Introduction to hyperprolactinemia

INTRODUCTION: Hyperprolactimia is the most common form of pituitary disease, which is characterized by galactorrhea and hypogonadism. If the patient has both galactorrhea and amenorrhea, it is called galactorrhea-abated syndrome, such as Chiari-Fromeel syndrome in postpartum; Forbes-Albright syndrome with pituitary tumors; non-postpartum without pituitary tumors It is called del Castillo syndrome. The main difference between the above syndromes is that there are two kinds of pituitary tumors and no pituitary tumors, and the other differences are only in the time of illness. Therefore, the names of these syndromes have recently been mentioned less frequently. Etiology: (1) Causes of the disease 1. Physiological hyperprolactinemia In normal healthy women, plasma prolactin increased during nighttime and sleep (2-6am), late follicular and luteal phase. Plasma prolactin is increased 5 to 10 times during pregnancy. The concentration of prolactin in amniotic fluid is higher than that in plasma after the second trimester. In lactating women, plasma prolactin concentrations are 1 times higher than non-pregnant women. Fetal and neonatal (≥ 28 weeks gestation - 2 to 3 weeks postpartum) plasma prolactin corresponds to maternal levels. Massage the breast and sucking the nipple to reflexively promote prolactin secretion. Plasma prolactin remained at a high level during the puerperium (within 4 weeks). Prolactin in non-breastfeeding women fell to non-pregnancy levels within 3 months. Prolactin is significantly elevated in fasting, insulin-induced hypoglycemia, exercise, stress, and sexual intercourse. 2. Pathological hyperprolactinemia (1) Hypothalamic-pituitary lesions: 1 hypothalamic non-functional tumors: including craniopharyngioma, invasive hypothalamic lesions, sarcomatoid disease, histiocytosis, glial cells Tumor and leukemia. 2 pituitary functional tumors: including pituitary adenomas (80% secretory prolactin), prolactinoma (prolactinoma), acromegaly (25% with hyperprolactinemia), Cushing syndrome (adrenal ACTH gland) Tumor, 10% with hyperprolactinemia, prolactin cell hyperplasia (80% with hyperprolactinemia). 3 Functional hyperprolactinemia: caused by inhibition of dopamine function, including primary vacuolar sella syndrome (5% with amenorrhea and galactorrhea) and secondary vacuolar sellar syndrome (10% with Hyperprolactinemia). 4 Inflammatory and destructive lesions: including meningitis, tuberculosis, syphilis, actinomycosis, injury, surgery, arteriovenous malformation, granulomatosis; pituitary stalk lesions, injury or tumor compression. 5 trauma, stress and Parkinson's disease. (2) thyroid and adrenal diseases: including primary and secondary hypothyroidism, pseudohypoparathyroidism, Hashimoto's thyroiditis. Adrenal diseases, including chronic kidney disease, Addison's disease, and chronic renal failure may have hyperprolactinemia. (3) ectopic prolactin secretion syndrome: including undifferentiated bronchogenic lung cancer, adrenal cancer and embryonal cancer. (4) Polycystic ovary syndrome. (5) Obstetrics and gynecology surgery and local irritation: including induced abortion, erosive hydatidiform mole or stillbirth, postpartum, hysterectomy, tubal ligation, oophorectomy. Local breast irritation, including papillitis, cleft palate, chest wall trauma, herpes zoster, tuberculosis, and chest wall surgery can also cause hyperprolactinemia. (6) drugs that promote prolactin secretion: 1 anesthetic drugs: including morphine, methadone, methionine enkephalin. 2 psychiatric drugs: including phenothiazines, including haloperidol, fluphenazine, chlorpromazine, tricyclic antidepressants, alpha peptides, chlordiazepines, amphetamines and diazepam. 3 hormone drugs: including estrogen, oral contraceptives, thyroid stimulating hormone releasing hormone (TSH-RH). 4 antihypertensive drugs: including methyldopa, reserpine, verapamil (icopidine). 5 affecting dopamine metabolism and functional drugs: including: A. dopamine receptor antagonists, including phenothiazine, haloperidol, metoclopramide, morphine, piperazine (pimozide); B. Dopamine reuptake blocker: nomifensine (phenisoquineamine); C. dopamine degrading agent, including reserpine, methyldopa; D. dopamine conversion inhibitor: apeptide. 6 monoamine oxidase inhibitor. 7 benzodiazepine derivatives: including dibenzoxazole nitrogen leather, carbamoyl chloride, inducible, imipramine, amitriptyline, phenytoin, diazepam, clonazepam. 8 histamine and histamine H1, H2 receptor antagonists: including serotonin, amphetamine and the like. H1 receptor antagonists, including meclizine, pyripramine. H2 receptor antagonist cyanoguanidine. 9 antiemetic drugs: including sulpiride, promethazine (purazine), perphenazine. 10 other: cyproheptadine. (B) the pathogenesis of pituitary prolactin (PRL) secretion is strongly controlled by the hypothalamic nodules - dopaminergic neurons in the funnel, so any damage to the hypothalamic lesions such as tumors, radiation damage and inflammation may make the pituitary PRL Increased secretion, resulting in high PRL. Some pituitary diseases (such as inflammation), if damaged by the pituitary stalk, can reduce the dopamine transported by the hypothalamus to the pituitary PRL cells and cause high PRL. Certain non-PRL pituitary tumors such as GH tumors, ACTH tumors, etc. can compress the pituitary stalk and cause high PRL. TRH has a strong effect on the secretion of PRL, while thyroid hormone can slightly inhibit the response of PRL cells to TRH, so high PRL can occur in primary hypothyroidism. 30% to 80% of patients with end-stage renal failure have mild to moderate high PRL, which may be due to accelerated dopamine metabolism in these patients. In cirrhosis, high PRL can be caused by abnormal metabolism of neurotransmitters. Some chest and breast diseases such as thoracic surgery, chest herpes, mastitis, etc. can also cause high PRL. Some non-endocrine gland tumors such as bronchial carcinoma can also secrete PRL, which produces high PRL, but is extremely rare. Symptoms: 1. General manifestations (1) Menstrual disorders: 4% of primary amenorrhea, 89% of secondary amenorrhea, less than 7% of menstrual thinning, menstruation, dysfunctional bleeding and luteal insufficiency accounted for 23% ~77%. (2) The typical amenorrhea-galactorrhea syndrome of galactorrhea is 20.84% in non-tumor hyperprolactinemia, 70.6% in tumor type, and 63%-83.5% in simple galactorrhea. The galactorrhea appears as a dominant or extruded breast, as a water sample, as a serum, or as a milk. More normal breasts. (3) The incidence of infertility is 70.7%, which may be primary or secondary infertility, and is associated with anovulation, luteal insufficiency or luteinized non-ruptured follicular syndrome (LUFS). (4) low estrogenemia and hyperandrogenism: decreased estrogen causes flushing, palpitations, spontaneous sweating, vaginal dryness, sexual pain, loss of libido, etc. Elevated androgen causes moderate obesity, seborrheic, acne and hirsutism. (5) visual acuity and visual field changes: pituitary tumors involving the optic nerve cross, can cause vision loss, headache, dizziness, hemianopia and blindness, as well as brain nerve II, III, IV dysfunction, fundus edema and exudation. (6) Acromegaly: When seen in PRL-GH adenoma, mucinous edema is seen in patients with hypothyroidism, and some patients have type 2 diabetes and osteoporosis. 2. Clinical classification (1) Tumor-type hyperprolactinemia: 71.61% of hyperprolactinemia, of which prolactin adenomas account for 46%, microadenomas account for 66%, giant adenomas account for 34%, a few For prolactin-growth hormone adenomas and suspected cell tumors. Most pituitary adenomas have a PRL ≥ 200 ng/ml, and some pituitary adenomas can naturally resolve. (2) Postpartum hyperprolactinemia: 30% of hyperprolactinemia occurs in pregnancy, childbirth, abortion, and 3 years after induction of labor. Plasma prolactin is slightly elevated, and patients with menstrual thinning, menstrual disorders, galactorrhea, and prognosis are better. (3) special hyperprolactinemia: rare, mostly related to trauma, stress factors, and some are extremely small adenomas. (4) iatrogenic hyperprolactinemia is caused by iatrogenic factors or drugs, mostly caused by other diseases (such as hypothyroidism), which can be naturally recovered after the cause is removed. (5) The latent hyperprolactinemia (OHP) is also called occult hyperprolactinemia. (1) The cause of the disease 1. Physiological hyperprolactinemia Normal healthy women during night and sleep (2-6am) Increased plasma prolactin in late follicular and luteal phase. Plasma prolactin is increased 5 to 10 times during pregnancy. The concentration of prolactin in amniotic fluid is higher than that in plasma after the second trimester. In lactating women, plasma prolactin concentrations are 1 times higher than non-pregnant women. Fetal and neonatal (≥ 28 weeks gestation - 2 to 3 weeks postpartum) plasma prolactin corresponds to maternal levels. Massage the breast and sucking the nipple to reflexively promote prolactin secretion. Plasma prolactin remained at a high level during the puerperium (within 4 weeks). Prolactin in non-breastfeeding women fell to non-pregnancy levels within 3 months. Prolactin is significantly elevated in fasting, insulin-induced hypoglycemia, exercise, stress, and sexual intercourse. 2. Pathological hyperprolactinemia Read more...