Abstract
INTRODUCTION: The frequency of pituitary adenomas (PAs) with simultaneous co-secretion of GH and PRL is approximately one-third, while the frequency of those producing both GH and TSH is relatively low. Such plurihormonal PAs, usually of the PIT-1 lineage, can be hormonally active or clinically silent. Here, we present a case of plurihormonal PA diagnosed with thyrotoxicosis and accompanied by papillary thyroid carcinoma (PTC). CLINICAL CASE: A 44-year-old male patient, who was considered for surgery with the diagnosis of multinodular goiter, was referred to our endocrinology clinic due to hyperthyroidism, and discordant thyroid function test. The patient complains of palpitations, tremors and sweating for 3 months. The patient stated that his thyroid hormones had not returned to normal with medication administered by an external center. On physical examination, there was no hormonal hypersecretion/hyposecretion phenotype other than multinodular goiter and hyperthyroidism. Elevated thyroid hormones (FT4:2.7 ng/dL;0.89-1.7 and FT3: 6.8 ng/dL;2-4.4) together with non-suppressed TSH of 2.6 uIU/mL (0.27-4.2) were consistent with secondary hyperthyroidism. Pituitary MRI showed an adenoma (11x8mm) (Fig.1a). Other anterior pituitary hormones included moderately elevated IGF-1 (286ng/ml; 1.4xULN for age and age-matched), borderline elevated PRL (15.3µg/L;4.04-15.2), and normal GH (1.02 ng/ml;0.3-2.47). Total testosterone and basal cortisol were normal. He also had clinically silent GH excess. In thyroid ultrasonography, there were nodules measuring 8 mm in the isthmus and 2.6 cm in the left lobe, in addition to the 3.0 cm diameter nodule in the right lobe for which FNAB was recommended. Transsphenoidal surgery (TSS) was performed after clinical euthyroidism was achieved with Lanreotide. Following surgery, thyroid functions tests and IGF1 level remained within normal limits. Histopathological examination confirmed a Pit-1-positive plurihormonal adenoma with strong immunoreactivity for TSH and GH and scattered PRL positivity, Ki-67 was<1% (Fig.2a). After euthyroidism was achieved, the histopathology of the right nodule for which FNAB was recommended was follicular adenoma. The patient, whose postoperative euthyroidism continued, underwent total thyroidectomy because pituitary residue was detected in MRI (Fig. 1b). In the pathology specimen of the thyroid follicular variant of PTC was detected histopathologically (Fig.2b). Apart from capsule invasion of the tumor, no vascular or lymphatic invasion were evident. CONCLUSION: This case highlights the possibility that differentiated thyroid carcinoma can co-exist with a pulirihormonal PA, a rare cause of thyrotoxicosis. Primary surgical treatments for both pathologies play an important role in both tumor control and thyrotoxicosis treatment. GH/TSH hypersecretion may also negatively impact the other tumor. Multidisciplinary evaluation and personalized treatment strategies are essential. [Figure: see text]