Prolactin plays a central role in variety of reproductive functions. The main biological action of prolactin is in mammary development and in inducing as well as maintaining lactation [7]. In addition, it also stimulates immune responsiveness and exerts metabolic effects [8]. It binds to specific receptors in the gonads, lymphoid cells and liver [9]. Plenty of mediators of central and peripheral origin take part in regulating prolactin secretion through a direct or indirect effect on lactotroph cells [5].

Prolactin secretion is under dual regulation by hypothalamic hormones, but the predominant signal is tonic inhibitory control of hypothalamic dopamine, which acts upon pituitary lactotroph D2 receptors. Factors affecting prolactin secretion are listed in Table 29.2 [10].

Hyperprolactinaemia can be physiological, pharmacological, pathological or idiopathic in origin. Physiological hyperprolactinaemia is usually mild or moderate and may cause temporary episodes of hyperprolactinaemia that do not warrant any treatment because repeat assays generally show normal prolactin levels. There are a number of pharmacological agents that may lead to hyperprolactinaemia, and discontinuation of the drug readily restores prolactin level to normal. During normal pregnancy, serum prolactin rises progressively to around 10–20 fold. Prolactinomas (prolactin-secreting adenomas) are the most frequent cause of chronic pathological hyperprolactinaemia and account for 25–30 % of functioning pituitary tumours [14]. Prolactinomas are of two types depending on their size: micro-adenomas (smaller than 10 mm) and macro-adenomas (10 mm or larger). Smaller tumours are generally very slow growing or static, but the larger ones require to be followed up regularly, and if their growth causes compression of surrounding neuronal tissue, surgical intervention may be required. A number of chronic systemic diseases also cause moderate rise in prolactin levels leading to disturbed reproductive function or galactorrhoea. Apart from these known reasons for high circulating prolactin levels, a large proportion of women presenting with symptomatic hyper-prolactinaemia are idiopathic in origin (Table 29.3) [15].

The predominant physiological consequence of hyperprolactinaemia is suppression of pulsatile GnRH. The clinical manifestations of conditions vary significantly depending on the age and the sex of the patient and the magnitude of prolactin excess. Clinical presentation in women is more obvious and occurs earlier than in men (Table 29.4). Presenting symptoms in women are manifold and range from those arising due to hypogonadism (oligo-ovulation, anovulation, menstrual irregularities, symptoms of hypo-oestrogenism) to those that occur by lactotroph stimulation of breasts causing galactorrhoea. In addition, these women can also present with neurological symptoms caused by mass effects of the tumour within or around the pituitary. Symptoms include headache, visual field loss, cranial neuropathy, hypo-pituitarism, seizures and cerebrospinal fluid rhinorrhoea [16].

It is worth noting that many women with hyperprolactinaemia do not have galactorrhoea, and many with galactorrhoea do not have hyperprolactinaemia. This is because galactorrhoea requires adequate oestrogen or progesterone priming of breasts. Conversely, isolated galactorrhoea with normal prolactin levels occurs due to increased sensitivity of the breast to the lactotrophic stimulus [17].

Approximately 3–10 % women with PCOS have co-existent hyperprolactinaemia [18]. Ovulatory dysfunction and hyper-androgenism both are commonly existing clinical presentations in patients with hyperprolactinaemia as well as in PCOS. Persistently elevated oestrogen levels are often found in women with PCOS which could result in prolactin elevation. However, it is still controversial whether they have cause-effect relationship or share a common mechanism or it is just a coincidental finding.

Prolonged hypo-oestrogenism secondary to hyperprolactinaemia may result in osteopenia [19]. Spinal bone mineral density (BMD) is decreased by approximately 25 % in such women and is not necessarily restored with normalization of prolactin levels [20, 21]. Hyperprolactinaemic women may present with signs of chronic hyper-androgenism such as hirsutism and acne, possibly due to increased dehydro-epiandro-sterone sulfate secretion from the adrenals [22], as well as reduced sex hormone-binding globulin leading to high free testosterone levels.

The management of hyperprolactinaemia should be individualized on the basis of clinical findings, underlying cause and the presence of hypogonadism or infertility. Asymptomatic women with hyperprolactinaemia and/or micro-adenomas, who are not concerned about fertility, may be followed without active intervention. Annual clinical review and prolactin assay might be sufficient if the clinical condition remains stable.