Endocrine Abstracts

JOINT2804

Introduction: Thyroid-associated ophthalmopathy (TAO) is predominantly linked to Graves’ disease, manifesting in approximately 25-50% of such patients. However, its association with Hashimoto’s thyroiditis (HT) is rare, with only isolated reports in the literature. The presence of recurrent TAO in HT is even more uncommon and presents unique diagnostic and therapeutic challenges. This case highlights recurrent moderate-to-severe TAO in a patient with HT, requiring systemic corticosteroid therapy.

Case Presentation: An 80-year-old female with a 15-year history of hypothyroidism secondary to HT, diabetes mellitus, and hyperlipidemia presented with progressive orbital symptoms, including erythema, swelling, diplopia, and burning sensations. Examination revealed bilateral proptosis (Hertel: 22 mm in the right eye, 23 mm in the left eye), conjunctival hyperemia, and a Clinical Activity Score (CAS) of 5/7, indicating active and moderate-to-severe TAO. The patient was receiving treatment with levothyroxine (75 µg/day), rosuvastatin (10 mg/day), and linagliptin (5 mg/day). Laboratory investigations demonstrated normal TSH (1.22 mIU/L), normal free T3 (4.05 pmol/L), normal free T4 (16.9 pmol/L), and significantly elevated thyroid receptor antibody (TRAb) (19.97 IU/L). Anti-thyroid peroxidase (Anti-TPO) and anti-thyroglobulin (Anti-Tg) antibodies were positive. Orbital magnetic resonance imaging (MRI) revealed no evidence of compressive optic neuropathy. The patient received a cumulative dose of 4.5 g of methylprednisolone over 12 weeks. Following treatment, the CAS decreased to 1/1, and the ophthalmopathy became inactive. However, 11 months after completing therapy, ocular symptoms recurred, with a CAS of 4/4 and an increased bilateral Hertel measurement of 24 mm. Thyroid function tests revealed TSH: 16 mIU/l, normal free T4 levels, and an elevated TRAb level of 27 IU/L. The levothyroxine dosage was increased and a 6-week course of methylprednisolone therapy was planned for active ophthalmopathy.

Conclusion: The pathogenesis of TAO in HT remains poorly understood, it may involve a different immunopathogenic mechanism, primarily mediated by TRAb and local inflammatory cytokines. Recent case reports have highlighted instances of TAO in patients with Hashimoto’s thyroiditis, even in the absence of TRAb. Corticosteroids are the first-line therapy for active disease. Our patient received a cumulative dose of 4.5 g of methylprednisolone over 12 weeks, leading to a temporary resolution of symptoms. However, relapse occurred 11 months post-treatment, requiring a second cycle of steroid therapy. Optimizing thyroid hormone replacement is crucial in hypothyroid TAO cases, as untreated hypothyroidism may exacerbate orbital inflammation. In summary, while TAO is uncommon in HT, clinicians should remain vigilant for ocular manifestations in these patients.