Evolution from Hypothyroidism to Thyrotoxicosis and Back to Hypothyroidism

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

Poster Board SAT-466
Yewxin Teh* and Matthew Gilbert
University of Vermont College of Medicine, Burlington, VT
Evolution from Hypothyroidism to Thyrotoxicosis and Back to Hypothyroidism

Yewxin Teh MD., Matthew Gilbert DO., MPH.

University of Vermont College of Medicine, Burlington, VT

Background: Hashimoto thyroiditis and Graves’ disease are the two most common autoimmune thyroid diseases. Graves’ disease following primary hypothyroidism is rare(1). We describe a case with three cycles of thyroid function evolution, starting with thyroperoxidase antibody-negative hypothyroidism, followed by Graves’ hyperthyroidism, and back to hypothyroidism.

Clinical Case: A 76-year-old woman with atrial fibrillation and osteoporosis was diagnosed with subclinical hypothyroidism two years ago with a TSH of 11.4 μIU/ml (0.4-4), free T4 of 0.8 ng/dl (0.5-1.5), and total T3 of 84 ng/dl (60-181). Thyroperoxidase antibody was negative. Levothyroxine (LT4) 25 μg daily was started and subsequently increased to 50 μg daily. Three months after initiation of LT4, TSH was 3.1 μIU/ml. One year later, repeat laboratory evaluation revealed thyrotoxicosis with a TSH of <0.01 μIU/ml, and free T4 of 1.7 ng/dl. The patient’s LT4 dose was reduced to 25 μg daily. Despite the decrease in dose, repeat blood work drawn two months later revealed persistent thyrotoxicosis (TSH of <0.01 μIU/ml and free T4 of 2 ng/dl). Levothyroxine was discontinued, and repeat laboratory testing four weeks later showed improvement in free T4 to 1.4 ng/dl and a TSH that remained suppressed at <0.01 μIU/ml. Thyroid stimulating immunoglobulin and TSH receptor antibody returned elevated at 3.7 TSI index (≤1.3) and >40 IU/L (0-1.75) respectively. Two months later during an evaluation in the endocrine clinic, she was clinically euthyroid and without thyromegaly. She denied exposure to iodine-containing medications or intravenous contrast. Repeat laboratory evaluation revealed a low, but improved TSH of 0.24 μIU/ml (0.35-5), and low normal free T4 of 0.8 ng/dl (0.8-1.8), suggesting a trend towards hypothyroidism.

Conclusion: This case describes alternations of thyroid function between hypothyroidism, hyperthyroidism and back to hypothyroidism. This could be caused by coexistence of TSH receptor antibody (TSHRAb) varieties, including stimulating, blocking and neutral TSHRAbs. Stimulating TSHRAbs result in Graves’ hyperthyroidism. Blocking TSHRAbs result in hypothyroidism and can be found in up to 15% of patients with autoimmune thyroiditis. Determination of thyroid function depends on the relative concentration and bioactivity of the different autoantibodies(2).

(1) Takasu N, et al. Graves’ disease following hypothyroidism due to Hashimoto’s disease: studies of eight cases. Clin Endocrinol (Oxf) 1990 Dec;33(6):687-98. (2) Kraiem Z, et al. Changes in stimulating and blocking TSH receptor antibodies in a patient undergoing three cycles of transition from hypo to hyperthyroidism and back to hypothyroidism. Clin Endocrinol (Oxf) 1992 Feb;36(2):211-4.

Nothing to Disclose: YT, MG

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