Patient's question:
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Doctor's answer:
Sex hormones include androgens and estrogens. Androgens are mainly testosterone and small amounts of dehydroepiandrosterone and androstenedione. The main metabolite of testosterone is androsterone. The main physiological functions of androgens are: 1. Stimulating the differentiation, maturation, and development of male internal and external genitalia during embryonic and postnatal periods; 2. Promoting the anabolic effect of protein synthesis; 3. Promoting the synthesis of erythropoietin in the kidneys and stimulating hematopoietic function in the bone marrow, etc. Estrogens include estrogen and progesterone. Estrogens are divided into estradiol and small amounts of estrone and estriol. The main metabolites of estradiol and estrone are estriol. Progesterone is mainly progesterone. The main metabolite of progesterone is allopregnanolone. The urinary excretion of allopregnanolone can be used as an indicator of luteal function. The main physiological functions of estrogens are: 1. Promoting the differentiation, maturation, and development of female internal and external genitalia, and synergistically forming the menstrual cycle with progesterone; 2. Effects on metabolism include promoting the liver to synthesize various transport proteins, reducing cholesterol, and promoting the synthesis of high-density lipoprotein, etc. The main physiological functions of progesterone are that progesterone primarily acts synergistically with estrogen on the endometrium to form the menstrual cycle, etc. Therefore, sex hormones are all steroid hormones. Common serum gonadal hormone tests include: 1. Testosterone (T) in males Normal male reproductive system function depends on the interaction between the hypothalamus, pituitary, and testes. It mainly promotes the development of the clitoris, labia, and mons pubis. It has an antagonistic effect on estrogen and has a certain impact on overall metabolism. The normal concentration of blood T in females is 0.7~3.1 mol/L. High blood T levels are known as hyper-Temia, which can cause infertility. Blood T levels are also elevated in polycystic ovary syndrome. T is the main and only clinically significant androgen in the male body. T secretion increases during puberty and remains high until the age of 40, then gradually declines with age. In young males, T secretion has a circadian rhythm, with a peak around 8 a.m. As age increases, this secretion rhythm disappears. Measuring morning T levels can best evaluate the degree of decline in male T levels. The proportion of free T in the blood circulation is very low, less than 2% of total T. Measuring free T levels in the male body can represent the level of biologically active T. T testing can be used to diagnose male sexual dysfunction or insufficient T secretion, as well as to evaluate male infertility. Elevated T levels are common in benign interstitial cell tumors of the testes, congenital adrenal hyperplasia, true precocious puberty, male pseudohermaphroditism, female masculinizing tumors, polycystic ovary syndrome, cortisol excess, and the use of gonadotropins, obesity, and late pregnancy. Low T levels are seen in male sexual dysfunction, primary testicular hypoplasia, hyperprolactinemia, hypopituitarism, systemic lupus erythematosus, hypothyroidism, osteoporosis, cryptorchiditis, and gynecomastia. 2. Human chorionic gonadotropin (HCG) Diagnosis of early pregnancy: HCG can be detected 5-7 days after fertilization, with serum HCG levels as an indicator for diagnosing early pregnancy, achieving a compliance rate of 98-100%. Diagnosis of trophoblastic cell tumors, observation of treatment efficacy, and prognosis assessment: Patients with molar pregnancy and choriocarcinoma have significantly higher serum HCG levels than normal pregnancy, and their secretion amount is positively correlated with the total number of cancer cells and the severity of the condition. Dynamically detecting HCG levels during treatment actually reflects the growth or regression of cancer cell clusters. This is of practical value for clinical treatment selection, efficacy observation, and prognosis assessment. Generally, serum HCG levels decrease to normal after molar pregnancy evacuation. If levels rise during follow-up, it suggests recurrence. Simultaneously measuring cerebrospinal fluid and serum HCG levels and calculating their concentration ratio helps determine whether choriocarcinoma has metastasized to the brain. Diagnosis of ectopic pregnancy: In cases of delayed menstruation without early pregnancy symptoms, high HCG levels, and no chorionic villi found during induced abortion, ectopic pregnancy should be considered. Management of threatened abortion: By dynamically monitoring HCG changes, if the HCG level does not decrease significantly and remains close to normal, active fetal preservation can be initiated. If HCG levels gradually rise and align with the gestational age after treatment, pregnancy can continue. However, if HCG levels gradually decrease and reach a certain extent, miscarriage is inevitable, and induced abortion should be performed to terminate the pregnancy. Differential diagnosis of incomplete abortion: After 4 weeks of miscarriage, HCG should return to normal, but in incomplete abortion, HCG levels remain higher than normal. If there is uterine cavity infection or incomplete uterine involution postpartum, HCG levels will be within the normal range. 3. Prolactin (PRL) The main physiological function of human PRL is to maintain lactation after childbirth and, together with ovarian hormones, to promote the development of breast ducts and glands before delivery. It mainly promotes the proliferation of the breast, milk production, and lactation. In non-lactating periods, the normal value of blood PRL is 0.08~0.92 mol/L. Levels higher than 1.0 mol/L indicate hyperprolactinemia, and excessive PRL can inhibit the secretion of FSH and LH, suppress ovarian function, and inhibit ovulation. 4. Human placental lactogen (hPL) Human placental lactogen (hPL), also known as human chorionic somatomammotropin (hCS), is produced and secreted by syncytiotrophoblast cells of the placenta. After secretion, most of it enters the intervillous space and placental sinusoids, rarely appearing in the fetal body. The function of hPL is to synergistically promote breast development and positive nitrogen balance with insulin and corticosteroids in pregnant women, which is beneficial for the accumulation of proteins during pregnancy. hPL also has an inhibitory effect on fat deposition, promoting lipolysis and increasing free fatty acid levels in the blood. When free fatty acids in the blood are more abundant than glucose, muscle tissue primarily uses free fatty acids as an energy source, reducing glucose uptake, which is favorable for the fetus to take up large amounts of glucose from the mother's blood. This function of hPL is a crucial condition for the rapid growth and development of the fetus. When there is abnormal lactation, infertility with unknown factors or causes, or pituitary adenomas, hPL testing is indicated. Excessive synthesis and release of prolactin can lead to hypogonadism syndrome, which is very common in women. Elevated prolactin levels in women can cause lactation, infertility with unknown causes, anovulation with amenorrhea, and in severe cases, significant estrogen reduction. Hyperprolactinemia is a common cause or factor leading to female infertility. Therefore, measuring prolactin is of great significance for diagnosing diseases affecting the female reproductive system. 5. Progesterone (P) P is secreted by the corpus luteum in the second half of the normal menstrual cycle, with concentration changes varying greatly depending on the menstrual cycle. After pregnancy, its concentration is further influenced by placental synthesis. P testing is widely used to confirm ovulation and as a reference for managing pregnancy-related complications such as threatened abortion and ectopic pregnancy in the first three months of pregnancy. The placenta can synthesize P from cholesterol in the mother's blood, starting to produce sufficient P from the 36th day of pregnancy. The raw material for placental synthesis of P is cholesterol, which comes from the maternal blood supply. It mainly promotes the transformation of the endometrium from the proliferative phase to the secretory phase. Blood P concentration is 0-4.8 mol/L before ovulation, 7.6-97.6 mol/L after ovulation, and 272-793 pmol/L in the post-ovulatory phase. Low blood P levels in the post-ovulatory phase are seen in luteal dysfunction and ovulatory dysfunctional uterine bleeding. In normal women, blood P levels are highest during the luteal phase and lowest during the follicular phase. Dynamic monitoring helps determine the ovulatory phase, assess luteal function, and study the mechanisms of various steroid contraceptives and anti-abortion drugs. In normal pregnancy, blood P levels rise starting from the 11th week, reaching a peak by the 35th week, with levels as high as 80-320 μg/L. In threatened abortion, P remains high; if there is a downward trend, miscarriage is possible. In multiple pregnancies, P levels are elevated. Pathological elevation of P is seen in diabetic pregnant women, molar pregnancy, granulosa cell tumors of the ovary, lipid cell tumors of the ovary, congenital adrenal hyperplasia, congenital 17α-hydroxylase deficiency, primary hypertension, etc. Pathological reduction of P is mainly seen in luteal dysfunction, polycystic ovary syndrome, anovulatory dysfunctional uterine bleeding, severe pregnancy dysfunction, fetal growth retardation, and stillbirth. 6. Estradiol (E2) In normal late pregnancy, estrone (E1), estradiol (E2), and estriol mainly come from ovarian secretion, with E3 being the metabolite of the first two in peripheral tissues. Since the placenta can also synthesize E1, E2, and E3, the estrogen levels in normal pregnant women continue to rise with gestational age. By the 7th week of pregnancy, placental estrogen production exceeds 50%, so after the first few weeks of pregnancy, the ovary is no longer a major source of estrogen. E2 is mainly secreted by the testes, ovaries, and placenta, and when released into the blood circulation, it is the most biologically active natural estrogen. E2 mainly promotes the transformation of the endometrium to the proliferative phase and the development of female secondary sexual characteristics. In normal pregnancy, E2 levels rise slightly and decline rapidly after placental delivery. In ovulating women, E2 in the blood circulation primarily comes from a group of maturing follicles, finally from a fully mature follicle ready to ovulate, and the corpus luteum formed from it. E2 levels vary greatly depending on the phase of the menstrual cycle. In postmenopausal women, E2 comes from the conversion of androgens outside the gonads, with low circulating concentrations and no cyclical pattern. In prepubertal children and males, circulating concentrations are also low and non-cyclical. E2 testing can be used as one of the diagnostic indicators for female precocious puberty, helps analyze male gynecomastia, assess female estrogen deficiency and excess, and is affected by the use of contraceptives, superovulation drugs, and estrogen replacement therapy, among others. In abnormal pregnancies, twin or multiple pregnancies, and diabetic pregnancies, E2 levels are generally elevated. In severe cases of preeclampsia, E2 levels are low, and if E2 is particularly low, it may suggest the possibility of fetal intrauterine death, requiring combined other tests for confirmation and timely management. In anencephaly, E2 levels are low. In molar pregnancy, E2 levels are low, with urinary E2 levels being only 1-12% of those in normal pregnancy. Blood E2 concentrations are 48-521 pmol/L before ovulation, 70-1835 pmol/L during ovulation, and 272-793 pmol/L after ovulation. Pathological causes of elevated E2 levels: 1. Ovarian disorders: Granulosa cell tumors, ovarian teratomas, lipid cell tumors, and sex hormone-producing tumors all indicate ovarian hyperfunction and increased E2 secretion. 2. Cardiovascular diseases: Myocardial infarction, angina, and coronary stenosis. 3. Other: Systemic lupus erythematosus, liver cirrhosis, and male obesity. Pathological causes of low E2 levels: 1. Ovarian disorders: Ovarian absence or hypoplasia, ovarian hypofunction, premature ovarian failure, primary ovarian failure, and ovarian cysts. 2. Pituitary amenorrhea or infertility. 3. Other: Hypothyroidism or hyperthyroidism, Cushing's syndrome, Addison's disease, Sheehan's syndrome, malignancies, extensive infections, renal insufficiency, focal lesions in the brain and pituitary, etc., can all lead to reduced plasma E2 levels. 7. Estriol (E3) Monitoring placental function: Poor placental function, placental sulfatase deficiency, and preeclampsia affecting uterine-placental circulation can all lead to decreased E3 levels. Generally, pregnant women with gestational age >42 weeks experience gradual placental function decline. Weekly detection of E3 concentrations 2-3 times will help identify clinical issues. If E3 remains persistently high, natural delivery can be awaited; if E3 levels decrease, it indicates that fetal-placental function is deteriorating, and the fetus may experience intrauterine complications, requiring timely induction of labor or cesarean delivery. Monitoring high-risk pregnancies: Regular dynamic detection of pregnant women's blood or urine E3 levels can help estimate gestational age; if E3 continues to rise, it suggests preterm labor; if several measurements are at the same level, it indicates term pregnancy; if levels gradually decrease, it is often indicative of postterm pregnancy; significant reduction suggests fetal intrauterine distress, requiring close monitoring of fetal movement and heart rate, and appropriate measures should be taken based on the situation; if plasma E3 levels <2 mg/L, the possibility of fetal intrauterine death is high. 8. Follicle-stimulating hormone (FSH) It primarily promotes the development and maturation of ovarian follicles. In women, FSH stimulates follicular growth and maturation by directly acting on receptors on granulosa cells. Like LH, elevated FSH levels indicate that the follicle is about to rupture, allowing for the prediction of ovulation and the diagnosis of ovulatory disorders, as well as the prediction of responses to superovulation drugs. Blood FSH concentrations are 1.5-10 mIU/ml before ovulation, 8-20 mIU/ml during ovulation, and 2-10 mIU/ml after ovulation. Generally, 5-40 mIU/ml is considered normal. Low FSH levels are seen during estrogen-progesterone treatment and Sheehan's syndrome. High FSH levels are seen in premature ovarian failure, ovarian insensitivity syndrome, and primary amenorrhea. If FSH levels are higher than 40 mIU/ml, they are ineffective against ovulation-inducing drugs such as clomiphene. 9. Luteinizing hormone (LH) It primarily promotes ovulation (in conjunction with FSH) and the formation of the corpus luteum and secretion of progesterone, allowing for the prediction of ovulation. In women, LH, follicle-stimulating hormone, and estradiol interact to promote the synthesis of ovarian hormones. LH testing is used to predict ovulation and diagnose ovulatory disorders, but it can also be affected by oral contraceptives, superovulation drugs, estrogen replacement therapy, and oophorectomy, among others. Blood LH concentrations are 2-15 mIU/ml before ovulation, 30-100 mIU/ml during ovulation, and 4-10 mIU/ml after ovulation. Generally, normal values outside of the ovulatory phase are 5-25 mIU/ml. Levels below 5 mIU/ml suggest hypogonadism, seen in Sheehan's syndrome; high FSH levels combined with high LH suggest ovarian failure. LH/FSH ≥3 is one of the diagnostic criteria for polycystic ovary syndrome. In human malignancies, the secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) is rarely observed. In 50% of malignant tumors, the cancer tissue contains estrogen receptors, while only 5% of normal benign breast tumor tissue does. Among estrogen receptor-positive tumors, 62% also have progesterone receptors. Tumors without estrogen receptors have only 8% with progesterone receptors. Clinical significance: Patients with receptor-positive tumors respond well to corresponding endocrine hormone therapy, while those without receptors have poor efficacy, with an average success rate of only 10%.