P-52 ASYMPTOMATIC MIXED PITUITARY MACROADENOMA IN A YOUNG MALE PATIENT

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Abstract Introduction Central hyperthyroidism due to a thyrotropin (TSH)-secreting pituitary adenoma is a rare cause of hyperthyroidism, representing 0.5-1.0% of all pituitary adenomas. The etiopathogenesis of TSH-secreting-adenomas is unknown and no definite role for various oncogenes has been proven. Plurihormonal pituitary adenomas reveal greater tumor recurrence and local invasion than do mono-secreting pituitary adenomas and therefore they need to be followed more closely. Clinical Case We present the case of a 19-year-old male who was admitted to the endocrinology clinic, was asymptomatic, and had abnormal thyroid tests during routine examinations. Laboratory tests revealed TSH 1.33 (normal RI), freeT4 2.5 (high), freeT3 6.78 (high), and the patient had tachycardia (pulse 120/min) on physical examination, but had no complaints. Thyroid antibody tests were negative, and ultrasonography revealed normal thyroid gland size and homogeneous parenchyma. Alpha subunit test was requested with suspicion of TSHoma and genetic test was requested considering thyroid hormone receptor resistance. In the pituitary panel tests, the patient's GH and IGF1 tests were found to be high for his age and gender, The lowest GH value in the GH-OGTT test was 3.95 ng/mL. LH was high but testosterone was within the normal reference range. The patient was found to have mandibular prognathism and his secondary sex characteristics were normal. Pituitary MRI revealed a nodular appearance on the left side of the pituitary gland, measuring 13x9 mm, hypointense on T1A, hyperintense on T2A, and showing contrast medium uptake. The infundibulum deviates to the right, and there is no pressure on the optic chiasm. Visual field test was normal. AlphaSubunit pituitary tumor marker value was found to be high at 1.9ng/mL (RIs ≤0.5). The genetic test for resistance to thyroid hormone, also came back normal. The patient underwent endoscopic transsphenoidal pituitary adenomectomy due to pituitary macroadenoma by an experienced neurosurgeon. No postoperative complications developed. In cytopathological evaluation, histochemical studies performed with silver stain showed that the reticulin roof was lost. In immunohistochemical studies, SF-1, PIT-1, LH (diffuse), GH (densely granular), TSH (rare) and LMWK (perinuclear cytoplasmic weighted) were positive. T-PIT and Prolactin were negative. Ki-67 proliferation index was 5%. Postoperative pituitary tests were normal and no deficiency was observed and no treatment was required. At the postoperative 3rd month follow-up, the lowest GH value in the GH-OGTT test was 0.16 ng/mL, and no residual mass was observed in the pituitary MRI. The patient, who had no postoperative complaints, is being followed up by the endocrinology clinic. Conclusion Mixed pituitary tumors are rare and can sometimes appear as silent tumors, but may be aggressive during follow-up, so better follow-up is necessary.Table 1:Pituitary panel biochemical results