AACE ePoster Library

COMPREHENSIVE EVALUATION OF THYROTROPINOMAS: EMORY UNIVERSITY 20-YEAR EXPERIENCE
AACE ePoster Library. Azzalin A. 05/14/15; 97739; 804
Dr. Alice Azzalin
Dr. Alice Azzalin
Login now to access Regular content available to all registered users.
Abstract
Rate & Comment (0)
Objective: Historically thyrotropinomas (TSHomas) represent 1% of pituitary adenomas, but up to 4% in recent series. Data on silent TSHomas is sparse. Classic presentation includes tumor mass effect and hyperthyroidism often incorrectly treated with thyroid surgery/ablation. We present a single center review of TSHomas.
Methods: Retrospective case series of histopathologically-proven TSH-adenomas operated between 1993-2013. TSHomas were classified as active (group A) and silent (group B) based on biochemical evidence of central hyperthyroidism (elevated thyroid hormones along with inappropriately normal/high TSH).
Results: Among 1628 operated pituitary adenomas, 20 were TSHomas (1.2%). In increments of 5 years, proportion of TSHomas was 1%, 1%, 0.04% and 1.77% respectively. Two thirds of active TSHomas were operated between 2009-2013.
Group A: 6 patients (5 men), age 41±12, presented with hyperthyroidism (3), incidentally discovered tumor (2) and acromegaly (1). One patient with incidentaloma was diagnosed with acromegaly and 10 months later developed hyperthyroidism. Preoperatively, 3 patients received somatostatin analogs (SSA), 1 antithyroid drugs (ATD) and 2 SSA/ATD. None had thyroid surgery/ablation. Mean FT4 was 2.68±2.73 ng/dL; TSH 6.50±3.68 mIU/L. Glycoprotein alpha subunit (GSU obtained in 5 cases) was uniformly high. IGF-1 was high in 2 and prolactin (PRL) in 1 case. Tumor diameter was 2.1±1.2 cm. All adenomas were plurihormonal and 5 stained for GH. Postoperatively, 4 patients became euthyroid, 1 had high TSH/normal T4 and 1 remained hyperthyroid. Residual tumor was identified in the latter who received SSA, ATD and radiation.
Group B - 14 patients (7 men), age 47±14 presented with acromegaly (6), mass effect (4), incidentaloma (3) and galactorrhea (1). Mean FT4 (1.00±0.24 ng/dL) and TSH (2.02±1.65 mIU/L) were lower than in group A (p<0.01). GSU (measured in 5 cases) was uniformly elevated; IGF-1 was high in 9 and PRL in 6. Tumor diameter was 2.0±1.0 cm. All adenomas were plurihormonal and 12 stained for GH. Postoperatively, 2 patients had residual tumor; 1 underwent radiation and 1 reoperation. One patient had recurrence at one year and received SSA and radiation.
Discussion: In our surgical series, active TSHomas have been detected with greater frequency in recent years. Silent TSHomas may secrete insufficient amounts of TSH to induce hyperthyroidism but exhibit high GSU. TSHomas frequently co-secrete GH, which may be clinically apparent.
Conclusion: TSHomas have a wide spectrum of manifestations and often require multimodality treatment. Correct biochemical diagnosis is essential for early detection and may improve outcomes.
Objective: Historically thyrotropinomas (TSHomas) represent 1% of pituitary adenomas, but up to 4% in recent series. Data on silent TSHomas is sparse. Classic presentation includes tumor mass effect and hyperthyroidism often incorrectly treated with thyroid surgery/ablation. We present a single center review of TSHomas.
Methods: Retrospective case series of histopathologically-proven TSH-adenomas operated between 1993-2013. TSHomas were classified as active (group A) and silent (group B) based on biochemical evidence of central hyperthyroidism (elevated thyroid hormones along with inappropriately normal/high TSH).
Results: Among 1628 operated pituitary adenomas, 20 were TSHomas (1.2%). In increments of 5 years, proportion of TSHomas was 1%, 1%, 0.04% and 1.77% respectively. Two thirds of active TSHomas were operated between 2009-2013.
Group A: 6 patients (5 men), age 41±12, presented with hyperthyroidism (3), incidentally discovered tumor (2) and acromegaly (1). One patient with incidentaloma was diagnosed with acromegaly and 10 months later developed hyperthyroidism. Preoperatively, 3 patients received somatostatin analogs (SSA), 1 antithyroid drugs (ATD) and 2 SSA/ATD. None had thyroid surgery/ablation. Mean FT4 was 2.68±2.73 ng/dL; TSH 6.50±3.68 mIU/L. Glycoprotein alpha subunit (GSU obtained in 5 cases) was uniformly high. IGF-1 was high in 2 and prolactin (PRL) in 1 case. Tumor diameter was 2.1±1.2 cm. All adenomas were plurihormonal and 5 stained for GH. Postoperatively, 4 patients became euthyroid, 1 had high TSH/normal T4 and 1 remained hyperthyroid. Residual tumor was identified in the latter who received SSA, ATD and radiation.
Group B - 14 patients (7 men), age 47±14 presented with acromegaly (6), mass effect (4), incidentaloma (3) and galactorrhea (1). Mean FT4 (1.00±0.24 ng/dL) and TSH (2.02±1.65 mIU/L) were lower than in group A (p<0.01). GSU (measured in 5 cases) was uniformly elevated; IGF-1 was high in 9 and PRL in 6. Tumor diameter was 2.0±1.0 cm. All adenomas were plurihormonal and 12 stained for GH. Postoperatively, 2 patients had residual tumor; 1 underwent radiation and 1 reoperation. One patient had recurrence at one year and received SSA and radiation.
Discussion: In our surgical series, active TSHomas have been detected with greater frequency in recent years. Silent TSHomas may secrete insufficient amounts of TSH to induce hyperthyroidism but exhibit high GSU. TSHomas frequently co-secrete GH, which may be clinically apparent.
Conclusion: TSHomas have a wide spectrum of manifestations and often require multimodality treatment. Correct biochemical diagnosis is essential for early detection and may improve outcomes.

By clicking “Accept Terms & all Cookies” or by continuing to browse, you agree to the storing of third-party cookies on your device to enhance your user experience and agree to the user terms and conditions of this learning management system (LMS).

Cookie Settings
Accept Terms & all Cookies