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Luteinizing Hormone (LH) and Prolactin-Releasing Pituitary Tumor; Possible Malignant Transformation of the LH Cell Line

Division d'Endocrinologie et Biochimie Clinique, Département de Médecine Interne CH-1011 Lausanne, Switzerland.
Division de Neuropathologie, Institut de Pathologie CH-1011 Lausanne, Switzerland.
Service de Pédiatrie, Centre Hospitalier Universitaire Vaudois CH-1011 Lausanne, Switzerland.

Address requests for reprints to: Dr F. Gomez, Division d'Endocrinologie et Biochimie Clinique, Centre Hospitalier Universitaire Vaudois BH-10, CH-1011 Lansanne, Switzerland.

A pituitary tumor was diagnosed in a prepubertal 13-yr-old girl, who had elevated plasma LH (58 mlU/ml) and PRL (93 ng/ml) levels; decreased GH, ACTH, and FSH secretion; and diabetes insipidus. After surgery, plasma LH and PRL declined, but not to normal levels. Conventional external radiotherapy to the pituitary was immediately followed by a decrease in LH to prepubertal values (0.7 mlU/ml), while PRL levels became normal only after a long course of bromocriptine therapy. The pituitary tumor was composed of two distinct cell types: small polygonal cells, which were PRL positive by immunohistochemistry, and clusters of pleomorphic large frequently mitotic polynucleated cells, which were LH positive, some of them also being positive for the -subunit or βLH but not for βFSH. Four years after surgery and radiotherapy, the patient deteriorated neurologically. Computed tomographic scan showed widespread frontal and periventricular tumor, which had the histological features of a poorly differentiated carcinoma. No PRL, LH, or or β-subunits were detectable on immunocytochemistry.

While the PRL-positive cells of the pituitary tumor displayed the histological and clinical features of PRL adenomas, the morphological characteristics of LH cells and the sharp decline of plasma LH levels after radiotherapy were suggestive of malignant transformation. In this context, the later brain tumor could have been the result of subependymal spread of the pituitary tumor after it lost its hormone-secreting capacity.

Received October 29, 1984.

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