SAT-581 Graves' Disease and Hashimoto's Thyroiditis: Two Ends of a Spectrum

Abstract

Autoimmune thyroid disease, characterized by the presence of specific anti-thyroid antibodies, is the most common cause of thyroid dysfunction and can lead to either hypo- or hyperthyroidism. In rare cases, thyroid function spontaneously shifts from one extreme to the other. A 32 year old man with an 8 year history of hypothyroidism was referred to our clinic for evaluation of hyperthyroidism. He had been on levothyroxine (LT4) replacement, requiring up to 300 µg qd until about 6 months before coming to our attention, when he sustained a 60 lb weight loss. TSH was suppressed and the LT4 dose was progressively decreased to 75 µg qd. On presentation, the patient was clinically euthyroid. He had no family history of thyroid disease. No thyromegaly was noted. Eye exam showed conjunctival injection without proptosis, chemosis, periorbital edema or abnormal extraocular movements. TSH was <0.01 µUI/ml (0.27-4.2) and FT4 1.91 ng/dl (0.8-1.8). Thyroid stimulating antibodies were positive at 418% (<123). LT4 was discontinued and, a month later, given persistence of hyperthyroidism, the patient was started on methimazole (MMI). Thyroid function initially normalized but hyperthyroidism recurred once the dose of MMI was tapered. The patient elected to undergo thyroidectomy 6 months later. Pathology was consistent with Graves disease. He was restarted on LT4 and euthyroidism was achieved 8 months later with 300 µg qd (2.9 µg/kg). Celiac disease screening was negative. A year after undergoing thyroidectomy, the patient experienced discomfort and bulging of the left eye without any vision changes. CT of the orbits showed mild enlargement of the extraocular muscles bilaterally and orbital fat expansion with left greater than right exophthalmos. Ophthalmologic evaluation confirmed active Graves’ orbitopathy (GO) with clinical activity score 4 and exophthalmos (left eye 23 mm, right eye 19 mm). Few cases of Graves’ disease following a diagnosis of autoimmune hypothyroidism have been reported. Both entities exist at opposite ends of the spectrum of thyroid autoimmunity. It is possible that, at the onset of disease, this patient preferentially produced thyroid blocking antibodies rather than thyroid stimulating antibodies, causing hypothyroidism. Alternatively, de novo thyroid stimulating antibodies were produced later in the course of disease. Contrary to what is observed with radioactive iodine treatment, the risk of GO is not increased after thyroidectomy, especially in patient with inactive GO. However prolonged hypothyroidism after definitive treatment of hyperthyroidism is a risk factor for GO and may have contributed to the patient’s clinical picture.