ESPE Abstracts

Introduction: Thyroid ophthalmopathy, also known as Graves ophthalmopathy, is an autoimmune condition that can affect the orbital and periorbital tissue. Antibodies stimulating the TSH receptor (TRAb) are thought to be involved in the pathogenesis of this disease. Our report describes a case of Graves’ ophthalmopathy presented solely with symptoms of the eyes with normal thyroid function tests and negative immunoreactive TSH receptor autoantibody.

Case presentation: A 14-year-old adolescent was referred to our hospital due to a 3-month history of mild protrusion of his left eyes and pain. On physical examination, his pubertal examination found that he is on tanner 4. His weight is 50 kg (-0,13 SD), height: 168 cm (+0,62 SD), the Body Mass Index (BMI) is 17.7 kg/m² (-0,61 SD). He had a normal blood pressure, no tachycardia, without any signs or symptoms of hyper- or hypothyroidism. Ophthalmological examination has revealed exophtalmous of the left eyes, conjunctiva was congested and there was a corneal lesion on his left eyes. Intraocular pressure and visual acuity were normal. Serum thyroid function tests were within the normal range. Anti-thyroid autoantibodies were all negative. Ultrasonography of the thyroid gland was performed and showed a normal-sized gland. We diagnosed this case as TRAb negative euthyroid Graves’ ophthalmopathy and the patient was treated with oral corticosteroids and local ophthalmic therapy, leading to a good improvement of the symptoms. However, following the thyroid profile in our patient, one year later, antibodies became positive, hyperthyroidism appeared and the patient was treated with Carbimazole.

Discussion: Our patient presented with symptoms, signs of Graves’ ophthalmopathy but with negative TRAb. Although TRAb in this case was initially negative but which subsequently became positive, suggesting the involvement of autoimmune etiology, establishing the definitive diagnosis of Graves’ ophthalmopathy was difficult. Mechanism suggested in Graves’ ophthalmopathy is that the autoantigen called calsequestrin derived from ocular muscles serves as a target of autoimmunity. Although its pathogenic role remains controversial. Calsequestrin is now recognized as a new and precise biomarker of ophthalmopathy in people with Graves' disease. In the present case, however, oral corticosteroid therapy and adjunct opthalmic therapy led to an improvement of the ocular symptoms.

Conclusion: The case highlights the difficulties in diagnosing a euthyroid patient with negative anti-thyroid autoantibodies. Hence the interest of regular monitoring over time in these patients. We also emphasize the interest of corticosteroids in the treatment of this disease.