By Jesús Ramón Giraudo and Julio Libman

Galactorrhea is defined as the inadequate secretion of milk by the nipple, inadequate or non-physiological being understood as the circumstance of not being related to postpartum lactation. It can be uni or bilateral. The quantity is variable; sometimes there is a spontaneous and abundant discharge while others it is necessary to squeeze the nipple to get some drops of milk secretion to appear. Neither the quantity nor the uni or bilaterality are related to the importance of the causative process.

Physiology and pathophysiology

The development of normal breast in non-lactating women depends on the action of estrogens, which induce the growth, division and elongation of the ducts and maturation of the nipple. The development of the alveoli requires the joint effect of progesterone and estrogens, in a ratio of 20: 1 to 100; 1. The formation of milk is one of the most complex endocrine phenomena, and requires, in addition to the prior preparation of the breast tissue by estrogens and progesterone, the presence of prolactin and lactogenic placental hormone, and the permissive action of insulin , corticosteroids, thyroxine, and somatotrophin.

Two neuroendocrine reflexes ensure the secretion of prolactin and oxytocin, contributing to the maintenance of lactation. Suction induces prolactin secretion via the nerve. In nonpregnant women, plasma prolactin is below 25 ng / ml and remains unchanged during the menstrual cycle. During pregnancy it increases and the postpartum levels, at the beginning of lactation, are several times higher than in women who do not breastfeed. Sucking or manual stimulation of the breasts causes a pronounced increase in prolactin, with an immediate response before 10 minutes, and levels of up to 300 ng / ml at 30 minutes. Suction also induces via reflex the secretion of oxytocin stored in the posterior lobe of the pituitary. Oxytocin acts as the efferent branch of the reflex, activating at the level of the breast the contraction of the myoepilelial cells that surround the alveoli. The milk is thus expelled into the canalicular system and the cisterns of the mammary gland, from where it is possible to extract it by suction.

Since the initiation of milk secretion requires the presence of prolactin, it is logical to consider galactorrhea as a manifestation of an alteration in the physiology of this hormone. Unlike other pituitary hormones, the predominant control of the hypo thalamus over prolactin secretion is inhibitory in nature; therefore, it is common for hyperprolactinemia and galactorrhea to occur in cases of hypolatalamic diseases or interruption of the pituitary stalk, provided that the pituitary maintains its integrity. Since the main physiological inhibitor of prolactin secretion is probably dopamine, drugs that interfere with dopamine neurotransmission or cause hypothalamic dopamine depletion frequently cause hyperprolactinemia and galactorrhea.

Prolactin responds easily to a variety of situations of physical and mental stress with an increase in its secretion rate, which can eventually lead to galactorrhea. This has practical relevance in interpreting the symptom and laboratory data.

The existence of a physiological prolactin-releasing factor is disputed, but thyrotrophin-releasing hormone (HRT) stimulates prolactin release, and the galactorrhea observable in hypothyroidism is likely due to increased production of that hormone. Likewise, estrogens, even in a small amount such as that found in oral contraceptives, stimulate prolactin secretion.

Causes of galactorrhea

  1. Normal hypothalamic inhibition deficiency for prolactin release, either by section of the pituitary stem or by the action of various drugs. A drug that causes catecholamine depletion, such as reserpine; alpha methyldopa, which acts as a false neurotransmitter, and dopaminergic antagonists such as phenothiazines, butyrophenones, and benzainides, can cause hyperprolactinemia and galactorrhea. The major neuroleptics, which are likely to antagonize dopaminergic action in the mesocortical and mesolimbic systems, are likely to cause hyperprolactinemia by antagonism of dopamine in the tuberoinfundibular system. Certain diseases of the central nervous system, such as encephalitis, meningitis, hydrocephalus, and pinealomas, would act by a similar mechanism.
  2. Increased prolactin-releasing factor, as in hypothyroidism.
  3. Autonomous increase in prolactin release, due to pituitary tumors, micro or macroproiactinomas. or by ectopic production, as in cases of bronchogenic carcinoma.
  4. Idiopathic.
  5. The administration of estrogens and various states of physical or psychological stress are capable of inducing hyperprolactinemia and galactorrhea, probably inhibiting the production of the prolactin inhibiting factor. They can also cause galactorrhea by reflex route various injuries of the chest wall, such as herpes zoster, tumors, thoracotomy, etc.

Interrogation and study methodology

The evaluation of a patient with galactorrhea begins with a careful medical history, where special attention is required to the intake of drugs and medications. Clinical manifestations of hypothyroidism should be sought, and it is important to remember, in this regard, that galactorrhea can present with a very mild or moderate picture of hypothyroidism, and that the existence of myxedema is not necessary for it to become evident. The development of neurological and / or visual manifestations (headache, loss of vision with reduction of the visual field) of a pituitary adenoma is characteristic of macroadenomas, although it should be borne in mind that on many occasions there are microadenomas, smaller than 10 mm, which they do not translate into a clinical picture of Mipoiisano Immoral Syndrome.

Endocrine evaluation includes the determination of thyroxine (T4) and thyroid stimulating hormone (TSH) to rule out hypothyroidism, and that of prolactin. Given the variations in the levels of the latter, it is necessary to quantify it in a pool of three samples, obtained at intervals of 20 minutes. Concentrations higher than 100 ng / ml suggest the existence of a pituitary adenoma. The diagnosis is made virtually true at levels above 200 ng / ml. A substantial proportion of patients with values ​​between 25 and 100 ng / ml are also carriers of prolactinomas, but in this range the majority correspond to hyperprolactinemias induced by drugs or other etiologies. Neuroradiological evaluation includes sella x-rays, polytomy, and computed axial tomography.