ODP533 Graves’ Ophthalmopathy in the Setting of Primary Hypothyroidism

Abstract

Abstract Background Graves’ ophthalmopathy (GO) is commonly associated with hyperthyroidism secondary to Graves’ disease (GD). Although rare, there have been case reports of it occurring in patients who are hypothyroid with underlying Hashimoto's thyroiditis (HT), as well as in euthyroid patients. It is thought that the mechanism behind developing GO in these patients is due to the presence of stimulating thyrotropin receptor antibodies (TRAB). Below we describe a case of GO developing in a patient who has hypothyroidism secondary to HT. Clinical Case A 53 years-old female non-smoker, known to have primary hypothyroidism (Hashimoto's thyroiditis) diagnosed at the age of 39 years, on levothyroxine 75 mcg/day. Presented to our endocrine clinic complaining of diplopia and periorbital swelling for the past 5 months. The diplopia occurs on left gaze while both eyes are open, it resolves with closure of either eye. No history of ocular surgeries, injections, or trauma. No previous hyperthyroid state or radioactive iodine therapy. On physical examination there was no goiter, bruit, palpable lymphadenopathy, tremor, or pretibial myxedema. Ophthalmic examination showed left sided upper and lower eyelid swelling, limited abduction with diplopia and mild punctate keratopathy. Laboratory investigation revealed TSH 3.6 mIU/L (0.250 - 5), T4 14.6 pmol/L (11.5 - 22.7), positive thyroid peroxidase antibody 173.9 units (> 100 units positive) and positive thyroid stimulating immunoglobulin 500IU/ml (Normal < 140). On ultrasound the thyroid gland was small and heterogeneous. MRI orbits demonstrated bilateral ocular proptosis with intraocular muscles enlargement particularly the medial, inferior, superior rectus as well as the levator palpebrae superioris muscles. Our impression was active moderate-severe isolated GO with aBackground of HT, clinically and biochemically euthyroid on levothyroxine. The patient was referred to an ophthalmologist and was started on a course of high dose oral prednisone tapered over 3 months. She reported a 50% improvement in her symptoms after the first month of therapy. Patient was then started and maintained on selenium 100 mcg oral twice daily with lubricating eyedrops. During her last clinic visit she had stable thyroid eye disease and there was no need for further medical or surgical intervention. Conclusion GO can occur in patients with HT due to the development of stimulating TRAB targeting thyrotropin receptors expressed on orbital fibroblasts. The incidence varies between studies from 2-7.5%. Awareness of this clinical presentation is important, as early detection and treatment can prevent visual complications. To date there are no clear guidelines on how to treat GO with underlying HT. Treating our patient with high dose steroids extrapolated from treating GO secondary to GD showed significant improvement in her symptoms. Presentation: No date and time listed