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Journal of Clinical Endocrinology & Metabolism Vol. 53, No. 1 165-173
doi:10.1210/jcem-53-1-165
Copyright © 1981 by the Endocrine Society.
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Anterior Pituitary Function after Transsphenoidal Selective Adenomectomy in Patients with Cushing's Disease*

AKIO KUWAYAMA, NAOKI KAGEYAMA, TOHICHI NAKANE, MASAO WATANABE and NORIO KANIE

Department of Neurosurgery, Nagoya University School of Medicine Showa-ku, Nagoya 466, Japan

Address requests for reprints to: Dr. Akio Kuwayama, Department of Neurosurgery, Nagoya University School of Medicine, 65 Tsurumacho, Showa-ku, Nagoya 466, Japan.

The anterior pituitary function in 25 patients with Cushing's disease was assessed before and after transsphenoidal adenomectomy. Pituitary adenoma was detected and removed in 24 cases, resulting in clinical remission in 22. Postoperative hypoadrenocorticism was observed in all of the cases with remission, necessitating substitution of glucocorticoid. One case had a recurrence after a year in remission. Plasma ACTH and cortisol rapidly decreased after surgery and remained at subnormal levels. However, diurnal rhythmicity of ACTH and cortisol appeared in 5 of 9 cases within 6 months after surgery and exhibited normal suppressibility in response to low dose dexamethasone. The impaired ACTH response to hypoglycemia was restored after surgery. The GH response to hypoglycemia and the TSH response to TRH were improved by correction of hypercorticism and became evident over time. These results suggest that preoperative impairment of anterior pituitary hormone secretion is secondary to hyperadrenocorticism and that ACTH hypersecretion by a primary pituitary adenoma is the primary etiology in Cushing's disease. We conclude that transsphenoidal pituitary exploration should be considered as a first choice of treatment of Cushing's disease because of its high clinical remission rate in association with normalization of other endocrine functions.

* Presented in part at the 6th International Congress of Endocrinology, February 13,1980, Melbourne, Australia. This work was supported by the Research Grant for the Intractable Diseases from the Ministry of Health and Welfare and Grant 457351 from the Ministry of Education, Science, and Culture of Japan.

Received October 14, 1980.




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