231 Unusual coexistence of differentiated thyroid cancer and thyrotropin- producing pituitary microadenoma: a case report 1 Muni A., 1 Rouhanifar H., 1 Zanaga M., 1 Zoccola R., 1 Testori O., 2 Versari P., 3 Ansaldi E, 3 Rosti G., 4 Arfini C., 5 Rolandi G. (1)Nuclear Medicine Unit, SS Antonio e Biagio Hospital of Alessandria, Italy (2) Neurosurgery Unit, SS Antonio e Biagio Hospital of Alessandria, Italy (3) Endocrinology Unit, SS Antonio e Biagio Hospital of Alessandria, Italy (4) Laboratory Unit, SS Antonio e Biagio Hospital of Alessandria, Italy (5) Radiology Unit, SS Antonio e Biagio Hospital of Alessandria, Italy fig. 1 MRI of the sella turcica. A pituitary microadenoma is shown fig. 2 MRI of the sella turcica after selective surgical removal of the microadenoma Background The TSH-producing pituitary adenoma represents only 2% of all pituitary cancers; it is a rare condition which becomes exceptional when associated with a thyroid differentiated carcinoma. Coexistence of these two pathologies is very rare: a survey of the specific literature found only four similar cases Case Report A 34-year-old euthyroid woman was referred from another institution for evaluation after thyroidectomy for thyroid papillary carcinoma. (pT 1 No Mx). After surgery, she wasn’t given any levothyroxine therapy, and four weeks later she received routine radioiodine ablation of the residual thyroid tissue. On this occasion, very high levels of TSH (620 mU/l) were found, with undetectable free thyroid hormones and 0.2 ng/ml thyroglobulin; the post therapy 131I scintiscan revealed only a small area of 131 I uptake in the thyroid bed. Levothyroxine treatment (0.15mg/d) was subsequently instituted, with the aim to be TSH-suppressive. Three months later, with normal FT3 and FT4, TSH was still 16 mU/l. Levothyroxine was increased to mg/d, but 8 months later TSH was 145 mU/l. She then came to our Nuclear Medicine Unit. Inadequate TSH secretion was suspected; it was confirmed by a MRI study, which demonstrated a pituitary microadenoma, and by the control of every pituitary hormone: only TSH was high. The patient underwent trans- sphenoidal resection of the microadenoma. The success of the operation was assessed four months later by MRI. TSH progressively fell to zero in six months (usually the fall is faster, so she will be restaged for persistence of residual TSH pituitary adenoma). One year later she was restaged under the stimulation of rhTSH: the 131 I WB scan was negative for persistence/ recurrence/ mts, thyroglobulin didn’t raise. She is now considered NED (no evidence of disease). Some considerations: In a patient on suppressive dose of l-thyroxine, high TSH levels with normal free hormones values must suggest that an unusual secretion of TSH is going on: a pituitary MRI will be suitable for the diagnosis. The different factors involved as etiological agents in thyroid cancer have in common long term thyroid follicle stimulation. On this base, a patient with a TSH-producing pituitary adenoma could be at high risk of developing thyroid cancer. Although very rare, the TSH-producing pituitary adenoma can play an important role in stimulating the multiplication of the thyroid differentiated neoplastic cells. In fact, on the one hand, TSH induces the expression of growth factors and of their receptors; it may contribute to an increased responsiveness to growth factor stimulated tyrosine kinase signalling with consequent proliferation. On the other hand, growth factor expression may increase proliferation regardless of the prevailing TSH levels. Patients operated both for differentiated thyroid carcinoma and TSH-producing pituitary adenoma require rhTSH for scanning and treatment with 131I, having a secondary failure to generate endogenous TSH. post therapy 131I scintiscan