LAUSR

Graves’ disease (GD), a common autoimmune disease clinically characterized by goiter, hyperthyroidism, and orbitopathy (GO), is caused by antibodies directed against the TSH-receptor (TRAb). These antibodies are responsible for hyperthyroidism and contribute to GO and, possibly, pretibial myxedema and acropachy. GD is first treated with thionamide antithyroid drugs (ATD), but requires thyroid ablation with either radioiodine or thyroidectomy when relapse after one or two thionamide courses occurs or if longterm ATD treatment, a safe alternative treatment for GD [1], fails or is not feasible. Total thyroidectomy is preferred when the goiter is large and multinodular, when nodules suspicious for malignancy or hyperparathyroidism coexist, when avoiding exposure to radiation is critical (as for women who desire to become pregnant or have recently delivered), or when a rapid resolution of the hyperthyroidism is desired [2]. Patient’s choice is also essential. GD is characterized pathologically by (1) hypertrophy and hyperplasia of thyrocytes, (2) stromal infiltration with hematopoietic mononuclear cells, and (3) increased vascularity. Histopathological heterogeneity, however, does exist. Goiter size, for example, can vary greatly, lymphocytic infiltration can range from minimal to mature germinal centers, and thyroid nodules can be present. It remains uncertain whether GD is responsible for the development or the aggressiveness of differentiated thyroid cancer (DTC), but some studies suggest that this might be the case [3, 4]. Aim of this retrospective study was to analyze the surgical pathology archive of the Department of Pathology of the Johns Hopkins Hospital to gain further insights on the GDDTC relationship.