Endocrine Abstracts

JOINT3882

Introduction: The presence of hyperthyroidism is no longer considered a protective factor against the development of thyroid cancer. The coexistence of differentiated thyroid cancer and Graves’ disease(GD) is a well-documented but rare phenomenon, with reported prevalence rates ranging from 0.1% to 9.8% in the literature. We present two cases of female patients with hyperthyroidism secondary to GD who were subsequently diagnosed with differentiated thyroid cancer.

Case Reports: Case 1: A 49-year-old female patient with a two-year history of GD was managed with antithyroid drugs (ATD). She developed drug-induced cholestasis as a side effect of ATD therapy. Clinical examination revealed bilateral firm cervical lymphadenopathies. Cervical ultrasound demonstrated a nodular thyroid structure, with the largest nodules located in the upper right lobe(14 mm)and the mid-left lobe, classified as EU-TIRADS IV. Due to ATD intolerance and the presence of cervical lymphadenopathies, the patient underwent total thyroidectomy with bilateral mediastino-recurrent lymph node dissection (MRLD). Histopathological analysis identified three foci of papillary thyroid carcinoma (PTC) without lymph node involvement. Postoperatively, the patient received an ablative dose of radioactive iodine (100 mCi), achieving a favorable biochemical and morphological response. Case 2: A 68-year-old female patient with GD exhibited resistance to medical treatment with ATD. A radical surgical approach was pursued, and she underwent total thyroidectomy with bilateral MRLD. Histopathological examination revealed a 2 cm papillary thyroid carcinoma in the right lobe and a 3 cm thyroid tumor with malignant potential in the left lobe. The tumor was classified as pT2NxMx. She received ablative therapy with 30 mCi of radioactive iodine, resulting in a good therapeutic response.

Conclusion: The pathogenesis underlying the association between GD and thyroid cancer remains incompletely understood. Cervical irradiation is a recognized risk factor for thyroid cancer, as it induces nuclear modifications that may initiate tumorigenesis. Additionally, it may contribute to the development of hyperthyroidism. Damaged thyroid cells with reduced hormone production may be subjected to increased thyrotropic stimulation, potentially promoting tumor proliferation. Furthermore, antithyroid therapy has been implicated in this association, as it normalizes previously suppressed TSH levels, which may facilitate tumor growth. Dobyns et al. reported a higher incidence of thyroid cancer in patients treated medically for hyperthyroidism compared to those managed with radioiodine therapy or surgery. The possibility of thyroid cancer in patients with GD should not be overlooked. A malignancy workup should be considered, and a diagnostic approach similar to that for any thyroid nodule should be applied. Early detection and appropriate management are crucial for optimizing outcomes in these patients.