ODP615 Emergence of Graves’ Ophthalmopathy in the Setting of Sudden Hypothyroidism: Possible Mechanisms Explored
Authors: Suelto Jeremy Anne , Isidro Maria Jocelyn 
Published: November 2022

Abstract

Background
Ninety percent of thyroid eye disease (TED) patients are hyperthyroid and at least 10% of TED occurs in the setting of euthyroidism or hypothyroidism. When Graves’ hyperthyroidism is diagnosed, 74% may not present with ophthalmopathy.

Clinical Case
A 58 year old woman diagnosed with Multinodular nontoxic goiter ﻿without nodule suspicious for malignancy was carefully monitored. No Levothyroxine treatment started. In 2017, patient had sudden onset of tremors, weight loss and palpitations. There were no signs of thyroid associated orbitopathy. Her TSH was &lt;0. 009 uIU/ml (0.30-4) and FT4 29. 06pmol/L (10-22). Thyroid scan showed elevated 2- and 24-hours RAI uptake (as high as 80%) in both lobes. She was started on Methimazole but developed adverse reactions hence RAI (10 mci) was given. A month after RAI, she was rendered hypothyroid with of TSH 73.48uIU/ml (0.27-3.75), FT4 2.257pmol/L (8.8-44). She was maintained on Levothyroxine and remained euthyroid for four years. One year post RAI, ultrasound showed a small sized thyroid gland (right lobe: 3×0.6×1.5cm and left lobe: 2.2×0.3×1.3cm). May 2021, she followed up due to bulging eyes with scratchy sensation. She was noncompliant with Levothyroxine for several months. TSH was elevated to 46.19 uIU/ml (0.3-4. 00) and FT4 12.35 pmol/L (10.20-22.50). Levothyroxine dose was adjusted and repeat TSH was normal to 0.38 uIU/ml (0.30-4. 00) with FT4 of 22.40 pmol/L (10.20-22.50). Despite euthyroidism, there were progressive eye protrusion, conjunctival redness, pain and blurring of vision. TSHrAb was elevated to 21.62 U/L (N: &lt;1 U/L). TSI was elevated to 6.59 IU/L (N: &lt;0.10). . MRI of the orbit showed findings suggestive of Graves’ ophthalmopathy. She was started on Prednisone 60mg/day. Repeat TSHrAb was 9.85 U/L (&lt;1U/L) after 3 weeks of steroids. Levothyroxine was stopped to check whether she had recurrence of Graves’ disease. When Levothyroxine was discontinued, there was worsening of eye disease and it was confirmed that patient was hypothyroid with TSH of 48.91 uIU/ml (0.55-4.78). Levothyroxine was resumed at 100mcg 1 tablet once daily and continued with Prednisone in tapering doses.

Conclusion
There were possible mechanisms that can lead to Graves’ ophthalmopathy in patients who had RAI and suddenly became hypothyroid. The rapid and protracted hypothyroidism caused increased secretion of TSH that stimulate antigen production by thyrocytes or induce proliferation in retro-orbital preadipocytes which express the TSH receptor. The protracted hypothyroidism can also be related to fluctuating TSHrAb post RAI. It was suggested that remission of TSH-receptor autoimmunity after RAI is less common. Clinicians should acquire baseline and monitoring of TSHrAb or ophthalmology consultation for all patients undergoing RAI regardless of whether they have eye signs or not. Maintenance of euthyroidism will help prevent emergence of Graves’ ophthalmopathy.
Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.