Surgical treatment of thyrotropin-secreting pituitary adenomas

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✓ Thyrotropin-secreting pituitary adenomas have been diagnosed more frequently as radiographic techniques and biochemical assays have improved; however, they remain uncommon and are unfamiliar to most neurosurgeons. This report concerns eight patients with hyperthyroidism, inappropriately elevated levels of serum thyrotropin and α-subunit, and radiographic evidence of pituitary tumor. All underwent surgery and had pathological confirmation of a thyrotropin-secreting adenoma, and most had been subjected to prior ablation of the thyroid gland. Only one tumor was a microadenoma; the others ranged in size from 1.4 to 12 cm, and invasion of parasellar structures was common. Thyrotropin, triiodothyronine, thyroxine, and α-subunit were measured preoperatively and at intervals postoperatively. Coexistent hormonal abnormalities (which occurred in all patients) included acromegaly and hyperprolactinemia and were also monitored. All four patients who had tumors less than 2 cm in diameter remain alive. Complete extirpation of tumor in these patients produced rapid correction of all hormonal abnormalities and resolution of clinical hyperthyroidism. The other four patients had larger invasive tumors: two died soon after surgery, one died of disseminated tumor 8 years after presentation, and one remains alive with residual tumor.

Tumors secreting thyroid-stimulating hormone are less easily cured by surgery than are other types of pituitary adenoma because of the large size and invasive features that many attain during the delay to diagnosis; medical therapy can subdue the tumor but not cure it. The experience with these patients establishes the importance of early diagnosis and surgical excision for successful treatment, and demonstrates the utility of modern diagnostic techniques for finding these lesions. As occurs in Nelson's syndrome after adrenalectomy for Cushing's disease, ablation of the target organ may allow the tumor to convert to a more clinically malignant form which is resistant to cure.

Article Information

Address reprint requests to: Edward H. Oldfield, M.D., Room 5D37, Building 10, Clinical Neurosurgery Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892.

© AANS, except where prohibited by US copyright law.

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    Magnetic resonance (T2-weighted) images after intravenous infusion of gadolinium in Case 3. Upper Pair: Images obtained before the patient's fourth operation. Lower Pair: Images obtained 1 month later after progressive cranial nerve deficits and recurrent epistaxis culminated in sudden and complete loss of vision in the right eye. The tumor has extended from the sella into the clivus, sphenoid sinus, nasopharynx, and soft palate and compresses the right optic nerve, both temporal lobes, and the inferior surface of the right frontal lobe.

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