SUPPRESSION OF PROLACTIN SECRETION BY LISURIDE THROUGHOUT THE MENSTRUAL CYCLE AND IN HYPERPROLACTINAEMIC MENSTRUAL DISORDERS

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Abstract
Normally menstruating volunteers and patients with hyperprolactinemic menstrual disorders were treated with lisuride hydrogen maleate (200 .mu.g b.i.d. [twice a day]), an ergoline derivative with dopaminergic properties. Within 3 h after an oral dose of 200 .mu.g lisuride, PRL [prolactin] levels decreased significantly in all subjects to a plateau which lasted up to 3 h. Thereafter a gradual increase of serum PRL was noted. In the normally menstruating volunteers lisuride treatment did not result in any significant change of gonadotropin or of sex steroid secretion, while basal and metoclopramide (MTCL) stimulated PRL release were significantly diminished. The inhibition of PRL secretion in patients with short luteal phases resulted in an increase of luteal progesterone output. In both treated groups ovulation occurred 1-5 days earlier in cycles on lisuride than in control cycles. LH-RH[luliberin]/MTCL tests performed in the patient bearing a pituitary prolactinoma before and after lisuride treatment revealed a continuous increase of pituitary LH [lutropin] pools, while PRL secretion decreased under lisuride therapy. Subsequently ovulation and menstruation occurred. Lisuride is a potent inhibitor of PRL secretion and has proven its clinical usefulness for treatment of hyperprolactinemic menstrual disorders. Application of lisuride resulted in an increase of luteal progesterone secretion in previously demonstrated corpus luteum insufficiency and in restoration of normal cyclical feedback mechanisms in tumorous hyperprolactinemic anovulation. The MTCL-PRL stimulation test is suitable to monitor PRL suppression during lisuride treatment, while LH-RH testing reveals the effectiveness of lisuride by demonstrating an increase of pituitary gonadotropin pools.

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