Diethylstilbestrol-induced prolactinoma: dose-related tumor growth and effect of catecholaminergic cells on prolactin tumor cells.

Abstract

Prolactinoma is a pituitary adenoma originating from prolactin-secreting epithelial cells of the adenohypophysis. Unfortunately, there appears to be a relatively high recurrence rate despite all pharmacological, radiological, and surgical therapeutic interventions. The aim of the present study was to evaluate the extent of involvement of the dopaminergic dysregulation hypothesis of prolactinomas. We transplanted, in rats, DES-induced prolactinoma cells into the adrenal medulla or under the renal capsule, two tissues rich and poor in catecholaminergic innervation, respectively.
Prolactinoma was dose-dependently induced in ovariectomized female rats implanted with 10 and 20 mg DES, and tumor cells taken from prolactinoma induced by 20 mg DES were either transplanted under the renal capsule or into the adrenal medulla.
Although the adrenal medulla, with its high dopamine content to inhibit prolactin secretion, was devoid of any tumoral development, a significant tumoral development was evident under the renal capsule, seemingly because of no inhibitory control over prolactin secretion coexisting with the dopamine deficiency of the tissue. Results are discussed for an alternatively possible regression and prevention of any relapse of prolactinoma, most possibly occurring because of tuberoinfundibular dopamine deficiency, by the implantation of another dopamine-rich tissue beside the tumoral mass.
Regression and prevention of any relapse of a tumoral outgrowth, most possibly occurring because of tuberoinfundibular dopamine deficiency, can well be alternatively achieved by the implantation of another dopamine-rich tissue beside the tumoral mass prolactinoma.