ECE2015 Eposter Presentations Thyroid (non-cancer) (160 abstracts)
1Department of Endocrinology and Metabolism, Uludag University Medical School, Bursa, Turkey; 2Clinic of Endocrinology and Metabolism, Sevket Yilmaz Training and Research Hospital, Bursa, Turkey; 3Department of Internal Medicine, Uludag University Medical School, Bursa, Turkey.
Classic thyroid hormone resistance (THR) occurs per every 400 000 live birth. THR should be considered along with TSH-producing adenomas when normal or high levels of TSH not consistent with hyperthyroidism is present. A 45-year-old female patient who was operated three times for multinodulary goitre had been treated with L-thyroxine. Mamillary biopsy had performed after detection of mass localized in right breast by mammography performed during regular follow-up, then right radical mastectomy was performed due to the diagnosis of ductal carcinoma. In thyroid USG examination, it was found that there were three to four nodules in right thyroid lobe sized 9×6.5 mm and nodules with hypoechoic solid-nature which largest of them was 16×11 mm in left thyroid lobe. In addition, there were also ovoid-shaped lymph nodes with fatty hiluses in both cervical lymphoid chains as two of them (largest one sized 26×5 mm) in right zone 3 and three of them (largest one sized 25×6 mm) in left zone 3. Thin needle aspiration biopsy was performed on thyroid nodules and cervical lymph nodes. Results were benign. Cella magnetic resonance imaging (MRI) was performed with diagnosis of secondary hyperthyroidism after detection of elevated TSH, fT3, and fT4 levels in thyroid tests. In cella MRI, it was found that there was an adenoma sized 11×9×10 mm in hypophysis gland. Other anterior hypophysis hormones were normal. There were no eyesight pathology. L-thyroxine treatment was ceased due to the euthyroid status of the patient. During tests performed for excluding THR, it was found that alfa subunit (ASU) level was in normal range (0.35) and molar ASU/TSH ratio was below 1. These results were consistent with THR. Then, TRH stimulation test was planned. TSH levels at 0, 15, 30, 45, and 60 min after TRH administration were obtained. It was observed that there was an extensive response consistent with THR in TSH levels with TRH test (TSH at 0 min: 8 mIU/ml, TSH at 15 min: 57 mIU/ml, TSH at 30 min: 76 mIU/ml, TSH at 45 min: 75 mIU/ml, and TSH at 60 min: 67 mIU/ml). Hypothyroidism symptoms were not observed in follow-up without medication. Adenoma size had not been changed in control sella MRI. Anterior hypophysis hormones were in normal range. Patient was enrolled in follow-up with the diagnosis of THR and non-functional hypophysis adenoma. In clinical practice, differentiation between TSH-secreting adenomas and THR is quite difficult. Predominance of hyperthyroidism symptoms and presence of macroadenoma in hypophysis make the possibility of TSH-secreting adenoma more convincing. However, most of the patients are asymptomatic. Considerable elevations in TSH levels increase the possibility of TSH-secreting adenoma although thyroid function tests are mostly same in both of these pathologies. TRH stimulation test is the most valuable test for diagnosing. Its sensitivity and specificity were reported as 90% and 8090% respectively. In conclusion, THR should be considered before diagnosing as TSH-secreting adenoma in patients evaluated for secondary hyperthyroidism and identified with hypophysis adenoma.