Hyperprolactinemia and hypogonadism in the human female
Rolland, R.; Corbey, R.S.
European Journal of Obstetrics Gynecology and Reproductive Biology 7(5): 337-348
1977
ISSN/ISBN: 0301-2115 PMID: 400856 DOI: 10.1016/0028-2243(77)90019-3Document Number: 439497
In 1937 pure preparations of ovine prolactin became available. It was not until 1970 that it was clearly shown that prolactin existed as a hormone in humans. During the second and third trimesters of human pregnancy, prolactin is present in both fetal and maternal plasma at levels above 50 ng/ml; the maximum at term is about 100 ng/ml. This increase parallels that of 17beta-estradiol. In the postpartum period prolactin remains elevated for a longer period in lactating women. Pituitary prolactin release is under tonic inhibition by the prolactin inhibiting factor (PIF) produced within the hypothalamus. Dopamine is the msot important catecholamine regulating PIF. Increased prolactin levels may interfere with follicular maturation leading to hypogonadism. Usually pathological hyperprolactinemia is a sign of hypothalamic disorder or pituitary tumor. Bromocriptine, a dopamine receptor agonist, is a potent inhibitor of puerperal lactation through its blockade of pituitary prolactin release. The incidence of hyperprolactinemia in patients with secondary amenorrhea is 13-20% regardless of the presence of galactorrhea. High prolactin with blunted response to thyrotropin releasing hormone but with thyroid stimulating hormone response preserved indicates that the patient will respond to bromocriptine. Lowering of pituitary prolactin secretion can be achieved surgically, medically, by irradiation, or by a combination of these methods. Bromocriptine, 2.5 mg twice daily, has been used. Oral contraceptives have not been used along with bromocriptine therapy. IUDs have been recommended.