Endocrine Abstracts

JOINT1085

Introduction: Thyroid-associated orbitopathy (TAO) is uncommon in patients with Hashimoto’s thyroiditis (HT), with a prevalence of 10.36% in those with hypothyroidism. In rare cases, hypothyroidism, orbitopathy, and elevated TSH-receptor autoantibodies (TRAbs) can be associated.

Case Presentation: A 62-year-old male presented with sight-threatening TAO and recently diagnosed hypothyroidism. Three months earlier, he had been started on levothyroxine (75 µg/day) for symptoms of asthenia, myxedema, constipation, and mild exophthalmos without signs of activity. Initial thyroid function tests revealed significantly elevated TSH (34 mIU/l [0.25-4.5]) and low free thyroxine (fT4) (3 pmol/l [12-22]). Upon admission to the ophthalmology department, the patient exhibited severe active orbitopathy, characterized by bilateral visual acuity of 3/10, restricted upward and abduction eye movements, and eyelid swelling. Laboratory investigations showed normal thyroid function (TSH: 4 mIU/l, fT4:11.6 pmol/l) under regular levothyroxine therapy, significantly elevated TRAbs (32 IU/l, normal <2 IU/l), and markedly high anti-thyroid peroxidase antibodies (Anti-TPO) (500 IU/ml, normal <50 IU/ml). Orbital MRI revealed bilateral, symmetrical hypertrophy of the extraocular muscles compressing the optic nerves at the apices and grade 3 exophthalmos. Thyroid ultrasound showed a heterogeneous, pseudonodular gland suggestive of thyroiditis. Treatment involved high-dose intravenous methylprednisolone (1000 mg/day for three consecutive days), achieving partial improvement, followed by a cumulative corticosteroid dose of 4.5 g administered over 12 weekly injections. Selenium supplementation (200 µg/day) was initiated, associated with levothyroxine therapy. At the six-month follow-up, ophthalmological evaluation revealed resolution of oculomotor restriction, absence of disease activity, and improved bilateral visual acuity (5/10). However, persistent TSH suppression, despite adjustments in levothyroxine dosage, led to a six-month interruption of therapy. Subsequent follow-up tests revealed TSH of 0.01 mIU/l[0.25-4.5], fT4 of 16 pmol/l[12-22], undetectable TRAbs levels, and persistently elevated Anti-TPO.

Conclusion: The literature describes different types of TRAbs, including thyroid-stimulating and TSH-blocking autoantibodies, each linked to distinct clinical syndromes. In this case, the predominance of blocking-type TRAbs may explain the presence of hypothyroidism. A multidisciplinary approach is crucial for optimizing outcomes in TAO, particularly in complex cases. Long-term follow-up is essential to monitor both thyroid function and ocular health.