Endocrine Abstracts

Introduction: Graves disease (GD) is an autoimmune disease in which thyrotropin receptor antibodies overactive the thyroid gland. Therefore, antithyroid drugs, radioactive iodine therapy, or surgical interventions are treatment options. In GD, pathology after thyroidectomy may include hypertrophy and hyperplasia in thyrocytes, mononuclear cell infiltration in the stroma, and increased blood supply. We presented a case with areas of necrosis and vasculitis due to GD in the pathological specimen obtained after a patient underwent a total thyroidectomy due to development of hepatotoxicity under antithyroid therapy.

Case: An 18-year-old female patient complained of palpitation, weakness, and fatigue. TSH was suppressed, fT4, fT3 and thyroid stimulating antibody were elevated. thyroid ultrasonography and scintigraphy also confirmed GD. After 2 months of methimazole she could not achieve adequate control and developed hepatotoxicity. Therefore she was switched to propylthiouracil and surgery was planned. On the histopathological examination, diffuse hyperplasia of thyroid follicular epithelial cells with nearly complete loss of colloid material was observed. The typical lobular structure was preserved, whereas the follicular pattern had been lost due to the pronounced lack of colloid. A focus of lymphocytic thyroiditis with accompanying pseudopapillary projections was present. Patchy areas of thyroid parenchyma showing coagulation necrosis were remarkable. In some small intraparenchymal venules, thrombotic vasculopathy was noticed. There was no cytological atypia and increased mitotic activity. Immunohistochemical test results (TTF-1 (+), PAX8 (+), calcitonin (-), GATA-3 (-)) were confirmatory of the thyroid follicular epithelial cell origin. There was no evidence of systemic vasculitis in his physical examination. Sedimentation, CRP, p-ANCA, c-ANCA, ANA, C3, and C4 were within normal ranges. PET CT did not show a systemic vasculitis.

Discussion: Vasculitis in the thyroid is not common. However, there have been few cases with giant cell arteritis or temporal arteritis in the thyroid artery. Antithyroid drug-associated vasculitis is generally ANCA-associated leukocytoclastic vasculitis and presents with skin manifestations. We did not find evidence of systemic manifestations in our case. Autoantibodies were negative. Due to absence of prominent nodular patterns, cytological atypia, increased mitosis, or solid growth pattern in histopathological examination; poorly differentiated thyroid carcinoma was excluded. The existing findings in the thyroidectomy material were evaluated as vasculitis localized to thyroid gland and related to GD.