Hyper PRLemia is the most common clinical disorder of the endocrine system with disorders of the hypothalamic-pituitary axis. Hyper PRLemia is significantly more common in women. There are many causes of hyperPRLemia, which are mainly classified into four categories: physiologic, pharmacologic, pathologic, and idiopathic. Clinical diagnosis of pathologic hyperPRLemia must be made with the exception of other causes of increased PRL. Normal human blood PRL level is not constant, PRL secretion has a diurnal rhythm, after sleep gradually rise, in the morning before waking up can reach the 24-hour peak, after waking up decline, 2:00 p.m. down to the trough of the day. Various stressful situations such as exercise, tension, cold, pain, and surgery; physiological states such as pregnancy, breastfeeding, touching the nipple, and ovulation; infections and fever, immune disorders, and systemic diseases of the body such as the liver or kidneys can cause an increase in serum PRL; and female hormones, sedative sleeping and psychotropic drugs, and H2-receptor blockers can rapidly cause a significant increase in serum PRL levels. After the exclusion of these reversible hyperPRLemia factors, persistent blood PRL elevation of 150-200 μg/L or more is usually suggestive of pituitary PRL-secreting adenoma, whereas only a few cases of mildly elevated blood PRL levels are confirmed to be pituitary PRL-secreting adenomas during follow-up. Pathological hyper-PRLemia mainly manifests in women of childbearing age as menstrual disorders, lactation, weight gain, etc., and in men as decreased libido, male infertility and even impotence. The potential threat of persistent hyperproliferative disorders is osteoporosis, and PRL macroadenomas also have a tumor-occupying effect, which can be manifested as growth disorders in children and adolescents with pre-pubertal onset. Magnetic resonance imaging (MRI) of pituitary PRL adenomas is the most valuable imaging method. Early therapeutic intervention is needed for clinically symptomatic hyperPRLemia and pituitary prolactin adenomas; asymptomatic mild hyperPRLemia can be followed and observed. The dopamine agonist bromocriptine (Bromocriptine) was clinically studied since 1969 and officially marketed in 1973, which has good efficacy in hyper-PRLemia, making 70%~90% of patients with pituitary PRL adenomas to decrease PRL level, inhibit lactation, shrink the tumor, and restore menstruation and fertility. This is an epoch-making progress in the history of pituitary adenoma treatment. Subsequently, newer dopamine agonists with stronger, longer-lasting effects and fewer side effects were introduced. Pharmacologic therapy has now become the treatment of choice for the majority of hyperproliferative, pituitary PRL adenomas. Surgical treatment is an option for the few cases that do not respond well to dopamine agonists or cannot tolerate the side effects. The primary surgical approach is microsurgery via the transnasal or oral-pterygoid sinus route, and individual suprasellar and paraspinal development of macroadenomas may require craniotomy. Postoperative residual tumors may be supplemented with radiation therapy and dopamine agonist medication. Patients with hypopituitarism may be treated with pituitary target gland hormone replacement therapy. Idiopathic hyperprolactinemia is not associated with pregnancy, medication, pituitary tumors, or other organic pathologies, but is due to a dysfunction of the hypothalamus-pituitary gland, which leads to increased PRL secretion. Most of them have mildly elevated PRL and have a long course of the disease, but can return to normal. The diagnosis of idiopathic hyperPRLemia is established when there is no medical cause and the cranial magnetic resonance fails to detect an adenoma. However, in some cases with menstrual disorders and PRL higher than 100 μg/L, the possibility of latent pituitary microadenomas needs to be guarded against, and should be closely followed up. Another type of hyper-PRLmia is macroprolactinemia. Macromolecular PRL anemia is a marked increase in serum PRL without clinical symptoms. This macromolecule PRL forms immune complexes with its IgG-type antibodies and has no biological effect in vivo because its high molecular weight cannot pass through the capillary wall or bind to target cell receptors, but because of its long half-life, it is easy to accumulate in the circulation, resulting in an increase in PRL. Hyperprolactinemia has also been reported in the 1 to 2 hours following seizures; anti-PRL autoantibodies have been suggested as a possible unknown cause of hyperprolactinemia; and the causal relationship between polycystic ovary syndrome (PCOS) and hyperprolactinemia is debated. The etiologic diagnosis of hyperprolactinemia requires a detailed history, appropriate laboratory tests, and imaging studies to rule out physiologic or pharmacologic causes of elevated PRL levels and to determine whether there is a clear pathologic cause. The most common cause is pituitary adenoma. History-taking The patient’s medical history needs to be tailored to the physiologic, pathologic, and pharmacologic causes of hyperPRLemia (see above) that may be relevant to the patient’s condition. The patient should be asked about her menstrual, labor and delivery, surgical, and past medical history, any history of related medications, and the presence of stress at the time of blood collection (e.g., exercise, sexual intercourse, mood swings, or pelvic exam). Other laboratory tests Including pregnancy test, thyroid function, renal function, etc., which are selected according to the medical history. Imaging tests After the above tests, mild hyper PRL without a clear cause or blood PRL 100μg/L should be confirmed by imaging tests (MRI or CT) of the cranium/pteronavicular saddle in order to exclude or determine the presence of intracranial tumors compressing the pituitary stalks or secretion of PRL and empty pteronavicular saddle syndrome, etc., and idiopathic hyper PRLemia if no clear cause is found. The goals of treatment for hyperPRLemia are to suppress PRL secretion, restore normal menstrual and ovulatory function, reduce breast milk production, and improve other symptoms such as headaches and visual dysfunction. After identifying hyper PRLemia, the first decision is whether treatment is needed. Pituitary PRL macroadenomas and microadenomas accompanied by amenorrhea, lactation, infertility, headache, osteoporosis and other manifestations require treatment; only increased blood PRL levels without the above manifestations can be followed up for observation. The next step is to decide the treatment plan and which treatment method to choose. For pituitary PRL adenomas, whether microadenomas or macroadenomas, dopamine agonist treatment can be preferred; for those patients with poor drug efficacy, large side effects and refusal to accept drug treatment can choose surgical treatment. For the choice of treatment, doctors should help patients to make appropriate choices according to their own conditions, such as age, fertility status and requirements, and with full respect for patients’ opinions while fully informing them of the advantages and disadvantages of various treatment methods.