Male precocious puberty

Introduction to male precocious puberty Precocious puberty refers to premature puberty development. It is generally defined that boys who develop puberty before the age of 9 and girls before the age of 8 can be divided into true (also known as central complete) precocious puberty and pseudo (also known as peripheral incomplete) precocious puberty. class. True precocious puberty refers to the hypothalamic-pituitary-gonadal axis being inappropriately prematurely active, leading to premature puberty development, which is the same as normal developmental period. The second sexual characteristic is consistent with genetic gender, can produce sperm or egg, and has fertility. ability. Pseudoprecocious puberty is an increase in sex hormones caused by factors other than the gonad center. Only the second sexuality develops, but the germ cells do not have the same maturity and fertility. Clinically true precocious puberty is more common than pseudo precocious puberty. basic knowledge The proportion of illness: 1% Susceptible people: male Mode of infection: non-infectious Complications: Giant Syndrome Giant Syndrome and Acromegaly Headache Nausea and Vomiting Hyperparathyroidism

Male precocious cause

(1) Causes of the disease

There are many causes of precocious puberty, and it is more common in the clinic to have female GnRH-dependent precocious puberty.

(two) pathogenesis

True precocious puberty

(1) idiopathic precocious puberty: generally sporadic, sporadic cases are more common in women (female: male is about 4:1), a few can be familial (may be autosomal recessive), the cause of this disease is unknown For some reasons, the inhibition of gonadal development by the hypothalamus may be out of control (as follows, the repression of the posterior hypothalamus in the posterior thalamus is lost), so that GnRH and pituitary gonadotropin are secreted prematurely, resulting in hypothalamic-pituitary- The premature initiation of the gonadal axis causes precocious puberty. The majority of female patients with this disease develop sexual development before the age of 8 (the order is first mammary gland development - pubic hair - menstrual cramps - mane appearing), labial development has pigmentation, vagina Increased secretions, the boy showed testicular penis growth, scrotal skin wrinkles increased with pigmentation, penile erection increased, and even sperm production, muscle increase, subcutaneous fat reduction, both sexes showed a long body, bone age in advance, and ultimately The bones are prematurely fused, so that when they reach adulthood, their body is shorter than normal, and the patient's sexual maturity is also early. Some patients may have a history of sexual intercourse or even a pregnancy.

Patients with serum LH, FSH levels increased, accompanied by increased levels of sex hormones, such as continuous blood collection, LH can be found to pulse secretion, idiopathic same-sex precocious puberty is ahead of the puberty process, artificial line is usually lower than normal The average age of the population is 2.5 years. Before the girl is 8 years old, the boy has sexual maturity before the age of 9 and can be diagnosed as precocious puberty.

In idiopathic homosexual precocity, sporadic cases are more common in women, female: male is about 4:1. In female patients, idiopathic homosexual precocious puberty is 8.5 times that of organic precocious puberty such as tumor. In male patients, organic precocious puberty accounts for 50% to 60% of all precocious puberty, and the pathogenesis of idiopathic precocious puberty is unclear. It is speculated that it may be caused by early hypothalamic activity.

Familial idiopathic precocious puberty mainly affects male members. Some families have morbidity in several generations. Extreme examples even have sexual signs of maturity at birth. The genetic pattern is limited to autosomal dominant inheritance in men, leading to sexual maturity. The reason is the activation of testicular function, the absence of pubertal changes in gonadotropin secretion, and there have been reports of familial precocious puberty involving female members. It is possible that different families have different genetic patterns.

Idiopathic true precocious puberty is the growth of the boy's testicles, increased scrotal skin wrinkles, pigmentation, penis and pubic hair growth, increased penile erection, even sperm production, increased muscle mass, reduced subcutaneous fat, girl mammary gland development, areola and nipple length Large, labia developa, pigmentation, increased vaginal discharge, pubic hair growth, menstrual cramps, ultrasound examination can find ovarian enlargement, in addition, the body's straight line growth accelerates, bone age is advanced, and eventually the epiphysis advances in advance, resulting in short stature, patient psychology, Intelligence is in line with the actual age.

The levels of LH and FSH are increased. For frequent blood collection, LH is pulsed and the level of sex hormones is correspondingly increased.

When the child has the clinical manifestations of precocious puberty, the testosterone in the peripheral blood is almost 100% increased in male children. The E2 is increased by about 50% in female children. The increase of simple sex hormone level is not enough to prove the centrality of precocious puberty. The centrality of probative precocity includes two points:

1 gonadotropin levels increased, a single determination of peripheral blood, the probability of FSH increased by 80% to 100%, LH is 20% to 70%, which may be related to the pulse mode of LH secretion, so it should be determined several times to make the correct Judging, such as the GnRH stimulation test, the secretion response of LH in children with precocious puberty is higher than that of children of the same age.

2 gonads grow up, the size of the testicles can be judged by palpation, and the ovary needs to rely on B-ultrasound to achieve the goal, followed by the exclusion of central nervous system organic disease, cerebrospinal fluid examination, brain CT scan or magnetic resonance imaging (MRI) helps to rule out diseases in the brain. If it proves the centrality of precocious puberty, and excludes intracranial lesions and other causes, it can be diagnosed as idiopathic same-sex precocious puberty.

Familial male precocious puberty patients have a positive family history, and all patients are male. The activated mutation of LH receptor gene in male leads to precocious puberty, while the activated mutation of FSH receptor causes ovarian tumor and leads to excessive secretion of estrogen. Pseudopregnant.

(2) Sexual precocious puberty caused by central nervous system diseases: mostly caused by organic brain diseases, including tumors (such as thalamic astrocytoma, glioma, neuroblastoma, hamartoma, pine cone) Body tumors, teratoma, etc.), infections (such as tuberculous granuloma, encephalitis, brain abscess, etc.), as well as cysts, hydrocephalus, brain trauma, etc. These factors may be affected by infiltration, scars, tumor compression, etc. Thalamic function, causing the function of the gonad axis system to start in advance, the exact mechanism is still unclear, but it has been found that the hamartoma itself can secrete GnRH, pineal tumor, teratoma can also secrete active substances with gonadotropin, pine cone Body tumors can also cause precocious puberty due to decreased melatonin.

The development of this type of precocious puberty is similar to idiopathic. The difference between the two types is that idiopathic can not detect the corresponding cause, and this type can find organic intracranial lesions, which can be obtained by cranial X-ray, CT, MRI, etc. Check to identify.

(3) Primary hypothyroidism with precocious puberty: young children due to hypothyroidism, bone age is significantly behind, severely associated with growth and mental retardation, but some patients may have precocious puberty, early genital development, skin pigmentation, girls Menarche and galactorrhea may occur, the mechanism may be decreased thyroid hormone, negative feedback to the hypothalamus, and increased secretion of TRH in the hypothalamus, while TRH not only stimulates the secretion of TSH from the pituitary, but also stimulates the secretion of PRL, LH and FSH in the pituitary. Increased, these hormones act on the gonads, the breast causes precocious puberty, this disease can be improved after treatment with thyroid hormone.

(4) Multiple bone fiber abnormalosis with Alzright syndrome: The patient has skeletal dysplasia, brown pigmented spots on the trunk skin, often accompanied by precocious puberty, the cause is unknown, and it is believed that the skull is hypertrophied to the base of the skull. Hypothalamic dysfunction, some cases may have increased gonadotropin secretion, while others are gonadotropins with functional ovarian cysts, and blood estrogen increases, so it is considered to be a gonadotropin-independent Sexual precocity, this disease is good for girls, boys are rare, girls show menstrual cramps, reproductive organs mature, breast development, their sexual development is not in the normal order (normal first breast development - pubic hair growth - menstrual cramps), and therefore It is different from true precocious puberty.

(5) Silver syndrome: This disease is associated with short stature, congenital half-body hypertrophy, precocious puberty, which was first reported by Silver in 1953. The disease has precocious puberty, the urinary gonadotropin is increased, the sexual development is early, and the bone age is Compared with sexual development, it is obviously delayed. The mechanism is unknown. After birth, the growth hormone is in the normal range. However, if a large amount of growth hormone is given, the growth of height can be accelerated rapidly, which is presumed to be related to the low sensitivity of the body cells to growth hormone.

(6) Williams syndrome: Williams syndrome is a hereditary disease with many organ developmental malformations, especially arterial stenosis, mainly due to abnormal elastin, whose genetic defect is 7q11 of chromosome 7. .23 microdeletion, due to the lack of 16 genes such as LIMK1, WBSCR1, WBSCR5, RFC2 and elastin genes in this area, patients with mental retardation and learning disabilities, special recognition and personality, often precocious pubic, 12 years old pubic hair Development has reached the Tanner III stage, the bone age is normal or advanced, and the cause of puberty development may be in the hypothalamus or pituitary.

(7) testotoxicosis: also known as familial male non-gonadotropin-independent sexual precocity with premature Leydig cell and germ cell developmental disorder (familial male-limited gonadotropin-independent sexual precocity with premature Leydig cell and germ cell maturation The syndrome was first reported in 1981, the penis of the child increased, sometimes there was a hypertrophic penis after birth, Leydig cells in the testis, Seroti cells matured in advance and had spermatogenesis, sometimes accompanied by Leydig cell proliferation, suffering from Longitudinal growth and skeletal age, muscle development, blood-based state of LH and FSH and GnRH excitatory levels as before puberty development, generally no LH pulse secretion characteristics, blood testosterone increased to adult levels, blood DHEAS levels It is equivalent to bone age, but higher than the normal age of the same age. The intrinsic feature is that GnRH agonists can not inhibit the maturation and proliferation of Leydig cells and germ cells, and the secretion of testosterone is not inhibited. Penile erection and ejaculation may have Fertility, LH secretion and response to GnRH at this time are the same as normal adults, indicating the presence of secondary GnR H-dependent puberty development factors, some adult patients have impaired sperm production, elevated blood FSH, occasionally intrinsic sporadic, but the majority are familial morbidity, there have been reports of a family of nine consecutive generations Women carry activated mutant LH receptor genes, while men are ill.

The etiology of the intrinsic has been basically ascertained. The LH/HOG receptor has a molecular weight of 80,000 to 90,000, and the receptor gene is located at 2p21. The LH/HOG receptor is a member of the G-protein coupled receptor family. There are at least 10 types of missense activating mutations, mainly occurring in the 542-581 segment, which cause premature puberty due to excessive and long-term stimulation of Leydig cells and germ cells due to activating mutations.

2. Male pseudo precocious puberty

Sexual precocity in this group of patients is not related to the hypothalamic-pituitary gonadal center, and is not the result of activation of the central nervous system GnRH pulse generator. This type of precocious puberty is incomplete.

(1) gonadotropin-producing tumors: HCG can be found in chorionic epithelial cancer or teratomas, and liver tumors produce LH-like substances, which promote the secretion of sex hormones. Since only one gonadotropin is produced, it cannot cause true precocious puberty. These patients are almost all male, with increased genital growth but no fertility.

(2) Premature androgen production: may be due to testicular Leydig cell tumor (one-sided increase in testis, plasma testosterone is significantly increased) or adrenal lesions (such as 21 hydroxylase deficiency or 11 hydroxylase deficiency caused congenital Adrenal hyperplasia, obstruction of cortisol synthesis, increased secretion of ACTH, stimulation of adrenal secretion of androgen increased) caused an increase in blood androgen levels, and a small number of iatrogenic or misuse of excessive androgen.

(3) Excessive estrogen production: such as ovarian granulosa cell tumor, ovarian cyst or estrogen-producing tumor, so that the female external genitalia and secondary sexual characteristics develop prematurely, but no germ cell maturation.

The above-mentioned excessive adrenal gland or gonadal disease caused by serotonin showed an increase in urinary 17-KS, and dexamethasone suppression test was often suggested as adrenal hyperplasia, but not as an adrenal or gonad tumor.

(4) Excessive use of exogenous androgens or estrogens: Tiwary et al reported that exogenous estrogen foods can cause pseudo-precocious puberty in women and return to normal after stopping.

Male precocious puberty prevention

Idiopathic precocious puberty is generally sporadic, and a few can be familial (may be autosomal recessive). Can do genetic testing, timely discovery. Minimize the effects of sex hormones in the environment: such as pollen, honey, royal jelly, chicken embryos, silkworm cocoons; animal foods that grow very fast, anti-season fruits, soybeans and their products, adult supplements such as ferrets, Cordyceps sinensis, ginseng, some advertised An oral liquid that allows children to grow taller and stronger, "high hormone" foods such as poultry necks, fried foods, etc. Adult washing and cosmetics, etc. Avoid contact with footage and text about sexual content in movies and magazines. Avoid excessive light exposure: turn off the lights at night. Exercise more, eat a balanced diet, avoid high-calorie foods, and prevent overweight and obesity.

Male precocious complication Complications Giant disease giant acromegaly and acromegaly headache nausea and vomiting hyperparathyroidism

Accelerated bone formation can eventually lead to a lifetime high below the target height. In the case of central nervous system diseases such as intracranial tumors, there may be headache, vomiting, vision changes or other neurological symptoms and signs; McCune-Albright syndrome may have bone Pseudocysts, deformation and fractures, may be associated with thyroid, adrenal gland, pituitary and hyperparathyroidism, such as nodular goiter, hyperthyroidism, adrenal nodular hyperplasia, excessive secretion of growth hormone to produce giant disease or limbs The end of the fat and other signs.

Male precocious puberty Symptoms 21-hydroxylase deficiency vaginal discharge increased male precocious pigmentation learning disorder

True precocious puberty

(1) idiopathic precocious puberty: generally sporadic, more common in women (female: male is about 4:1), a few may be familial (may be autosomal recessive), the cause is unknown, women often Development occurs before the age of 8 years, the order is first breast development pubic hair menstrual cramps mane hair, labia development (with pigmentation), increased vaginal secretions.

Males develop sexual development before the age of 9, testicles, penis grow, scrotal skin wrinkles increase with pigmentation, penile erection increases, even sperm production, muscle increase, subcutaneous fat reduction.

Both sexes are characterized by a long body and a long bone age, which can lead to premature fusion of the bones, shortening the adult height, and premature sexual maturity. A few may have a history of sexual intercourse or pregnancy.

(2) Sexual precocious puberty caused by central nervous system diseases: its clinical manifestations are similar to those of idiopathic ones. Only this type may have neurological organic lesions related to the identification, mainly based on cranial X-ray, CT, MRI, etc. an examination.

(3) Primary hypothyroidism (hypothyroidism) with precocious puberty: a small number of premature infants with hypothyroidism may be associated with precocious puberty, may be due to decreased thyroid hormone levels, negative feedback, resulting in increased hypothalamic TRH secretion, TRH not only stimulates the secretion of TSH from the pituitary, but also stimulates the secretion of PRL, LH and FSH, leading to precocious puberty.

(4) multiple bone fibrosis (Albright syndrome) with precocious puberty: patients with skeletal dysplasia, brown pigmented spots on the trunk skin, often accompanied by precocious puberty, the cause is unknown, occurs in girls, boys are rare, their sexuality The developmental order is different from normal: normal development is usually first breast development pubic hair growth menstrual cramps, and the disease is first menstrual cramps (reproductive organs are mature), and then mammary gland development.

(5) Silver syndrome with precocious puberty: intrinsic short stature, congenital half-body hypertrophy with precocious puberty, normal growth hormone levels at birth, but if a large number of growth hormone treatments are given later, height growth can be rapidly accelerated, speculated with target cells It is associated with low sensitivity to growth hormone, and the characteristic of precocious puberty is that bone age is significantly delayed compared to sexual development.

(6) Williams syndrome with precocious puberty: Intrinsic with many organ malformations, especially the genetic defect of arterial stenosis, the genetic defect is LIMK1.WBSCR1.WBSCR5.RFC2 and elastin in 7q11.23 locus 16 genes such as genes are deleted, and the clinical manifestations are mental retardation, learning disabilities, special cognition and personality, often accompanied by precocious puberty, and differential diagnosis based on detection of gene deletion.

(7) Testicular poisoning with male precocious puberty: This disease is also known as familial male non-gonadotropin-dependent precocious puberty with Leydig cells and germ cell developmental predisposition, patients with penile enlargement, and some have hypertrophy at birth The penis, testicular Leydig, Sertoli cells mature in advance and have spermatogenesis, sometimes accompanied by Leydig cell proliferation, longitudinal growth and bone age of the child, muscle development, penile erection and ejaculation can have fertility, a few adult patients sperm Most of the disorders are familial and a few are sporadic, and the disease is caused by missense mutations in the LH/HCG receptor gene (2p21).

(8) causing precocious puberty after treatment of congenital adrenal hyperplasia: congenital adrenal hyperplasia such as 11-beta hydroxylase and 21-hydroxylase deficiency patients, after treatment with glucocorticoids or simultaneous mineralocorticoids, The level of plasma ACTH is inhibited, and the adrenal gland produces a decrease in gonadal steroids. However, due to the delay in diagnosis and treatment, the patient's bone age is advanced. If the threshold of puberty is reached, the patient may have activation of the hypothalamic-pituitary-gonadal axis function. Precocious puberty, as well as patients who have previously been treated with gonadal steroids.

2. pseudo precocious puberty

The main difference between the clinical manifestations of pseudo-precocious puberty and the trueness is its sexual development. The maturity is incomplete, that is, it only shows the developmental performance of some accessory characteristics, but no germ cells (sperm and follicle) mature. No fertility.

Male precocious examination

Laboratory inspection

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, increased again after puberty began, before the start of puberty, 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, elevated blood progesterone suggests a luteal tumor, a common precocious reproductive hormone change.

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) The clomiphene stimulating test has certain value for judging the hypothalamic-pituitary-gonadal axis formation: it is less useful, but it has been used less frequently. Before the test, FSH and LH were used as the basal level, followed by taking clomiphene 100mg. For 5 consecutive days, FSH was retested on the 6th day. After LH, if the basal value was increased by 50%, 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.

Film degree exam

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 of CT and MRI head examination can understand intracranial lesions, especially to help identify intracranial tumors, is also important for the exclusion of secondary precocious puberty, and idiopathic precocious puberty Normal, 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 part of the pituitary (level 1 obvious depression, level 2 mild depression, level 3 flat, level 4 Mild bulging, 5 prominent bulging), it is considered that pituitary grading has important value in the diagnosis of precocious puberty in prepubertal children. Those with grade 4 or higher can highly suspect central precocious puberty.

Diagnosis and identification of male precocious puberty

diagnosis

The hypothalamic, pituitary, gonad and adrenal organic lesions must be excluded based on detailed clinical data and necessary laboratory tests. Laboratory tests should first determine whether precocious puberty is gonadotropin-dependent, and LH/FSH pulsed secretion helps. Identification of the two.

Imaging examination is mainly used to search for pituitary and gonad tumors. If there is no organic disease, it can be traced, but the LH receptor gene mutation may be excluded.

The cause of gonadotropin independent precocious puberty is mainly in the gonads and adrenal glands, which are caused by excessive secretion of gonadal hormones. However, it must be noted that some gonadal tumors are also self-synthesized and similar to hypothalamic hamartomas. Secretion of gonadotropins.

Differential diagnosis

According to the etiology and laboratory tests, whether the early precocity is gonadotropin-dependent, hypothalamic, pituitary, gonad and adrenal organic disease, premature puberty of boys before the age of 9 often prompted by organic lesions.

1. Simple early breast development, part of central precocious puberty (PICPP): The clinical features of simple breast early development are small age of onset, more common in girls from 6 months to 2 years old, only mild development of the breast, or symmetry Or only unilateral development, and often cyclical changes, no growth overspeed and bone age leading phenomenon, the vulva still maintains a naive type, no yin, mane growth, a kind of puberty development variation, may have a family history. FSH was significantly elevated after GnRH challenge (normal pre-puberty girls also increased after challenge), but LH did not increase significantly, most <5 0u="" l="" fsh="" lh="">1. It is worth noting that PICCP is converted to CPP without any clinical warning. Therefore, regular follow-up is required after diagnosis of PICPP, especially if the breast is repeatedly enlarged or persistent, and the test is repeated if necessary.

2. CPP transformed from non-central precocious puberty, such as congenital adrenal hyperplasia, must pay attention to monitoring the occurrence of CPP during the treatment of primary disease.

3, congenital hypothyroidism associated with precocious puberty: a special type of precocious puberty, early children with elevated blood LH basal value, but not increased after GnRH challenge, the disease is longer after the conversion into a real CPP. Short stature is an important feature.

4, pseudo-precocious puberty: caused by exogenous diseases such as adrenal diseases, gonad diseases and drugs. Its clinical characteristics are: sexual development does not occur according to normal developmental rules, often there is a lack of secondary sexual characteristics, such as female ovarian tumor caused by precocious pubic pubic hair, male CAH, adrenal tumor, penis increased without corresponding The testicles are enlarged, and the contraceptives are mistreated. The skin pigmentation of the nipple, areola and perineum is very obvious, especially with breast enlargement, female labia majora, swelling of the labia minora, and increased vaginal discharge. Have vaginal bleeding.

Identification points of true and pseudo precocious puberty:

Breast enlargement, after a considerable period of time (usually about 2 years), regular menstruation should be considered as true precocious puberty; if the breast is enlarged soon, menstruation may be pseudo precocious.

True precocious puberty is generally accompanied by increased growth rate and bone maturity, and the bone age exceeds the actual age.

The high-value LH and FSH in the blood were determined to be true precocious puberty, and the low-value ones were pseudo-precocious puberty. If necessary, the LHRH stimulation test was used to identify.

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