PSAT357 Preventing Progression of Ophthalmopathy Using a 'Block-Replace' Treatment Strategy in Labile Graves’ Disease

Abstract

Abstract Introduction Graves’ disease is an autoimmune disorder that most commonly causes hyperthyroidism. Pathogenesis usually involves the stimulation of TSH receptors by antibodies, but in rare cases can alternate between hyper- and hypothyroidism. In this case report, we describe a patient who had labile thyroid function with persistent ophthalmopathy, requiring a temporizing "block and replace" strategy for treatment. Case Description A 53-year-old woman with a history of GERD and fibroids presented to her primary care physician with a month-long history of hand and leg tremors, weakness, heat intolerance, palpitations and worsened anxiety. She also developed eye irritation and enlargement. Thyromegaly was noted on examination. Thyroid function tests showed that TSH was <0.01 (0.45-5.33 uIU/mL) and Free T4 was 2.48 (0.61-1.12 ng/dL). TRab was 21.2 (<1.75 IU/L). Thyroid ultrasound revealed heterogeneous enlargement with increased vascularity representing thyroiditis. CT orbit revealed mild bilateral ocular proptosis with normal extraocular muscle. She was diagnosed with Graves’ disease complicated by ophthalmopathy and she was started on methimazole and metoprolol. Repeat labs six weeks later improved to TSH of 0.01 and total T4 of 6.5 (4.50-11.70 ug/dL). Unfortunately, follow up labs 2 months later revealed overt hypothyroidism, with TSH of 134 with total T4 0.9. Methimazole and metoprolol were discontinued and 75mcg of levothyroxine was started. One month later, TSH was suppressed again to 0.11 and Total T4 was 17.8, so methimazole was again added with the intent of suppressing hyperthyroidism while simultaneously replacing levothyroxine to avoid hypothyroidism. Given the difficulty of maintaining a euthyroid state and ongoing symptomatic ophthalmopathy, she eventually underwent total thyroidectomy and started levothyroxine post operatively. Pathology of the thyroid gland was consistent with Graves’ disease. Discussion Graves’ disease is typically treated with anti-thyroid medical therapy (thioamides such as methimazole), which is titrated to a euthyroid state. In our case, the patient's thyroid function varied widely on methimazole, potentially representing variable stimulating and blocking functions of TRab. As periods of hypothyroidism can worsen ophthalmopathy, a "block and replace" treatment strategy was adopted, which involves a thioamide and levothyroxine concurrently to achieve a biochemically euthyroid state. While a Cochrane review has suggested there is no improvement in relevant outcomes using this approach, it was useful in our case as a bridge to surgical management1.