I. Etiological diagnosis of hyperprolactinemia
A detailed medical history, laboratory tests, and imaging examinations are used to rule out physiological or pharmacological factors causing elevated PRL levels and to clarify whether there is a clear pathological cause. The most common cause is pituitary adenoma.
1. History taking
The patient’s medical history should be tailored to the physiologic, pathologic, and pharmacologic causes of hyper-PRLemia. Patients should be asked about their menstrual history, childbirth history, surgical history, past medical history, any history of taking related drugs, and any stressful conditions (such as exercise, sexual intercourse, mental and emotional fluctuations or pelvic examination) at the time of blood collection.
2.Other laboratory tests
Including pregnancy test, thyroid function, kidney function, etc., according to the medical history to choose to carry out.
3.Imaging examination
After the above tests, it is confirmed that mild hyper-PRL without a clear cause or 100μg/L blood PRL should be examined by cranial/saddle imaging (MRI or CT) to exclude or determine whether there is an intracranial tumor that compresses the pituitary stalk or secretes PRL and empty saddle syndrome, etc. If there is no clear cause, it is idiopathic hyper-PRLemia.
The main imaging tests for saddle lesions are CT and MRI. Although some lesions can be diagnosed with certainty by MRI scan, it is recommended to perform enhanced MRI of the saddle area at the same time to detect the lesions with a higher rate, and if necessary, dynamic enhanced MRI of the saddle area should be performed.
The goals of treatment for hyper-PRLemia are to suppress PRL secretion, restore normal menstruation and ovulation, reduce lactation, and improve other symptoms such as headaches and visual dysfunction.
After hyper-PRLemia is identified, the first step is to decide whether treatment is needed. Pituitary PRL macroadenomas and microadenomas with amenorrhea, lactation, infertility, headache, osteoporosis and other manifestations need to be treated; those with only increased blood PRL levels and no such manifestations can be followed up and observed. The next step is to decide the treatment plan and which treatment method to choose. For pituitary PRL adenomas, whether they are microadenomas or macroadenomas, dopamine agonist therapy is the first choice; for those patients with poor drug efficacy, high side effects and those who refuse to accept drug therapy, surgery is the treatment of choice.
For the choice of treatment method, doctors should fully respect patients’ opinions and help them make appropriate choices according to their own conditions, such as age, fertility status and requirements, while fully informing them of the advantages and disadvantages of various treatment methods.
II. Drug therapy
Dopamine agonist therapy is indicated for all patients with hyper-PRLemia with menstrual disorders, infertility, headache, osteoporosis, lactation, optic sympathetic* or other cranial nerve compression, including pituitary PRL adenomas. The most commonly used are bromocriptine, cartegolide and quinagolide.
1. Bromocriptine
Treatment is increased gradually from a small dose, i.e. starting with 1.25 mg at bedtime and increasing to the required therapeutic dose. If the response is not significant, it can be increased to the therapeutic amount within a few days. The common dose is 2.5mg~10mg per day, divided into 2~3 doses. 5mg~7.5mg per day has been effective in most cases. Dose adjustment is based on blood PRL level. Bromocriptine treatment can achieve good results in 70%-90% of patients, as shown by the reduction of blood PRL to normal, disappearance or reduction of lactation, reduction of pituitary adenoma, restoration of regular menstruation and fertility, and in men, restoration of libido and sperm production, and correction of male infertility.
It is worth noting that bromocriptine only inhibits the growth of tumor cells and makes them fibrotic, but does not destroy them.
The side effects of bromocriptine are mainly nausea, vomiting, dizziness, headache and constipation, which disappear within a short period of time in most cases. A gradual dosing method starting with small doses may reduce side effects, and if intolerance becomes apparent at increasing doses, the incremental dose may be reduced. Raynaud’s phenomenon and abnormal heart rhythm may occur at high doses. The most serious adverse effect of this drug is postural hypotension in a small number of patients at the first dose, and loss of consciousness in some patients. Do not use concomitant drugs that increase blood PRL during bromocriptine treatment.
About 10% of patients who are not sensitive to bromocriptine, have unsatisfactory efficacy, or have severe headache, dizziness, gastrointestinal reactions, constipation, etc. that do not disappear and cannot tolerate the therapeutic dose of bromocriptine, can be replaced by other drugs or surgical treatment.
2.Other drugs
Cartegolide and quinagolide are highly selective dopamine D2 receptor agonists, which are substitutes of bromocriptine and have more powerful PRL inhibition with relatively less side effects and longer duration of action. Patients with PRL adenomas that are resistant to bromocriptine (unsatisfactory with 15 mg of bromocriptine daily) or intolerant to bromocriptine treatment are still more than 50% effective when switched to these new dopamine agonists. Quinagolide is given once daily at 75μg to 300μg; cartegolide is given only once or twice a week at the usual dose of 0.5mg to 2.0mg, with better patient compliance than bromocriptine.