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Journal of Clinical Endocrinology & Metabolism Vol. 57, No. 6 1093-1101
doi:10.1210/jcem-57-6-1093
Copyright © 1983 by the Endocrine Society.
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Pituitary Adenomas in Acromegalic Patients: An Immunohistochemical and Endocrinological Study with Special Reference to Prolactin-Secreting Adenoma*

NORIO KANIE, NAOKI KAGEYAMA, AKIO KUWAYAMA, TOSHICHI NAKANE, MASAO WATANABE and AKIRA KAWAOI

Department of Neurosurgery, Nagoya University School of Medicine Showa-ku, Nagoya 466
the Department of Pathology, Nihon University School of Medicine Itabashi-ku, Tokyo 173, Japan

Address requests for reprints to: Norio Kanie, M.D., Endocrine Division, Department of Medicine, New York University Medical Center, 550 First Avenue, New York, New York 10016.

To establish a functional classification of purification of pituitary adenomas in acromegalic patients, we used immunoperoxidase-staining techniques specific for GH and PRL. Surgical specimens from 55 acromegalic patients were studied. GH was demonstrated in all adenomas and PRL was found in 25 of them (45.5%). Immunohistologically, GH- and PRL-containing adenomas could be divided into 3 types. In type 1(11 patients), immunoreactive PRL was present in single cells surrounded by immunoreactive GH cells. In type 2 (6 patients), immunoreactive PRL cells formed clusters. In Type 3 (8 patients), immunoreactive PRL and GH cells demonstrated a mosaic pattern, and it was difficult to determine which were in the majority. A double immunostaining method revealed 15 adenomas in which individual cells contained both GH and PRL.

Hyperprolactinemia was present in 21 patients, 15 of these had immunoreactive PRL cells (type 1, 4 patients; type 2, 3 patients; type 3, 8 patients). There was no correlation between the size of the adenoma and its type. Endocrinologically, all patients with type 2 and 3 adenomas had an abnormal serum GH response to TRH administration; all type 3 patients had a substantial serum PRL response to TRH administration. Type 3 is considered to be an actively PRL-secreting adenoma, resulting in hyperprolactinemia.

* This work was supported by a Research Grant for Intractable Disease from the Japanese Ministry of Health and Welfare and Grant 457351 from the Ministry of Education, Science, and Culture of Japan.

Received April 13, 1983.







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Copyright © 1983 by The Endocrine Society