SUN-568 Steroid Induced Psychosis Complicating the Treatment of Graves Ophthalmopathy

Abstract

Introduction: Graves‘disease is an autoimmune disorder in which the thyroid is activated by antibodies to the thyrotropin receptor. The annual incidence in women over a 20-year period is around 0.5 per 1000, with the highest risk of onset between the ages of 40 and 60 years; it is thus the most prevalent autoimmune disorder in the United States1. This is 1/10 as common in men as in women. Treatment of Graves’ disease can be complicated by intrinsic aspects of the disease itself and also by effects of the therapy chosen. Case report: A 49 year old man presented to our emergency department with a three month history of palpitations, weight loss, heat intolerance, sweating, eye irritation and tremors. Physical examination revealed tachycardia (107 bpm), a fine tremor to the outstretched hands, bilateral stare, diffuse thyromegaly with bruit. Labs: TSH < 0.005 (0.35-3.4 uIU/ml), TT3 604 (70 -190 ng/dl), TT4 25.28 (4.5 - 12.1ug/dl), TSI 341 (< 140 %). Treatment was started on methimazole 10mg TID and propranolol 20mg TID. He had homogenous activity with a 24 hour uptake of 78 % on thyroid isotope scan. Diagnosis of Graves ’ disease was made and he was treated with 6.1 mCi of RAI. One month later, the patient presented with stare, conjunctival chemosis, lid lag, increased lacrimation, restricted extra ocular muscle movements worse on upward gaze, and periorbital edema. He was seen by Ophthalmology and started on prednisone 60 mg PO daily, with improvement in ocular findings. Two weeks thereafter was started, patient presented with agitation and anxiety. TSH was 0.006, TT4 9.4, TT3 88. Steroid induced psychosis was diagnosed and the prednisone dose was reduced, then gradually tapered off. The psychosis resolved. Post 131I Hypothyroidism developed and he became euthyroid with L-thyroxine replacement. Discussion: Graves’ ophthalmopathy occurs in a mild form in 25% to 50% of patients with Graves’ disease, with about 3% to 5% of patients having severe eye disease. Smoking, high levels of pre-treatment T3 (more than twice the upper limit of normal) and RAI induced release of retro orbital antigens cross reacting with thyrotropin receptor antigen are associated with an increased risk of ophthalmopathy .The risk of developing ophthalmopathy is around 20% after RAI and the risk of severe ophthalmopathy is around 7%1. At least 12 months follow-up after RAI is essential as ophthalmopathy usually develops or worsens within 6 months after RAI but can occur even after 2 years. Early treatment with glucocorticoids in appropriately selected patients is recommended for active, moderate to severe and sight-threatening disease. Serious neuropsychiatric effects occur in about 6% of patients who receive steroids.3 Although the effects of glucocorticoids are unpredictable, the administered dose is the most significant risk factor for the development of neuropsychiatric symptoms. Dosage reduction typically results in clinical recovery.