Female precocious puberty

Introduction to female precocious puberty Premature precocious puberty (premature precocious puberty), that is, puberty development is significantly advanced, because each normal child has a large variation in the onset of puberty development, it is difficult to determine the absolute limit of normal and precocious puberty at the beginning of puberty. It is generally believed that the girl has a mammary gland before the age of 8 years. Any one or more secondary sexual characteristics such as enlargement, pubic hair growth, mane growth, or menarche begin before the age of 10, that is, female precocious puberty, and some scholars advocate that children's puberty and sexual development are earlier than the average normal child development. Precocious puberty is more than 2 or 2.5 standard deviations, and female precocious puberty accounts for about 0.2% of all women. basic knowledge The proportion of illness: 10% Susceptible people: women Mode of infection: non-infectious Complications: ovarian cysts

Female precocious puberty

(1) Causes of the disease

Gonadotropin increase (45%):

Caused by increased gonadotropin, increased gonadotropin causes follicular development, and even ovulation and fertility, this is homosexual precocity or complete precocious puberty, the most typical case is Lina Medinam in Peru, she is 5 years and 10 months At the time of pregnancy, the cesarean section is delivered.

Increase in gonadal steroids (46%):

Caused by increased gonadal steroids, such as increased estrogen, homosexual precocity, and increased androgen, heterosexual precocious puberty, incomplete precocious puberty, no fertility.

(two) pathogenesis

1. True precocious puberty is completely homosexual precocious, due to the early development of the gonad axis, premature puberty, sexual maturation process in normal puberty sequence, hypothalamic-pituitary-gonadal axis function, ovulation menstrual cycle, fertility force.

(1) idiopathic precocious puberty (idiopathic precocious puberty) also known as constitutional or functional precocious puberty, is a common cause of true precocious puberty in children, accounting for 80% to 90% of girls precocious puberty.

The cause was unknown. After careful examination, no pathological changes were found. However, about half of the children had abnormal EEG, basal levels of gonadotropin and sex hormones increased, LH pulse frequency and amplitude, and GnRH stimulation response were in normal puberty range. Within its pathogenesis, it has not yet been fully understood. It may be that the inhibition of gonad development in the central nervous system or the hypothalamus is out of control due to certain unclear reasons, and the premature secretion of GnRH or pituitary gonadotropin in the hypothalamus is increased. As a result, the disease has a family predisposition, males are more obvious, girls are more sporadic, rare, autosomal recessive inheritance, family history positive children with a late onset, relatively mild condition (boys in 7 After the age, girls are more than 6 years old, and the incidence of boys is more than girls.

Generally, the mammary gland develops first, followed by pubic hair. In most cases, the pubic hair appears along with the development of the external genitalia. With the development of the external genitalia, the mane and menstruation appear, the menstrual cycle begins to irregular, no ovulation, when the ovaries After full maturity, the menstrual cycle gradually changes and ovulation occurs. At this time, girls may have pregnancy. There are reports of a 5.5-year-old girl who is pregnant in the literature. During sexual development, her height, weight gain and bone maturity are accelerated. This rapid growth Mainly because the gonadal steroid hormone can stimulate the elevation of GH and IGF-1, but not all patients develop faster, but also have a slow development rate or a fast and slow time. Because of the early closure of the epiphysis, there is a high childhood, adulthood. Short stature development curve, about 1/3 of the children's adult height is less than 152cm, the development of teeth and intelligence is generally consistent with their age, except for the height of the patient is lower than the general group, the rest are normal, and their mental state is commensurate with the actual age, sex Growth hormone binding protein (GHBP) is significantly elevated in precocious patients, but with height, age, youth stage, IGF-1 and Irrespective of ketone / estradiol levels, which may be associated with increased body fat content.

Precocious puberty girls do not have premature amenorrhea, but the risk of developing breast cancer in adulthood is often higher than that of normal people. Gonadal steroid hormones, LH and LH pulse frequency and amplitude are like puberty, girls who are sick from 6 years old are often accompanied Adrenal function is early in advance.

(2) true precocious puberty caused by central nervous system diseases: central nervous system tumors or non-neoplastic diseases such as hydrocephalus, infection, cysts, trauma, etc. can cause true precocious puberty, accounting for about 10% of female precocious puberty, more than half of them For tumors, common tumors include pineal tumor, optic glioma, hypothalamic hamartoma, saddle teratoma, neurofibroma, astrocytoma, ependymoma.

How the intracranial lesions stimulate puberty has not been known so far, may be the local infiltration of intracranial tumors, scar structure and increased intracranial pressure, affecting the nerve pathway of the GnRH pulse generator in the brain, GnRH pulse appears in advance, and start Adolescent development, symptoms of precocious puberty, such as hamartoma is a non-progressive growth of tumors composed of ectopic hormone secreting neurons, fiber bundles and glial cells, ectopic GnRH secretion cells pulsed release GnRH, it has been reported that the GnRH-containing fibers in this tumor are connected to the hypothalamic median ridge, but the GnRH release caused by hamartoma is not controlled by the intrinsic central nervous system. It is an atopic CnRH pulse generator, a misconfiguration. The age of onset of tumor-induced precocious puberty is often small, mostly less than 3 years old, and can be combined with central nervous system abnormalities, such as epilepsy, dementia and other changes. Due to the extensive application of CT and MRI in recent years, the diagnosis rate of this disease is increasing year by year. About 10% of patients have sexual precocity, in addition, arachnoid cyst can also cause hypothalamic, pituitary dysfunction, physiological precocious puberty.

The development of sexual characteristics in patients with precocious puberty caused by central nervous system disease is similar to that of idiopathic, except for the development of sexual characteristics, accompanied by other corresponding symptoms of intracranial disease, such as polydipsia, polyuria, fever, obesity or excessive Weight loss, mental abnormalities, mental retardation, headache, vomiting, convulsions, limb paralysis and visual impairment. It is worth noting that a considerable number of patients have slow growth of intracranial tumors, often first with precocious puberty, and then gradually appear intracranial Symptoms and signs of high pressure or damaged nerve tissue, the mechanism of hydrocephalus causing precocious puberty and amenorrhea is not yet clear. About 22 cases of hydrocephalus combined with amenorrhea and several cases of precocious puberty have been reported. After hydrocephalus drainage treatment, large Some cases can cause the initiation and maintenance of the normal reproductive cycle. It is believed that the mechanism leading to abnormal function of the reproductive system may be related to GnRH, but the exact pathway of hydrocephalus affecting the GnRH system of the hypothalamus is still unclear, possibly with mechanical compression, ischemia, The destruction of the nerve conduction feedback pathway is related.

(3) True precocious puberty caused by other causes: congenital adrenal hyperplasia such as 11-hydroxylase and 21-hydroxylase deficiency patients treated with glucocorticoids or simultaneous mineralocorticoids, plasma ACTH levels are inhibited, adrenal gland The production of gonadal steroids is reduced, but due to the delay in diagnosis and treatment, the patient's bone age is advanced. If the bone age limit value of puberty is reached, the patient may have activation of hypothalamic-pituitary-gonadal axis function, causing precocious puberty, which has been used in the past. This is also the case with patients treated with gonadal steroids.

2. Female pseudo-precocious pseudo-precocious puberty is incomplete homosexual precocity, is the gonad or adrenal gland-derived estrogen or exogenous estrogen excessively stimulates the target organ, causing the development of secondary sexual characteristics, menstrual cramps, Normal hypothalamic-pituitary-gonadal axis function is not established, so there is no fertility.

(1) neoplastic pseudoprecocious puberty: follicular cysts and ovarian tumors (granulosa cell tumor, vesicular cell tumor, etc.) are the most common causes of female pseudoprecocious puberty, "autonomic" follicular cysts, which secrete estrogen. Promote sexual development and vaginal bleeding, the secretion of estrogen concentration fluctuates greatly, most ovarian tumors are bilateral, gonadotropin levels are inhibited, LH is slow to respond to GnRH stimulation, B-ultrasound helps follicular cysts and parenchyma Sexual ovarian tumors are identified, but many patients need to be diagnosed by exploratory laparotomy. Follicular cysts generally do not require surgery. Recently, an ovarian tumor derived from residual adrenal tissue has been reported to cause pseudo-precocious puberty. Determined by the P450C11P and P450 C21 specific genes expressed in the adrenal cortex, ovarian teratoma, chorionic epithelial carcinoma, germ cell tumor, liver tumor, if only chorionic gonadotropin (HCG) is secreted, does not cause female sex Precocious (unless estrogen is secreted at the same time), because in the absence of FSH, pure HCG, LH can not stimulate ovarian synthesis of estrogen, adrenal feminine tumor It can cause pseudo precocious puberty, which is derived from a tumor estrogen secreted androstenedione or transformed from an outer gland.

The main lesions of Peutz-Jeghers syndrome are mucosal skin pigmentation, digestive tract polyps and tumors, incomplete precocious puberty due to tumor secretion of estrogen, and occasionally associated with supporting cell-stromal cell tumor.

Recently, Speiser et al reported a case of a 10-year-old girl with portal hypertension due to neonatal portal vein shunting and hepatocyte steroid hormone metabolism, resulting in increased blood sex hormone levels, and precocious ovarian and ovarian prolapse The patient developed pubic hair at 6 years old, 7 years old breast development, 10 years old with obvious acne and clitoris hypertrophy, and blood basal hormone levels were determined: androstenedione 413ng/dl, testosterone 226ng/dl, E2160pg/ml, liver transaminase Normal, coagulation index is mildly abnormal, ACTH stimulation test shows glucocorticoid hormone production defects, dexamethasone inhibition test shows male enedioneone and testosterone mildly decreased, LHRH stimulation test shows LH, FSH shows puberty-like reaction, B-ultrasound The ovarian enlargement and multiple follicles were detected. The bilateral ovarian enlargement was detected. The pathological examination was vesicular cell hyperplasia. The immunohistochemistry showed that the stromal cells had the expression of steroid synthase. The blood androstenedione was 1 month after operation. There was no change in testosterone, and E2 decreased to 56 pg/ml. Leuconide acetate significantly reduced testosterone levels, followed by oral contraceptive treatment, down to 50 ng/ml, menstruation Cycle recovery, this case reminds us to pay attention to the history of portal hypertension and blood sex hormone levels in children with precocious puberty.

(2) McCune-Albright syndrome: This disease is characterized by irregular skin brown pigmentation spots, slow progression of multiple bone dysplasia and precocious puberty (multiple bone dysplasia). See, because the G protein complex Gs subunit mutation caused by continuous activation in the absence of LH, and therefore attributed to the GnRH-independent precocious type, due to autonomic activation of the ovary, autonomous cystic follicles, increased estrogen secretion There is no ovulation in the ovary, sometimes there are multiple vesicular follicles, sometimes a single larger follicular cyst, while ovarian asymmetric cysts can be spontaneously atresia, but not inhibited by GnRH agonists, the basic level of LH is at prepubertal level, LH pair The GnRH reaction is not sensitive but responds to aromatase inhibitors.

The disease may also involve other endocrine diseases such as thyroid (nodular hyperplasia with toxic goiter), adrenal gland (multiple proliferative nodules with adrenal hyperfunction), pituitary (pituitary tumor with GH or PRL secretion) and thyroid Paragonads (adenomas or hyperplasia) and other diseases, resulting in excessive secretion of thyroxine, adrenocortical hormone and GH, PRL and other hormones, it is considered to be a multiple endocrine adenoma syndrome.

(3) Hypothyroidism: hypothyroidism in young children and adolescents, most children with delayed growth, sexual development retardation, amenorrhea, a small number of precocious puberty, manifested as mammary gland development, enlarged labia minora, vaginal mucus smear visible Changes in the effects of estrogen, generally no pubic hair growth, some children will have irregular vaginal bleeding, but often no growth in puberty, but short stature, bone age often lags behind the actual age, single or multiple small ovarian Cyst.

The exact mechanism of this disease is still unclear. FSH is slightly higher than normal, and FSH pulse secretion increases at night. It is inferred that there are two reasons:

1 The hypothalamic GnRH pulse generator is slightly activated, which stimulates the secretion of pituitary FSH without exciting LH secretion. Gnumbach et al believe that pituitary gonadotropin is cross-reactive with the feedback mechanism of thyroid hormone, so the cells secreting gonadotropin are like Like TSH secreting cells, it responds to thyroid hormone deficiency.

2 The release of TRH in the hypothalamus increases, causing an increase in FSH secretion, often accompanied by an increase in PRL, so galactorrhea may occur, and GH declines, so bone maturity is delayed without height and length.

(4) Asymmetric short stature dysplasia syndrome (Russell-Silver syndrome): This disease is rare, due to brain dysfunction caused by short stature, delayed bone age, abnormal development of head and facial bones and precocious puberty, showing an inverted triangle Face, mouth down, body is obviously asymmetrical, refers to the phalanx and the fifth finger (toe) inward bend, short deformity.

(5) Exogenous estrogen-induced pseudo-precocious puberty: including estrogen-containing drugs such as oral contraceptives and other estrogen-containing foods can cause, young girls eat oral contraceptives, breast development and vaginal bleeding , nipple, areola brown pigmentation, there are reports of this disease caused by the young girl sucking oral contraceptive mother's milk.

3. Sexual developmental variation

(1) Precocious thelarche: refers to the development of one or both breasts before the age of 8 years, no other sexual development, no bone age, early in the age of 2 years old, rarely more than 4 years old, It can naturally subside after a few months or years, a few can continue to adolescence, sometimes the development of breast development is slow, there is a hard knot, the nipple development is not obvious, the effect of estrogen on vaginal cells is not obvious, the uterus does not increase, estrogen The level is slightly higher or normal, the ovary generally does not increase, there may be single or several small follicles, follicles can sometimes disappear, sometimes appear, and often consistent with changes in the breast, FSH reaches puberty level, responds to GnRH, LH before puberty The level of no significant response to GnRH.

The mechanism of its pathogenesis is unknown, and may be:

1 temporary FSH and / or LH secretion, promote follicular development, estrogen temporarily increased;

2 prepubertal breast tissue is more sensitive to low levels of estrogen in the circulation;

3 The secretion of gonadotropin in the neonatal period was not stopped in time, and the gonadotropin in the body caused the secretion of estrogen, maintaining a certain level in the circulation;

4 premature breast development, serum sex hormone binding globulin (SHBG) increased, non-SHBG-bound testosterone and free testosterone decreased, decreased bioavailability, may lead to changes in the proportion of estrogen / androgen in the breast.

In addition, it has been found that the clinical type between simple premature breast development and central precocious puberty, Stanhope reported that 10 patients with spontaneous gonadotropin secretion and ovarian enlargement in addition to premature breast development The morphological changes of the ovary are somewhere in between. The treatment with GnRH-A is ineffective, suggesting that the mammary gland is not dependent on gonadotropin. The cyclical changes are probably due to abnormal follicular proliferation. This condition is called variation. Type of breast premature development (thelarche variant), it is reported that girls who have had premature breast development in childhood often have hyperinsulinemia, decreased IGFBP-1 and SHBG, and increased free androgen index, thus suggesting premature breast development Children should be followed up for long-term follow-up.

(2) Adrenal function early emergence (pubic hair early appearance): refers to the pubic hair, the early development of mane hair without other sexual development, a sexual developmental variation, often occurs in children after the age of 6, as early as only a few months Because of the premature secretion of adrenal androgen or the excessive sensitivity of hair follicles to androgen stimulation, but also reported cases of ovarian cysts temporarily secreted androgen, DHEA, DHEAS, androstenedione and testosterone, urinary 17-ketone Elevated steroids, the degree of elevation is comparable to that of normal hair development stage II, gonadotropin is not high, GnRH responds like prepuberty, bone age and body length are slightly higher than the actual age, but no bone over-maturation, There is no sudden increase in growth. If the bone age is too high and the testosterone reaches the level of puberty, the steroid hormone synthase deficiency may be considered. The disease is generally self-limiting, without treatment, and can enter the puberty normally.

(3) Single sexual precocity: It is a rare sign of incomplete sexual precocity. The clinical manifestation is that the girl has a single menstrual inflow, but no other sexual development, usually in the 1st to 6th year old. It is often transient, prognosis is good, estrogen levels fluctuate as high as pre-pubertal estrogen levels, gonadotropin does not increase, may be associated with increased transient ovarian function, and some are seen in children with ovarian cysts.

4. Excessive secretion of androgenetic premature androgen causes masculinization in women. Congenital adrenal hyperplasia or adrenogenital syndrome is impaired by 21 hydroxylase or 11-hydroxylase, and glucocorticoid synthesis is blocked. Reduced inhibition of pituitary ACTH, increased synthesis of ACTH, stimulate adrenal hyperplasia, including reticular cell proliferation, increased synthesis of androgen, in addition, 17-hydroxyprogesterone and progesterone can not be converted to glucocorticoid, and torogen Increase, such as the onset of embryo development within 20 weeks (positive value of the urethra, vaginal formation), the vulvar gender is blurred, become a female pseudohermaphroditism; after the onset, after birth, heterosexual precocity can occur, in addition, adrenal adenoma Or adrenal cancer or ovarian testicular cell tumors, etc., can secrete too much androgen and cause masculinization in women.

Female precocious puberty prevention

With the improvement of people's living standards and the increasing number of only children, it is more common to give supplements to healthy children. According to the survey, about 15% of children develop ahead of time and have a tendency to precocious puberty. In order to prevent the occurrence of precocious puberty, it should be Note the following:

1. Children should take nutritional nourishing agents under the guidance of doctors, supplement nutrition according to physiological needs. Children with precocious puberty often take ginseng royal jelly, pollen, chicken embryo baby, licorice, cordyceps and other tonics. These foods contain various nutrients. Substance, but also contains gonadotropin-like substances. Children who ingest too much of these supplements may induce precocious puberty, so it is very important to prevent children from eating supplements.

2. Society, schools and parents should pay attention to avoiding media factors that are not suitable for children, because these media factors can directly stimulate children's cerebral cortex activity, and cause children to have wrong sexual attitudes in advance.

3. To prevent false precocious puberty caused by misuse of contraceptives, mothers of childbearing age should keep the contraceptives in good condition.

4. The family should create an educational environment suitable for the child's physical and mental development, so that the child has a rich and rich life content, avoiding the child's dressing with the adult, so that the child is physiologically and psychologically consistent with the age characteristics, and maintain a beautiful innocence.

Female precocious complication Complications ovarian cysts

Generally, there is no complication, but the epiphysis is closed early, and the last one is short. Some girls with precocious puberty show depression or excessive behavior, and may have ovarian cysts.

Female precocious puberty symptoms common symptoms abdominal pain abdominal mass vaginal bleeding pigmented spot convulsion masculine visual impairment

Before the age of 8 or 2 times the standard deviation of the local average menarche age, the girl may have sexual maturity such as menstruation, mammary gland development and pubic hair growth. It can be diagnosed as precocious puberty, and then determined to be true or pseudo precocious, and seek The cause should first be excluded from diseases that are harmful to the body, such as central nervous system diseases, ovarian, adrenal tumors and other non-endocrine abnormalities caused by vaginal bleeding, such as inflammation, foreign bodies, trauma or genital tract tumors. Mistaken birth control pills, breastfeeding mothers taking contraceptives, whether or not to take nutrient foods containing sex hormones, history of head trauma 1 to 2 months ago, and history of birth, convulsions, epilepsy and infection, Is there a family history of precocious puberty, understanding the age of onset, the speed of disease and growth, and whether there is headache or visual impairment during the course of the disease.

Pay special attention to the physical examination:

1 should record the length of the body (the ratio of the upper body to the lower body), chest circumference, arm circumference, weight, pay attention to the distribution of fat, the state of the body, record the staging of sexual development and the development of the external genitalia, generally with the development of the breast is equivalent to the bone age 11 Age, menstrual cramps are equivalent to about 13 years of bone age to evaluate gonad development;

2 systemic examination should also pay attention to McCune-Albright syndrome, hypothyroidism, silver syndrome and other unique signs, such as skin pigmentation spots, abnormal skull shape, and attention to the presence or absence of signs of nervous system abnormalities, should pay attention to the skin when examining Skin pigmentation changes, acne, hair growth, excessive sebum secretion, and masculine performance;

3 abdominal, pelvic examination, pay attention to whether there is abdominal pain, abdominal mass and so on.

Female precocious examination

1. Determination of sex hormones and gonadotropins The secretion of sex hormones and gonadotropins has obvious age characteristics. FSH in blood of 2 years old male and female children, estradiol in boys and testosterone in boys are higher, after 2 years old Significantly decreased until the beginning of puberty, the blood testosterone <1.75nmol/L, estradiol <37.5pmol/l, testosterone <0.7nmol/L, estradiol <75.0pmol/L When true precocious puberty, LH, FSH increased, and there were periodic changes. There was a day-night fluctuation before the establishment of a periodic feedback relationship, and increased during nighttime sleep. Serum FSH, LH, testosterone and children with idiopathic precocious puberty The content of estradiol is higher than that of normal children of the same age, but there is no overlap between the normal high limit and the pathological low limit, so there is no strict limit, so the diagnostic reference value is small (especially early), if necessary, DHEAS, pregnancy The relationship between ketone, 17-hydroxyprogesterone, HCG, DHEAS and actual age and bone age can reflect the adrenal function, which is helpful for the diagnosis of true precocious puberty. When gonadotropin is not elevated, estrogen should be considered. Ovarian or adrenal tumor, if androgen Increased elevation should be considered for heterologous HCG secretion, and elevated blood progesterone suggests a luteal tumor.

2. GnRH or clomiphene stimulation test can understand the functional status of the hypothalamus-pituitary.

(1) GnRH stimulation test: LH is seen 30 minutes after the injection of GnRH in true precocious puberty, FSH is increased by 2 times or more than the basal value, while pseudo precocious puberty and hypothalamic-pituitary-gonadal axis function are not fully mature. Non-reactive or low-response, premature breast development, the response of this test is a significant increase in the peak of FSH, and LH reaction is not obvious, in the past, the simple reaction to promote LH, can identify premature breast development and central sex Early maturity, in recent years, the study found that infants under the age of 4 with simple breast premature development, the peak value of LH reaction in this test can be >20 U / L, so that infants under 4 years old can not be identified by LH reaction alone to identify simple breast premature Development and central precocious puberty, but to determine the reactivity of FSH to GnRH stimulation, it is generally considered central precocious puberty, LH/FSH>1 after GnRH stimulation, and simple mammary gland development, LH/FSH<1.

(2) Clomiphene stimulation test: It has certain value for judging the maturation of the hypothalamic-pituitary-gonadal axis, but it has been used less frequently. Before the test, FSH and LH were used as the basal level, followed by taking clomiphene 100mg continuously. After 5 days, the FSH was retested on the 6th day. If the baseline value increased by 50% after LH, the hypothalamic-pituitary-gonadal axis matured, which was helpful to identify true and pseudo precocious puberty.

3. Urine 17-ketone determination of congenital adrenal hyperplasia or adrenal cancer patients, increased urinary 17-ketone, feasible dexamethasone inhibition test, adrenal cancer patients with increased urinary 17-ketone can not be inhibited by low-dose dexamethasone, congenital adrenal gland Cortical hyperplasia has elevated plasma 17-hydroxyprogesterone, elevated plasma 11-deoxycorticosterone, and increased gestational gestrositol.

4. FT3, FT4 and TSH measurements help to reflect thyroid function.

5. Vaginal exfoliated cell smear to check estrogen levels, true precocious puberty, estrogen levels change periodically, while pseudo precocious puberty is persistently elevated.

6. If the basal body temperature is biphasic, it indicates that there is ovulation, which is true precocious puberty. There is no relevant information at present.

Other auxiliary inspections:

1. X-ray photograph of the left wrist was used to determine the bone age. Those with bone age exceeding the actual age of 2 years old were considered as precocious puberty, and those with delayed bone age indicated hypothyroidism.

2. Sella X-ray photograph, fundus, visual field examination, etc., to help understand whether there is intracranial lesion, saddle calcification suggesting craniopharyngioma, pineal calcification and sella enlargement, deformation suggesting intracranial tumor, intracranial Tumors can cause optic edema and visual field changes in the fundus.

3. EEG, brain topography, brain organ damage, often abnormal changes, some children with idiopathic precocious puberty, diffuse abnormalities in EEG, including abnormal slow wave with paroxysmal activity and tip Waves, spikes, etc. change.

4. Abdominal and pelvic B-ultrasound, can understand the adrenal gland and ovary, uterine size and morphology, and ovarian conditions.

5. CT and MRI examination: CT and MRI head examination can understand intracranial lesions, especially help to identify intracranial tumors, it is also valuable for the exclusion of secondary precocious puberty, and idiopathic precocious puberty It is normal, and it is also valuable for the identification of adrenal tumors and ovarian tumors. Some people use MRI to diagnose central precocious puberty according to the degree of concave surface in the upper pituitary (level 1 obvious depression, grade 2 mild depression, grade 3 flat, 4 Grades are slightly convex, and grade 5 is obviously protruding. It is considered that pituitary grading is of great value in the diagnosis of precocious puberty in prepubertal children. Those with grade 4 or higher can be highly suspected of central precocious puberty.

Female precocious puberty diagnosis

diagnosis

The disease depends on detailed medical history, comprehensive physical examination and necessary laboratory examinations and other auxiliary examinations, and requires careful follow-up observation to diagnose the cause. Idiopathic precocious puberty can only be completely excluded. The disease that causes precocious puberty can be diagnosed. During the follow-up, special attention should be paid to the possibility of early and slow-moving subclinical intracranial tumors. Children with precocious puberty caused by organic brain lesions, endocrine changes and bone age The characteristics are similar to those of idiopathic, but special examinations such as CT, MRI, EEG, EEG topography, and head X-ray may reveal abnormal signs, and there may be intracranial instruments before or after the development of sexual characteristics. The corresponding symptoms and signs of sexual diseases.

Differential diagnosis

Early stage of precocious puberty is not easy to differentiate from simple premature mammary gland development. However, if the rigorous follow-up observation is not difficult, the size of premature puberty and ovarian size is significantly increased, and the LH/FSH after GnRH stimulation is often >1. In the uterus of premature breast development, the size of the ovary does not change, and the LH/TSH is often <1 after stimulation. For those with early adrenal function, attention should be paid to the identification of adrenal hyperplasia and androgen-producing tumors. The former only shows pubic hair. And the mane is early, there will be no other sexual development, and the latter is accompanied by increased body hair, height, weight, rapid growth, bone age, acne, and thick voice.

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