precocious puberty
Introduction
Introduction to sexual precocity Precociouspuberty refers to the early appearance of puberty, that is, women have gonad enlargement and secondary sexual characteristics before the age of 8, or menstruation before the age of 10, men develop before the age of 9, according to the different pathogenesis, precocious puberty Can be divided into two categories: gonadotropin-releasing hormone (GnRH)-dependent precocious puberty (true precocious puberty) and non-GnRH-dependent precocious puberty (pseudo-precocious puberty); the former is called central precocious puberty or complete precocious puberty, The latter is called peripheral precocious puberty. In addition, incomplete sexual precocity, such as simple breast early development, simple pubic hair is early, and some scholars fall into the variability of puberty development. basic knowledge The proportion of illness: 1% Susceptible people: children Mode of infection: non-infectious Complications: acromegaly
Cause
Precocious puberty
Sexual precocity of the intracranial source (10%):
Sexual precocity of intracranial origin The premature appearance of genital tract development or function caused by hypothalamic or pituitary lesions, except for ovarian follicle maturation and ovulation, which is the same as that found in normal children. Most of the intracranial sources of precocious puberty are lesions or tumors at the bottom of the third ventricle. These lesions often involve the posterior part of the hypothalamus, especially the tuber cinereum: mammillary bodies and optic chiasm ( Optic chiasm), congenital brain defects or encephalitis may be associated with premature signs of premature development, neurological examination can often be diagnosed, Mc Cune-Albright syndrome is too early sexual development, accompanied by multi-bone fibrous development Poor (polyostotic fibrous dysplasia), skin pigmentation and other endocrine disorders, are congenital defects of the hypothalamus.
Some children with sexual activity related to intracranial diseases can initially have no neurological symptoms. From the types of precocious puberty that are initiated by many intracranial lesions, it is very important to find the location and characteristics of the disorder.
Precocious puberty due to intracranial disease can be explained by the ability of the posterior hypothalamus to inhibit the production of gonadotropins and their release from the anterior pituitary. Therefore, lesions in the posterior hypothalamus can destroy or inhibit some of the usual regulation of the pituitary gland. The mechanism of the stimulation strength of the posterior gland, so that the control effect of the hypothalamus on the pituitary is relieved, thereby increasing the production of gonadotropin, leading to the activity and sexual development of the gonads. In other cases, it can be directly stimulated by the pituitary gland. And.
Unexplained sexual precocity (40%):
Uncertain cryptogenic sexual precocity Approximately 80-90% of constitutional sexual precocity has no obvious cause. It is often classified as a central nervous-derived precocious puberty according to the cause, because the patient may have small and unconfirmed The hypothalamic lesions, some patients have a family history of precocious puberty, it is appropriate to say that this condition is unknown, because the source of this type of precocious puberty is very little known.
Precocious puberty caused by ovarian tumors (25%):
Ovarian tumors causing sexual precocity Ovarian tumors are worthy of emphasis as precocious puberty, but in childhood, feminine tumors are common. In the majority of feminine mesenchymal tumors in childhood, the rapid growth in body development and bone age develops along with adolescent female body type, genital maturation and breast enlargement, and pubic hair appears, but it is not as premature as true homosexual development. Pelvic tumors often can not be touched, vaginal secretions increased, vaginal smears showed enhanced estrogen effect, irregular vaginal bleeding, the incidence of precocious puberty caused by estrogen tumors, higher than the cause of unclear, urinary estrogen and 17 Ketone sterol levels can be higher than normal children of the same age, but such cases are generally no ovulation, can not be pregnant, occasionally follicular non-neoplastic ovarian cysts can lead to precocious puberty, removal of cysts (containing a large amount of estrogen) can alleviate precocious puberty Development, but if there are gonads remaining, small cysts can still increase, and precocious puberty can continue.
1. Other adrenal tumors that produce hormones in precocious puberty can cause heterosexual precocity or a mixed type of sexual maturation. Exogenous estrogens are often misused by their young mothers due to improper medication or other sources. The contraceptive pill can cause precocious puberty; children with hypothyroidism can also have precocious puberty, the latter has cross-feedback effect between thyroid hormone and gonadotropin, and excessive secretion of gonadotropin from pituitary .
2, temporary sexual precocity (transitory sexual precocity) is less, but not uncommon, children often have one or more secondary sexual characteristics to accelerate development, most of these children have physical development and breast development (about 50%), with vagina The bleeding is up to 45%, the vaginal smear smear, the epithelial cells show a significant estrogen effect, this premature sexual development can continue normal development for several months, and then enter normal puberty at normal age.
Occasionally, the endometrium is particularly sensitive to estrogen, which can cause uterine bleeding without other precocious puberty. Gynecological examination can not determine the true cause of uterine bleeding. Hormone determination is normal. Uterine bleeding stops naturally after several months of recovery. .
Children with temporary precocious puberty or premature endometrial response should be followed closely for several years until other causes (including uterine bleeding) are excluded.
Pathogenesis
1. Pathophysiological characteristics
(1) Hypothalamus-pituitary-gonadal axis: The human body grows from a fetus to a complete sexual maturity and fertility, the hypothalamus (gonadotropin releasing hormone, GnRH)-pituitary (gonadotropin, Gn)- The regulation and activation of the gonad (sex hormone) axis (HPG axis) also undergo a series of changes. The hypothalamic-pituitary-gonadal axis is mainly regulated by two mechanisms: one is a sex hormone-dependent negative feedback regulation mechanism, that is, a certain concentration of sex hormones. It can inhibit the secretion of GnRH and Gn, mainly in the 2 to 3 years old; one is the intrinsic inhibition mechanism of the central nervous system, such as adrenergic drugs can stimulate the release of GnRH, endogenous enkephalin can inhibit the release of GnRH Naltrexone, an opioid receptor antagonist, can completely inhibit the secretion of Gn, mainly in the 3 to 10 years old.
At 12 weeks, the fetus has secreted GnRH, which promotes the secretion of luteinizing hormone (LH) and follicle stimulating hormone (FSH) from the pituitary. At 20 weeks, the GnRH secretion peaks, and then the secretion of gonadotropin and sex hormones increases. At the time, due to the large amount of secretory hormones in the placenta and the central nervous system of the fetus, the two regulatory mechanisms inhibit the active hypothalamic-pituitary-gonadal axis from negative feedback. After birth, the sex hormones from the placenta are interrupted. The feedback effect is weakened, so Gn and sex hormone secretion increase again and may last for half a year.
From infancy to pre-puberty, the intrinsic inhibitory mechanism of the central nervous system and the negative feedback of sex hormones keep the hypothalamic-pituitary-gonadal axis in a state of inhibition. Before puberty, girls' follicle-stimulating hormone (FSH) levels are higher than luteal production. LH, the girl's FSH / LH is often greater than the boy, regardless of men and women, LH after GnRH injection showed prepubertal reaction, FSH can only be seen within one year before the start of puberty, LH's 24h secretion increased rather than secreted frequency Increase.
Near puberty, the central nervous system inhibits the secretion of GnRH in the hypothalamus, and the sensitive threshold of hypothalamic negative feedback to sex hormones is gradually adjusted, that is, low levels of sex hormones are insufficient to exert an inhibitory effect, thereby activating the hypothalamic GnRH impulse source, GnRH The impulse source generator is located at the central base of the hypothalamus. The central base of the hypothalamus contains GnRH neurons with transducer action. GnRH neurons convert the neural signals from the hypothalamus into chemical signals - GnRH, signals. With pulsed release, the frequency and amplitude of GnRH pulsed release regulate the release of pituitary Gn. As the frequency and amplitude of GnRH secretion increase, the frequency and amplitude of Gn secretion in the pituitary gland also increase, and the amount of sex hormone secretion increases.
GnRH is difficult to detect due to the small amount of secretion, but the pulse secretion of Gn can reflect the pulse release of GnRH indirectly. At the beginning of puberty, the frequency and amplitude of LH night pulse release and LH to GnRH injection can be seen first. After the reaction is enhanced, this characteristic can last for adults, FSH rises earlier than LH in puberty, and FSH increases (10-11 years) in girls before boys (11-12 years), but GnRH The intensity of FSH after injection was not significantly different from that before puberty. Therefore, the increase of pulsed release frequency of GnRH in puberty increased the ratio of LH/FSH, and the increase of LH/FSH ratio was characteristic of puberty.
(2) puberty development staging: 95% of normal girls secondary sexual characteristics (such as breast enlargement) in 8 to 13 years old, 95% of normal boys secondary sexual characteristics (such as testicular enlargement) in 9 to 13.5 years old Second sexual signs such as pubic hair, menstruation and penis enlargement accompanying normal youth progression, are divided into I to V stages according to Tanner stage, and girls from 2 months to 2.5 years of menstrual menarche, the boy from The testicles increased to the average of 3 years after spermatorrhea, and the growth of girls' puberty accelerated in the early stage of puberty. The growth of boys' puberty accelerated in the middle of youth. The average height of girls was 25~27cm, and the height of boys was 28~30cm. It takes about 2 to 4 years for sexual characteristics to begin to mature. Although the physical development of precocious children is greatly changed, psychological, cognitive and social (social adaptation) are still in childhood.
2. Pathogenesis
(1) True precocious puberty: True precocious puberty is the real advance of puberty, and the hypothalamic-pituitary-gonadal axis function is activated early. The response of LH to GnRH prematurely and its pulse secretion form has reached the level of puberty.
1 idiopathic precocious puberty: due to neuroendocrine dysfunction, premature initiation of GnRH pulse secretion, refers to the comprehensive examination of the intrinsic children failed to find any organic lesions leading to puberty development, the disease including sporadic Most) and familial, familial precocious pubic involving boys, may be restricted to male chromosomal recessive diseases by a father who is involved in the disease, and it is found that LH-R gene activating mutations cause familial masculinity Early maturity, after the development of the LH-R mutation in the embryonic stage, the child can see the big penis at birth, and the obvious precocious puberty occurs at the age of 3 to 4 years. The pathogenesis is that the mutant LH-R activates G prematurely. Protein, stimulated Leydig cells synthesize and secrete large amounts of androgens, and women with LH-R gene mutations do not express them, and can transmit disease-causing genes to male offspring.
2 secondary precocious puberty: secondary to central nervous system diseases, tumors located in the hypothalamus, such as interstitial hamartoma, glioma, craniopharyngioma, etc., these tumors destroy the nerve channel that inhibits GnRH secretion In order to increase the secretion of GnRH, some tumors may have cells that release GnRH. The children with these tumors have precocious puberty as the first symptom, and will be accompanied by symptoms caused by tumor compression, such as headache, epilepsy or visual field changes. In addition, encephalitis, tuberculosis, head injury or congenital malformations (such as brain hypoplasia, microcephaly, hydrocephalus) can destroy the hypothalamic and pituitary channels or the hypothalamus loses higher central control and increases activity, induced Precocious puberty.
(2) pseudo-precocious puberty: pseudo-precocious puberty is a non-neuroendocrine-induced precocious puberty, intrinsic to non-gonadotropin-dependent precocious puberty, but the result of increased non-central-dependent hormones in the blood, the source of sex hormones:
1 iatrogenic or artificial misuse of excessive sex hormones;
2 The female (androgen) hormone that promotes the early development of sexual characteristics is not caused by the stimulation of the hypothalamic-pituitary-gonadal axis, but the testis (ovary) is stimulated by non-pituitary-derived gonadotropins.
Prevention
Precocious puberty prevention
1. Popularize scientific parenting knowledge, precocious puberty and blind tonic. Some parents blindly buy higher, increase mental health products, or do not analyze the real reasons for children's anorexia, blindly give health care products that can not enhance their appetite for children who do not like to eat, but do not know, Health products that generally increase appetite often contain hormone components. Long-term use can cause elevated levels of hormones in children's blood, leading to precocious puberty.
Popularizing dietary balance knowledge, due to the improvement of nutrition, superior family living conditions, and the reduction of diseases, children's growth and development have accelerated. Some parents are too tonic, such as sputum sputum together in the soup, among which animals Endocrine glands such as the thyroid gland and gonads contain hormone substances, which can enter the human body through meals, leading to an increase in sexual development and precocious puberty.
2. Harnessing environmental pollution to avoid environmental hormones, children, detergents, pesticides and plastics industries to the environment and its decomposition products, can produce a series of hormone-like pollutants in the natural world, such as alkylated phenol in detergents Classes, additives used in the manufacture of plastic products, plasticizers such as phthalates and bisphenol A, up to 70 kinds, these substances are discharged into the environment every day.
If the water source is contaminated, the food is absorbed through the skin and ingested by the child, it can cause abnormal development of the reproductive organs and bones. Therefore, environmental hormones can be used as a direct cause of pseudo-precocious puberty, if it is received in the early stage of the embryo. The role of substances can also lead to barriers to gender differentiation.
3. Avoid mistaking the contraceptive. A 5-year-old girl misunderstood her mother's contraceptives, causing estrogen to increase to precocious puberty. This phenomenon is not uncommon, especially in rural areas.
4. Children with precocious puberty may also be affected by certain diseases (such as intracranial tumors, heredity, etc.). Therefore, parents should pay attention to observe the development of children, especially hair, genitals, beards, larynx, etc. Development, once the child is found to have secondary sexual characteristics prematurely, should go to the endocrinology examination and treatment in time to avoid the disease.
Complication
Precocious complication Complications, acromegaly
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 Terminal hypertrophy, etc.; exogenous sex hormones can cause breast enlargement, vaginal bleeding, ovarian cysts.
Symptom
Symptoms of precocious puberty Common symptoms Psychological age is greater than physiological age Parathyroid function Hyperthyroidism Male precocious vaginal bleeding Goiter Ovarian cyst Female precocious infant Blackhead acne pubic hair early development
1. Central precocious puberty 50% of children with central precocious puberty begin to develop earlier than 6 years old, women have breast development, small labia majora, estrogen-dependent changes in vaginal mucosal cells, uterus, ovarian enlargement, pubic hair Menarche, males show testicular and penis enlargement, pubic hair appears, muscles develop, the sound becomes thicker, both men and women have accelerated growth, bone ripening accelerates, and eventually can lead to a lifetime high below the target height, accompanied by intracranial tumors, etc. In the case of central nervous system lesions, there may be headache, vomiting, vision changes or other neurological symptoms and signs.
2. Peripheral precocious puberty Peripheral precocious puberty, also known as pseudo-precocious puberty, clinical manifestations of secondary sexual characteristics, but non-pubertal mobilization, and no relationship with the activity of the hypothalamic-pituitary-gonadal axis, but endogenous or external It is related to elevated levels of sex hormones.
(1) Familial hypertestosteroneemia: only found in male autosomal dominant precocious puberty, the cause is due to mutations in the gene encoding LH receptor, so that the LH receptor on the cell membrane is continuously activated, blood testosterone levels reach Adolescent or adult level, but LH secretion mode and LHH challenge test LH reaction showed prepubertal reaction, manifested as bilateral testicular enlargement, accelerated growth and accelerated bone maturation, testicular biopsy showed interstitial cell maturation and seminiferous tubule development .
(2) McCune-Albright syndrome: typical clinical manifestations of coffee milk spots, multiple cystic fibrous dysplasia and peripheral precocious puberty, skin coffee milk spot distribution often does not exceed the midline, located in bone lesions Ipsilateral body, multiple cystic fibrous dysplasia is chronic progressive, bone lesions often involve long bones of the extremities, pelvis, skull, pseudo-cysts, deformation and fractures, the incidence of girls is higher than boys, but also 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 acromegaly.
Female precocious puberty often begins within 2 years of age. Later, vaginal hemorrhage can be seen. LH and FSH levels are inhibited. The response to GnRH is low. Estrogen levels often fluctuate between normal and significantly elevated, often periodic, possibly with ovaries. Cyst size changes, ovarian cysts often show an increase and decrease alternately, boys precocious puberty is rare, and their testicular symmetry is increased. When the bone age is close to 12 years old, the GnRH impulse source is activated, and the true and false precocious puberty overlap.
The cause of McCune-Albright syndrome is due to mutations in the Gas subunit encoding a guanosine triphosphate (GTP)-binding protein on a somatic cell, Gas activates adenylate cyclase, and GTP-binding protein is a signal transduction pathway in hormones. One link.
(3) Tumors: Adrenal cortical tumors are one of the main causes of pseudo-precocious puberty in both male and female. Adrenal cortical tumors (adenomas, carcinomas) secreting androgen-based, and aggretic hyperplasia caused by adrenal hyperplasia Precocious puberty and girls' heterosexual precocity, growth deceleration is the difference between this disease and other precocious puberty. Determining the lesion should depend on the imaging examination of the adrenal gland.
Gonadal tumors are the cause of pseudo-precocious puberty in both male and female, and the incidence is low. The Leydigs cell tumor of the testis often presents with unilateral testicular enlargement, while males caused by congenital adrenal hyperplasia or adrenal tumors. Precocious puberty often causes bilateral testicular enlargement.
Solid tumors of the ovary (such as granulosa cell tumors) secrete estrogen, which can lead to darkening of the areola and labia. Pelvic ultrasound is still an important means of ovarian tumor diagnosis.
Germ cell tumor or teratoma of the central nervous system and hepatoblastoma located in the periphery, teratoma, choriocarcinoma can secrete HCG, often cause precocious puberty, more men than women, laboratory tests for blood, cerebrospinal fluid and The level of HCG in urine is significantly increased, the level of blood testosterone is significantly increased, and the feedback of blood LH level is decreased. The blood testosterone level and alpha-fetoprotein increase produce male precocious puberty, so the pathogenesis is due to HCG secreted by tumor. Increase blood testosterone levels, trigger peripheral precocious puberty, HCG effect similar to LH, can stimulate testicular stromal cell proliferation without spermatogenesis.
(4) Exogenous sex hormones: foods, drugs, beauty products and other sexual hormones can also cause precocious puberty. You should carefully ask about the medical history, pay attention to whether the child has accidental contact or take birth control pills, and mistakenly take birth control pills can cause breasts. Increase, vaginal bleeding, the areola can be significantly dark brown.
3. puberty variation
(1) Premature thelarche: Intrinsic refers to the development of only one or two breasts before the age of 8 without other secondary sexual characteristics (pubic hair, uterine size and labia minora changes), common in 2 Within the age of 4 years, it occurs less frequently after 4 years old, and a few last for a long time. Long-term follow-up found no effect on the health, growth and fertility of the child. The level of estrogen in the blood can be normal or slightly elevated, and blood sex hormones are combined. Proteins are often elevated, but no increase in FSH. FSH responds to GnRH stimulation more than normal controls. Ovarian B-ultrasound can be seen repeatedly with one or more cysts larger than 5 mm in diameter. The appearance of cysts is related to changes in breast size. The size of the sex, ovary and uterus is prepubertal. Since the early development of simple breast is not easy to distinguish from true precocious puberty, continuous observation is very important.
(2) premature pubarche: simple pubic hair early development can be seen in both sexes, most of them appear pubic hair or with mane around 6 years old, but no hypothalamic-pituitary-gonadal axis, no other Development of accessory sexual characteristics, some children may have mild growth acceleration and advanced bone age (in the normal ~-2SD range), blood dehydroepiandrosterone, 17-hydroxyprogesterone, 17-hydroxypregnenolone, The level of androstenedione can reach the level of pubic hair stage II in normal children. After ACTH stimulation, dehydroepiandrosterone can be elevated, but 17-hydroxyprogesterone, 17-hydroxypregnenone is not as elevated as congenital adrenal hyperplasia. The disease is high and the course of the disease is non-progressive. The true youthful puberty begins at the normal age, and the intrinsic need to be distinguished from the lesions that cause other androgen secretion in childhood.
Examine
Precocious puberty
Endocrine examination mainly includes determination of FSH, LH, estradiol, testosterone, and 17-hydroxyprogesterone base value.
The FSH and LH peaks after LHRH stimulation test are important for judging pituitary function and central precocious puberty. The excitatory test uses intravenous LHRH 100g/m2, and before and after injection, 30 and 60 minutes, blood LH and FSH are taken separately. Considering the pituitary dysfunction, blood can be collected again in 90 minutes, normal puberty or true precocious puberty, LH peak appearance time is 15 ~ 30min, LH peak is more than 3 times higher than the basic value, if the base value <1TU / L, even if LH peaks more than 3 times higher than the baseline value can not be considered as adolescent response; LH / FSH > 1.0; pre-puberty children or pseudo-precocious puberty did not respond.
1. Left-handed positive X-sex hormones can accelerate bone maturity. Therefore, judging bone age according to left-handed X-ray is valuable for evaluating puberty development. Bone age over actual age of 1 year can be regarded as advance, and the earlier the development, the bone age is ahead. The more bone age is a more accurate indicator of menarche, and the life expectancy can be predicted based on bone age, height and actual age.
2. Uterine, ovarian and testicular B-ultrasound can observe the size of the uterus and ovary, the number and size of follicles in the ovary, whether the ovary has cysts and tumors, and whether the testicles have tumors.
3. Skull X-ray or CT and MRI examination of small-age girls and all boys with confirmed central precocious puberty should be performed by CT or MRI to exclude intracranial space-occupying lesions.
Central precocious puberty can be caused by central organic lesions. Those who have not found primary lesions are called idiopathic precocious puberty. Because intracranial tumors are an important cause of central precocious puberty in boys, boys with central precocious puberty should Conventional hypothalamic, pituitary CT or MRI examination, tumors are generally found in the posterior hypothalamus, pineal body, median bulge, the third ventricle bottom, intracranial tumor caused by central precocious puberty, precocious puberty, puberty development age Early, there is often a higher peak of LH and a peak of FSH.
Diagnosis
Precocious puberty diagnosis
diagnosis
The diagnosis of precocious puberty must first exclude diseases that are more harmful to the body such as central diseases and tumors, ovarian and adrenal tumors, and vaginal bleeding caused by non-endocrine abnormalities, such as inflammation, ectopic, traumatic and tumor, etc. Complete or incomplete sexual precocity.
Generally, breast development and pubic hair growth precedes menarche for several months. The only characteristic of some children with precocious puberty is premature thelarche or premature pubarche, but most of them are accelerated by physical development.
The main purpose of the diagnostic procedure for female homosexual precocity is to clarify the cause of accelerated sexual maturation. About 90% of cases are of constitutional type (especially those with unknown or idiopathic), but this is explained in any case. Before, other causes must be ruled out.
In the medical history, you should know whether there are predisposing factors, such as the intake of sex hormones and nutritious foods, and understand the age of onset, the speed of disease and the growth.
Physical examination should record the length, weight and sexual development of the staging, external genital development, abdominal and pelvic examination, systemic attention to McCune-Albright syndrome, specific signs of hypothyroidism and nervous system abnormalities.
Laboratory diagnosis should be based on bone age and reproductive hormone determination (such as FSH, LH, E2, DHAS if necessary, testosterone, progesterone, 17-hydroxypregnancy and HCG). The relationship between DHAS and chronological age and bone age can reflect the initial adrenal function. Now, it is helpful for the diagnosis of true precocious puberty. The X-ray of the wrist can determine the bone age and understand the progress of the development process. The positive lateral X-ray of the sella turcica can determine whether the pituitary has any lesions, such as Suspicious, can further CT or / and MRI to confirm the diagnosis, central true precocious puberty in addition to adrenal function, there are functional activities of the hypothalamus and pituitary, therefore, GnRH stimulation test can understand the function of the pituitary Status, FT4 and TSH help to reflect thyroid function, cT or MRI head examination can understand the tumor of the brain, ultrasound examination of the abdomen and pelvis can understand the size and shape of the adrenal gland and ovary, as well as follicular condition, sign development, vaginal bleeding, The short stature, the actual age of the bone age, suggests that the thyroid function is hypothyroidism. If accompanied by an increase in PRu, galactorrhea may occur.
If the sexual characteristics develop and the GnRH test responds to adolescent mode, it is true precocious puberty. If the nervous system is examined and there is no abnormality in the head imaging examination, it is most likely to be idiopathic. The brain should be noted. Small lesions are not easy to find long-term observation and follow-up, so as to avoid missed diagnosis. When gonadotropin is not elevated, heterogeneous HCG secretion is considered. The estrogen secreted by the ovary often accelerates growth, bone maturation, and breast development is equivalent to 11 years of bone age; Menstrual cramps are equivalent to about 13 years of bone age. The rise of blood progesterone suggests luteal tumor, sexual development, vaginal bleeding, and short stature. If the bone age is less than the actual age, it suggests hypothyroidism. If accompanied by elevated PRL, it may appear. Lodging milk.
Differential diagnosis
First of all, it should be differentiated from early development of the breast and/or early pubic hair. Both are partial precocious puberty, no bone growth or slight growth rate, and the increase of sex hormone secretion is not obvious. In addition, the presence of intracranial lesions should be detected. Early appropriate treatment, other non-gonadal precocious GnRH test negative, abdominal B-ultrasound can rule out adrenal or ovarian tumors, in addition to multiple bone fiber dysplasia with precocious puberty identification, detailed history, careful and comprehensive physical examination and necessary The laboratory test helps to identify.
In congenital adrenal hyperplasia and adrenal cortical tumors, the penis enlarges, the testicles are relatively small or no testicular enlargement, the primary hypothyroidism boy has enlarged testicles, but no male sex, testicular stromal tumors (Leydigs) Cell tumor often causes unilateral testicular enlargement.
