Résumé

Hyperprolactinaemia is a condition of elevated serum PRL. Normal PRL levels in women and men are <1087 picomol/L (25 nanograms/mL or 25 micrograms/L or 500 milli-units/L) and 870 picomol/L (20 nanograms/mL or 20 micrograms/L or 400 milli-units/L), respectively. [1] [2] [3]

Hyperprolactinaemia is the most common endocrine disorder of the hypothalamus-pituitary axis. The prevalence of hyperprolactinaemia ranges from 0.4% in an unselected normal adult population to 5% in a family planning clinic. It increases to 9% in women with amenorrhoea and occurs in 25% of those with galactorrhoea. Among women presenting with concomitant amenorrhoea and galactorrhoea, 70% are hyperprolactinaemic. The condition also accounts for 5% of men who present with impotence or infertility. [2] [3] Although uncommon, hyperprolactinaemia can also present in children.

The hormone PRL is a 199-amino acid peptide synthesised and secreted by lactotroph cells in the anterior pituitary gland; 80% of circulating PRL exists as a 23 kd monomer. Dimeric PRL (also known as big PRL) has a molecular weight of 50 kd to 60 kd and accounts for 10% to 15%; the remainder is macroprolactin (also known as big-big PRL), a high molecular weight (>150 kd) complex of monomeric PRL and IgG. [4] [5] PRL is also produced by numerous extrapituitary tissues, including various brain regions, lymphocytes, mammary epithelial cells, and tumours, as well as the decidua, myometrium, lacrimal gland, thymus, and spleen. [6] Although it derives from an ancestral hormone common to GH and human placental lactogen, PRL displays little structural homology with these hormones. [4]

The main action of PRL is to stimulate breast epithelial cell proliferation and induce milk production. In addition to its lactogenic role, PRL promotes the formation and action of the corpus luteum and suppresses the pulsatile secretion of GnRH. GnRH results in decreased levels of FSH and LH. [6] Moreover, it plays a direct inhibitory role in spermatogenesis and steroidogenesis, as its receptors have been detected in Sertoli and Leydig cells in the testes. [7]

PRL secretion is pulsatile and controlled predominantly by the inhibitory effect of dopamine released from the hypothalamus. Dopamine acts through its D2 receptors on lactotroph cells. Other inhibitory factors are endothelin peptides, [8] tumour growth factor-beta 1, [9] and calcitonin. [10] Oestrogens stimulate the proliferation of lactotroph cells, resulting in an increased quantity of these cells in pre-menopausal women, especially during pregnancy. PRL production is also stimulated by TRH, vasoactive intestinal peptide, and oxytocin. [4]