Thyrotoxicosis in Pregnancy Following Long-standing Autoimmune Hypothyroidism

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SAT 449-497-Thyroid Neoplasia & Case Reports
Clinical
Saturday, June 15, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SAT-495
Nupur Bahl*1 and Geetha Gopalakrishnan2
1Brown Univ, East Providence, RI, 2Alpert Medical School of Brown U, East Providence, RI
Introduction/Background:

Chronic autoimmune (Hashimoto's) thyroiditis generally results in a cell- and antibody-mediated destruction of thyroid tissue requiring thyroid hormone replacement. Although hypothyroidism is typically permanent in Hashimoto’s thyroiditis, remission can occur indicating it is not always caused by thyroid gland destruction. We report a case of a 38 year old with a 5 year history of Hashimoto’s thyroiditis who presents with thyrotoxicosis during pregnancy requiring PTU therapy.

Clinical Case:

Patient was diagnosed with Hashimoto’s hypothyroidism in 2007 at which time her anti-TPO Ab was 8175.6 (1-60 IU/mL). She was started on levothyroxine and titrated to 75 mcg/day with TSH maintained in the normal range. A thyroid US showed autoimmune thyroiditis without nodules. Pertinent medical history includes a miscarriage in 2007, delivery of healthy twins in 2008 requiring thyroid hormone replacement of 100 mcg/day to maintain a TSH of 1-2 uIU/mL, and preterm premature rupture of membrane at 17 weeks resulting in fetal demise in 2010.

Subsequently her thyroid hormone dose was titrated down based on thyroid function tests and eventually stopped in 2011 when she developed symptoms of palpitations, tremor, hyperdefecation, and heat intolerance. Labs 1 month after discontinuing thyroid hormone showed a positive pregnancy test, TSI 357 (<140), TSH <0.003 (0.35-5.5 uIU/mL), TT3 231 (80-180 ng/dL), and FT4 1.54 (0.8-1.8 ng/dL). She was diagnosed with Graves disease and noted to be 6 weeks pregnant. She was treated with PTU during the first trimester and transitioned to MMI in the 2nd trimester. MMI was titrated off 3 months prior to delivery with T3 and T4 levels maintained in the upper end of normal range. She delivered a healthy baby boy. In the post-partum period, she again developed hypothyroidism for which thyroid hormone replacement was restarted.

Conclusion:

This case demonstrates the role of both blocking and stimulating antibodies in the pathogenesis of autoimmune thyroid disorders. Although most cases of Hashimoto’s thyroiditis results in hypothyroidism and requires increases in thyroid hormone replacement during pregnancy, stimulating antibodies and the risk of maternal and fetal thyrotoxicosis should also be considered in these patients with autoimmune thyroid dysfunction.

Disclosure: GG: Investigator, Amgen, Investigator, Novartis Pharmaceuticals, Investigator, Takeda, Investigator, Roche Pharmaceuticals, Investigator, Novo Nordisk. Nothing to Disclose: NB

*Please take note of The Endocrine Society's News Embargo Policy at http://www.endo-society.org/endo2013/media.cfm