HIPERPROLACTINEMIA Y AMENORREA PDF

Medications[ edit ] Prolactin secretion in the pituitary is normally suppressed by the brain chemical dopamine. Drugs that block the effects of dopamine at the pituitary or deplete dopamine stores in the brain may cause the pituitary to secrete prolactin. These drugs include the typical antipsychotics : phenothiazines such as chlorpromazine Thorazine , and butyrophenones such as haloperidol Haldol ; atypical antipsychotics such as risperidone Risperdal and paliperidone Invega ; [4] [5] gastroprokinetic drugs used to treat gastro-oesophageal reflux and medication-induced nausea such as that from chemotherapy : metoclopramide Reglan and domperidone ; less often, alpha-methyldopa and reserpine , used to control hypertension ; and also estrogens and TRH. A benzodiazepine analog, etizolam , can also increase the risk of hyperprolactinaemia. However, since prolactin is antagonized by dopamine and the body depends on the two being in balance, the risk of prolactin stimulation is generally present with all drugs that deplete dopamine, either directly or as a rebound effect. Specific diseases[ edit ] Prolactinoma or other tumours arising in or near the pituitary — such as those that cause acromegaly may block the flow of dopamine from the brain to the prolactin-secreting cells, likewise, division of the pituitary stalk or hypothalamic disease.

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E-mail: moc. This article has been cited by other articles in PMC. 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. In women with hyperprolactinemic amenorrhea one important consequence of estrogen deficiency is osteoporosis, which deserves specific therapeutic consideration.

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. Initially, even though this hormone was recognized in relation to lactation in women, lately immense interest has been focused on prolactin with respect to its effect on reproduction.

Hyperprolactinemia is a condition of elevated prolactin levels in blood which could be physiological, pathological, or idiopathic in origin. Similarly elevated prolactin levels could be associated with severe clinical manifestations on one side of the spectrum or be completely asymptomatic on the other side.

Unlike other tropic hormones secreted by the anterior pituitary gland, prolactin secretion is controlled primarily by inhibition from the hypothalamus and it is not subject to negative feedback directly or indirectly by peripheral hormones.

It exercises self-inhibition by a counter-current flow in the hypophyseal pituitary portal system which initiates secretion of hypothalamic dopamine, as well as causes inhibition of pulsatile secretion of gonadotropin releasing hormone GnRH. This negatively modulates the secretion of pituitary hormones responsible for gonadal function. It occurs more commonly in women. The prevalence of hyperprolactinemia ranges from 0. Its secretion is pulsatile and increases with sleep, stress, food ingestion, pregnancy, chest wall stimulation, and trauma.

Macroprolactin: Even though monomeric 23 kDa form is the predominant form, prolactin is also present in different molecular forms on which the bioactivity of the hormone depends. Such forms are rarely physiologically active but may register in most prolactin assays. Many commercial assays do not detect macroprolactin. Polyethylene glycol precipitation is an inexpensive way to detect the presence of macroprolactin in the serum.

However, it also exerts metabolic effects, takes part in reproductive mammary development[ 8 ] and stimulates immune responsiveness. Plenty of mediators of central, pituitary, and peripheral origin take part in regulating prolactin secretion through a direct or indirect effect on lactotroph cells. The predominant signal is tonic inhibitory control of hypothalamic dopamine which traverses the portal venous system to act upon pituitary lactotroph D2 receptors.

Other prolactin inhibiting factors include gamma amino butyric acid GABA , somatostatin, acetylcholine, and norepinephrine. The second signal is stimulatory which is provided by the hypothalamic peptides, thyrotropin releasing hormone TRH , vasoactive intestinal peptide VIP , epidermal growth factor EGF , and dopamine receptor antagonists.

Serotonin physiologically mediates nocturnal surges and suckling-induced prolactin rises and is a potent modulator of prolactin secretion. Histamine has a predominantly stimulatory effect due to the inhibition of the dopaminergic system. Estrogen stimulates the proliferation of pituitary lactotroph cells especially during pregnancy. However, lactation is inhibited by the high levels of estrogen and progesterone during pregnancy. The rapid decline of estrogen and progesterone in the postpartum period allows lactation to commence.

During lactation and breastfeeding, ovulation may be suppressed due to the suppression of gonadotropins by prolactin, but may resume before menstruation resumes.

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