FRI555 A Misdiagnosis Of TSH-secreting Adenoma With Thyrotoxicosis In A Patient With Graves’ Disease

Abstract Disclosure: J. Huynh: None. A. Makawi: None. G. Elshimy: None. Introduction: Modern healthcare relies on laboratory and imaging results for accurate diagnosis and medical decision-making. However, the collection and distillation of laboratory results is a multi-step process with the potential for error at each stage. This may result in diagnostic errors. A review of salient cases is one avenue to improving awareness of the risk for failure in the laboratory assessment process. We present one such case of a patient initially referred to neurosurgery for management of a thyroid stimulating hormone (TSH) secreting microadenoma, which is a rare disease and accounts for less than 1% of all pituitary adenomas, with incongruent laboratory presentation including elevation in TSH and free T4. Endocrinology consultation prompted further investigations which led to the diagnosis of Graves’ disease with a concomitant nonfunctional pituitary microadenoma. Case Presentation: This is a case of a 61-year-old white male who presented with 30-lb weight loss, insomnia, palpitations, and diaphoresis. Initial thyroid stimulating hormone (TSH) from outside facility was > 90 mcIU/mL with elevated free T4 of 23.4 pg/mL. MRI of the brain shows a 3x3 mm pituitary microadenoma raising concern for an atypical case of TSH-secreting adenoma. The patient referred to Neurosurgery for evaluation by primary care. Endocrinology was consulted for evaluation prior to any surgical intervention. A large goiter was noted on exam. Clinical presentation was highly concern for Graves’ disease. Repeated labs included undetectable TSH with FT4 of 4.4 pg/mL and free T3 12.9 pg/ml. TPO-ab was elevated at 17.1 IU/mL. TSIg index was low. Ultrasound of the thyroid gland revealed a normal thyroid without nodules. He was diagnosed with Graves’ disease and was initiated on methimazole and propranolol with symptomatic improvement. His pituitary panels continued to show suppressed TSH pre and post treatment with no other significant pituitary abnormalities hence the diagnosis of a concomitant nonfunctional pituitary microadenoma was made. Discussion: Ultimately, the initial TSH-secreting microadenoma has deemed a misdiagnosis and he was subsequently treated appropriately for Graves’ disease with normalization of thyroid functions. Standard of care for any laboratory abnormalities is to assess for reproducibility of the result. In our patient, subsequent in-house and outside assays were unable to demonstrate elevation of both TSH and FT4. Instead, the patient had suppressed TSH with elevated FT4, without evidence of nodules consistent with Graves’ disease. Treatment of Graves’ disease differs greatly from the treatment of TSH-secreting pituitary adenoma, which includes surgical resection, radiotherapy, and/or, a somatostatin analog based on the clinical picture. Correct diagnosis prevented our patients from unnecessary surgical complications and lifelong morbidity. Presentation: Friday, June 16, 2023