Hyperprolactinemia

Abstract

Prolactin (PRL) is an anterior pituitary hormone which has its principle physiological action in initiation and maintenance of lactation. In human reproduction, pathological hyperprolactinemia most commonly presents as an ovulatory disorder and is often associated with secondary amenorrhea or oligomenorrhea. Galactorrhea, a typical symptom of hyperprolactinemia, occurs in less than half the cases. Out of the causes of hyperprolactinemia, pituitary tumors may be responsible for almost 50% of cases and need to be investigated especially in the absence of history of drug induced hyperprolactinemia. In women with hyperprolactinemic amenorrhea one important consequence of estrogen deficiency is osteoporosis, which deserves specific therapeutic consideration. Problem in diagnosing and treating hyperprolactinemia is the occurrence of the ‘big big molecule of prolactin’ that is biologically inactive (called macroprolactinemia), but detected by the same radioimmunoassay as the biologically active prolactin. This may explain many cases of very high prolactin levels sometimes found in normally ovulating women and do not require any treatment. Dopamine agonist is the mainstay of treatment. However, presence of a pituitary macroadenoma may require surgical or radiological management.

Gliomas in the Sellar Turcica Region: A Retrospective Study Including Adult Cases and Comparison with Craniopharyngioma

“…The hormones that were predominately affected in our study were PRL and GH. PRL is secreted in the anterior pituitary and regulated by inhibition from the hypothalamus; when the hypothalamus-pituitary axis is affected by nearby lesions, the inhibition may be blocked, and the PRL level may rise [28]. As sellar lesions, both sellar glioma and craniopharyngioma have the potential to affect the PRL level.…”

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“…PRL is synthetized by lactotrophs in the anterior pituitary gland, immune, mammary, uterine, fat and epithelial cells. Its secretion is pulsatile (4 to 14 secretory pulses each lasting 67 to 76 minutes over 24 hours) and increases with stress, sleep, pregnancy, chest wall stimulation, and trauma [5][6]. Several factors exert a stimulatory effect on PRL secretion like thyrotropin releasing hormone (TRH), vasoactive intestinal peptide (VIP), epidermal growth factor, oxytocin, serotonin and opioid peptides.…”

“…Also, hyperprolactinemia decreases pulsatile excretion of gonadotropin-releasing hormone (GnRH) from hypothalamus, where consequently supressed luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion inhibits ovulation. In women, there are low levels of oestrogen and inhibited secretion of progesterone, while in men levels of testosterone are normal or decreased [5]. Chronic hyperprolactinemia can result in decreased bone mass in both sexes [17].…”

“…Treatment with DA is advisable in patients with symptomatic idiopathic hyperprolactinemia. Treatment with DA can induce ovulation in 80-90% of patients and in the remaining patients gonadotropin stimulation can be added [5].…”

New aspects of postmenopausal osteoporosis treatment with micronized estradiol and progesterone

“…Osteoblasts suppress the secretion of resorptive cytokines IL-1, IL-6, and TNF-α, which act as paracrine regulators of osteoblasts. Since the 1960s, estrogens have been used to treat osteoporosis owing to their enhancement of the expression of vitamin D 3 receptors, growth hormone receptors, and the osteoprotegerin gene [18], and their regulatory action on the thyroid gland [19]. Estrogens, like testosterone, stimulate bone metabolism [20].…”