During pregnancy, the expansion of TREG cells present in the mother's circulation is capable of regulating coincidental autoimmune responses through the phenomenon of linked suppression which is responsible for the amelioration of autoimmune disease such as GD in pregnancy. A rapid fall in these cells postpartum exacerbates autoimmunity. Spontaneous transformation of Hashimoto's thyroiditis into GD in the postpartum is rare. Awad et al. recently reported a case of hypothyroidism who spontaneously developed GD during pregnancy. They concluded that pregnancy was a trigger for the shift in the antibody properties and concentrations, and the balance between the stimulating and blocking TRAb may impact the clinical presentation of the mother and the newborn. The present case is possibly an example of switching of TBAb to TSAb postpartum. A small proportion of TBAb-positive hypothyroid patients treated with LT4 switch to TSAb and hyperthyroidism. LT4 therapy rarely induces or enhances thyroid autoantibody levels. The emergence of TSAb after LT4 administration may be sufficient to counteract TBAb inhibition. This could be the explanation for the present case to remain euthyroid even after 6-month follow-up. The functional switching of TRAb emphasizes the need for careful monitoring of women with AITD during pregnancy and postpartum as the clinical course is unpredictable.
The occurrence of Graves' ophthalmopathy postpartum in this case of AITD is mild and probably due to the autoimmune alteration. However, the ophthalmopathy was transient and resolved spontaneously parallel with the picture of thyrotoxicosis, difficult to draw any conclusion.
The TRAb in this case behaved as TBAb in the neonate and as TSAb in the mother postpartum. The neonate had transient congenital hypothyroidism probably due to TBAb. Although the assay was not done in this case, the clinical picture is that of TBAb-mediated transient congenital hypothyroidism. Transplacental transfer of TBAb is a rare cause of transient primary hypothyroidism in newborn infants, causing only about 1%–2% of cases. The infants have hypothyroidism because the antibodies are cleared slowly and the half-life of TBAb is 21 days. These antibodies do not interfere with the formation, migration, and growth of the thyroid gland and therefore do not cause permanent primary CH. The TBAbs do not cross the placenta till 16 weeks and therefore could not play a role in early thyroid embryogenesis. All mothers have underlying AITD. This suggests that only children born to mothers with underlying AITD are at a risk for the development of TBAb-induced congenital hypothyroidism. The diagnosis of transient congenital hypothyroidism due to TBAb should be suspected whenever congenital hypothyroidism is diagnosed in the child of a mother with hypothyroidism due to AITD, particularly with Eutopic thyroid tissue on the thyroid ultrasound.
| Conclusions|| |
The conclusions of the present case would be: (1) Close monitoring of AITD in pregnancy and postpartum is necessary due to the immune switching in this period. (2) The suspicion of transient congenital hypothyroidism due to TBAb should be high in neonates born to mothers with AITD.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Garber JR, Cobin RH, Gharib H, Hennessey J, Klein I, Mechanick J, et al
. ATA/AACE guidelines for hypothyroidism in adults. Endocr Pract 2012;18:988-1028.
Lu R, Burman KD, Jonklaas J. Transient Graves' hyperthyroidism during pregnancy in a patient with Hashimoto's hypothyroidism. Thyroid 2005;15:725-9.
Weetman AP. Immunity, thyroid function and pregnancy: Molecular mechanisms. Nat Rev Endocrinol 2010;6:311-8.
Awad S, Dutton H, Shaw J, Keely E. Pregnancy and autoimmune thyroid disease: Alternating between hypothyroidism and hyperthyroidism and the role of thyrotropin receptor antibodies. AACE Clin Case Rep 2017. [In Press]. Doi: http://dx.doi.org/10.4158/EP161660.CR
McLachlan SM, Rapoport B. Thyrotropin-blocking autoantibodies and thyroid-stimulating autoantibodies: Potential mechanisms involved in the pendulum swinging from hypothyroidism to hyperthyroidism or vice versa. Thyroid 2013;23:14-24.
Wall JR, Lahooti H, Hibbert EJ, Champion B. Relationship between clinical and immunological features of thyroid autoimmunity and ophthalmopathy during pregnancy. J Thyroid Res 2015;2015:698470.
Brown RS, Bellisario RL, Botero D, Fournier L, Abrams CA, Cowger ML, et al.
Incidence of transient congenital hypothyroidism due to maternal thyrotropin receptor-blocking antibodies in over one million babies. J Clin Endocrinol Metab 1996;81:1147-51.
[Table 1], [Table 2]