Precocious puberty is defined as the development of pubertal signs at a younger age than the accepted lower limits for the onset of puberty. In girls, breast development before the age of 8 years, appearance of sexual pubic hair before the age of 8 years or beginning menses before the age of 9.5 years is traditionally considered as precocious puberty. This is accompanied by rapid growth rate, advanced skeletal maturation and increased levels of gonadotropins and/or sex steroids.
This document discusses precocious puberty in a 3 year old girl. On examination, she had breast enlargement and pubic hair development consistent with Tanner stages B3 and Ph2. Lab tests found elevated LH and FSH. Ultrasound showed enlarged uterus and ovaries. The document then reviews physiology of puberty, Tanner staging of breast and pubic hair development, defines precocious puberty, and discusses causes and treatment options like GnRH agonists or surgery.
Precocious puberty is defined as the onset of secondary sexual characteristics before age 8 in girls and 9 in boys. It can be classified as central (gonadotropin-dependent) or peripheral (gonadotropin-independent) puberty. Central puberty is treated with GnRH agonists to slow progression, while peripheral causes like tumors require treatment of the underlying condition. Evaluation involves assessing pubertal development, growth, bone age, and hormone levels to distinguish central from peripheral puberty and identify any lesions.
The document discusses pubertal disorders and their classification, causes, diagnosis, and management. It begins by defining key terminology related to puberty and describing the normal physiology and regulation of the hypothalamic-pituitary-gonadal axis during puberty. Pubertal disorders are classified as either precocious or delayed puberty. Causes of delayed puberty include hypergonadotropic hypogonadism due to genetic defects or acquired conditions, and hypogonadotropic hypogonadism caused by tumors or CNS disorders that disrupt the HPG axis. Assessment of pubertal development involves the Tanner staging system.
This document discusses precocious puberty, defined as the onset of secondary sexual characteristics before age 8 in girls and 9 in boys. It describes the different types (true/central, pseudo/peripheral, mixed), potential causes including brain lesions, hypothyroidism, and tumors, signs and symptoms, diagnostic tests, and treatment which typically involves GnRH agonists. Specific conditions discussed in more detail include hypothalamic hamartomas, hepatoblastoma, McCune-Albright syndrome, and familial male precocious puberty. Incomplete forms of precocious puberty like premature thelarche and adrenarche are also summarized.
Here are the key considerations for this patient:
- She is postmenopausal based on her age
- With an intact uterus, estrogen-only hormone therapy would put her at increased risk for endometrial cancer
- As she is asymptomatic, hormone therapy may not be needed
- Screening for osteoporosis, cardiovascular risk, and breast cancer should be discussed based on risk factors
- Lifestyle modifications like calcium/vitamin D, exercise, not smoking can help prevent diseases of menopause
- Close monitoring without hormone therapy is a reasonable option given her age and lack of bothersome symptoms
The priorities would be assessing risk factors, discussing screening recommendations, and supporting lifestyle changes to promote health during men
Delayed Puberty Topics in Adolescent Gynecology Delayed Puberty Topics in A...MedicineAndHealth14
This document discusses delayed puberty in adolescent girls. It begins by outlining normal pubertal development and defining delayed puberty. Delayed puberty is then classified into three categories: hypergonadotropic hypogonadism (43%), hypogonadotropic hypogonadism (31%), and eugonadism (26%). For evaluation and management, the document recommends obtaining a history, physical exam, initial labs (TSH, prolactin), and a progestational challenge to determine gonadotropin levels and identify underlying causes. Treatment strategies aim to correct the underlying pathology, prevent disease complications, and provide sex steroids.
This document provides information on delayed puberty, including its definition, causes, evaluation, and treatment. Delayed puberty can be functional, due to hypogonadotropic hypogonadism, or hypergonadotropic hypogonadism. The most common cause is constitutional delay of growth and puberty. Evaluation involves medical history, physical exam, lab tests like LH, FSH and bone age. Treatment depends on the underlying cause, but aims to induce normal pubertal development and growth. For constitutional delay, watchful waiting is often recommended, while permanent hypogonadism requires hormone therapy like testosterone to initiate puberty.
This document discusses precocious puberty in a 3 year old girl. On examination, she had breast enlargement and pubic hair development consistent with Tanner stages B3 and Ph2. Lab tests found elevated LH and FSH. Ultrasound showed enlarged uterus and ovaries. The document then reviews physiology of puberty, Tanner staging of breast and pubic hair development, defines precocious puberty, and discusses causes and treatment options like GnRH agonists or surgery.
Precocious puberty is defined as the onset of secondary sexual characteristics before age 8 in girls and 9 in boys. It can be classified as central (gonadotropin-dependent) or peripheral (gonadotropin-independent) puberty. Central puberty is treated with GnRH agonists to slow progression, while peripheral causes like tumors require treatment of the underlying condition. Evaluation involves assessing pubertal development, growth, bone age, and hormone levels to distinguish central from peripheral puberty and identify any lesions.
The document discusses pubertal disorders and their classification, causes, diagnosis, and management. It begins by defining key terminology related to puberty and describing the normal physiology and regulation of the hypothalamic-pituitary-gonadal axis during puberty. Pubertal disorders are classified as either precocious or delayed puberty. Causes of delayed puberty include hypergonadotropic hypogonadism due to genetic defects or acquired conditions, and hypogonadotropic hypogonadism caused by tumors or CNS disorders that disrupt the HPG axis. Assessment of pubertal development involves the Tanner staging system.
This document discusses precocious puberty, defined as the onset of secondary sexual characteristics before age 8 in girls and 9 in boys. It describes the different types (true/central, pseudo/peripheral, mixed), potential causes including brain lesions, hypothyroidism, and tumors, signs and symptoms, diagnostic tests, and treatment which typically involves GnRH agonists. Specific conditions discussed in more detail include hypothalamic hamartomas, hepatoblastoma, McCune-Albright syndrome, and familial male precocious puberty. Incomplete forms of precocious puberty like premature thelarche and adrenarche are also summarized.
Here are the key considerations for this patient:
- She is postmenopausal based on her age
- With an intact uterus, estrogen-only hormone therapy would put her at increased risk for endometrial cancer
- As she is asymptomatic, hormone therapy may not be needed
- Screening for osteoporosis, cardiovascular risk, and breast cancer should be discussed based on risk factors
- Lifestyle modifications like calcium/vitamin D, exercise, not smoking can help prevent diseases of menopause
- Close monitoring without hormone therapy is a reasonable option given her age and lack of bothersome symptoms
The priorities would be assessing risk factors, discussing screening recommendations, and supporting lifestyle changes to promote health during men
Delayed Puberty Topics in Adolescent Gynecology Delayed Puberty Topics in A...MedicineAndHealth14
This document discusses delayed puberty in adolescent girls. It begins by outlining normal pubertal development and defining delayed puberty. Delayed puberty is then classified into three categories: hypergonadotropic hypogonadism (43%), hypogonadotropic hypogonadism (31%), and eugonadism (26%). For evaluation and management, the document recommends obtaining a history, physical exam, initial labs (TSH, prolactin), and a progestational challenge to determine gonadotropin levels and identify underlying causes. Treatment strategies aim to correct the underlying pathology, prevent disease complications, and provide sex steroids.
This document provides information on delayed puberty, including its definition, causes, evaluation, and treatment. Delayed puberty can be functional, due to hypogonadotropic hypogonadism, or hypergonadotropic hypogonadism. The most common cause is constitutional delay of growth and puberty. Evaluation involves medical history, physical exam, lab tests like LH, FSH and bone age. Treatment depends on the underlying cause, but aims to induce normal pubertal development and growth. For constitutional delay, watchful waiting is often recommended, while permanent hypogonadism requires hormone therapy like testosterone to initiate puberty.
Precocious puberty refers to the early onset of sexual maturation before 8 years in girls and 9 years in boys. It can be classified as true precocious puberty, which is GnRH-dependent, or pseudoprecocious puberty, which is GnRH-independent. Evaluation involves physical exam, lab tests, imaging and bone age assessment. Treatment depends on the type but may include GnRH analogues to suppress early puberty.
Precocious puberty can be caused by central or peripheral conditions. Central precocious puberty is gonadotropin dependent and caused by organic brain lesions or idiopathically. Peripheral precocious puberty is gonadotropin independent and caused by conditions like McCune-Albright syndrome or adrenal tumors. Hypothyroidism can also cause precocious puberty by elevating TSH levels and interacting with FSH receptors. Evaluation involves assessing pubertal progression, growth, hormonal levels, and imaging. Treatment depends on the underlying cause, and may involve surgery, medication like GnRH agonists, or treating the primary condition in cases of hypothyroidism.
Precocious puberty refers to the onset of puberty before age 8 in girls and age 9 in boys. It can be caused by central activation of the hypothalamic-pituitary-gonadal axis or peripheral problems affecting the ovaries, testes or adrenal glands. Treatment typically involves suppressing early hormone production through GnRH analogues to delay puberty and allow for normal adult height. Parents can help children cope by educating them about the changes, monitoring for emotional impacts, and offering praise and support through participation in other activities rather than focusing on appearance.
This document provides an overview of paediatric endocrinology for adult endocrinologists. It discusses various growth and puberty related conditions seen in paediatric endocrinology practice including short stature, precocious and delayed puberty, congenital hypothyroidism, and growth hormone deficiency. It also covers approaches to evaluating growth using height measurements and bone age assessments. Case examples are presented to illustrate various conditions.
This document provides information on evaluating and treating delayed puberty. It defines delayed puberty and discusses the main causes, which include constitutional delay of puberty, hypogonadotropic hypogonadism, and hypergonadotropic hypogonadism. Evaluation involves assessing medical history, physical exam including Tanner staging, lab tests of hormone levels, bone age, and imaging if needed. Treatment depends on the underlying cause, and may include observation, sex hormone therapy, or treating any underlying medical conditions.
This document discusses delayed puberty in children. It begins by defining normal puberty and factors that can affect the timing of puberty. It then defines delayed puberty and describes the main types as hypogonadotropic hypogonadism, characterized by low gonadotropins, and hypergonadotropic hypogonadism, characterized by high gonadotropins. The document outlines the evaluation and management of delayed puberty, including history, physical exam, laboratory tests, and treatment approaches depending on the underlying cause. Treatment may involve hormone replacement therapy, addressing underlying medical conditions, or observation in cases of constitutional delay.
This document discusses precocious puberty, including central precocious puberty and peripheral precocious puberty. Central precocious puberty is the early activation of the hypothalamic-pituitary-gonadal axis, leading to the onset of secondary sexual characteristics before age 8 in girls and 9 in boys. Peripheral precocious puberty is caused by external sex hormones and may be isosexual or heterosexual. McCune-Albright syndrome is a rare cause of peripheral precocious puberty associated with patchy skin pigmentation and fibrous dysplasia. Treatment for central precocious puberty involves suppressing puberty with GnRH agonists to help increase adult height potential.
Precocious puberty is when sexual and physical maturation occurs earlier than normal. It can begin as early as age 6-7 in girls and before age 9 in boys. This is caused by the early release of hormones from the hypothalamus and pituitary gland. Treatment aims to stop further sexual development and rapid growth to allow children to reach their full adult height. Medications that block sex hormones are commonly used, and can help reverse physical changes and return behavior to age-appropriate levels. Precocious puberty affects girls more often than boys and carries health risks if not properly treated.
Disorders of pubertal development can involve delayed, premature, or arrested puberty. The document discusses the normal physiology of puberty and various conditions that cause abnormalities in pubertal development, including central precocious puberty, peripheral precocious puberty, premature adrenarche, constitutional delay of growth and puberty, and pubertal arrest. Evaluation and management of disorders of pubertal development involves assessment of signs of puberty, auxiliary investigations, and potential treatments depending on the underlying cause.
Precocious puberty refers to the onset of sexual maturation before age 8 in girls and age 9 in boys. Common signs in girls include breast development, pubic hair growth, growth spurts, and menstruation. In boys, signs are enlargement of the testes or penis, pubic hair growth, growth spurts, and voice deepening. The causes can include brain injuries, infections, thyroid issues, or primary sex organ abnormalities. Treatment involves lowering sex hormone levels with medications like LHRH to stop further sexual development. Supporting the child emotionally is also important.
Additional important history:
- Family history of precocious or early puberty
- Developmental milestones
- Medications/supplements
Examination:
- Bone age X-ray
- Pelvic/abdominal ultrasound
- MRI brain
Differential diagnosis:
- Central precocious puberty
- Peripheral precocious puberty (e.g. McCune-Albright syndrome)
- Pseudoprecocious puberty
Investigations:
- LH, FSH, estradiol
- Chromosome analysis
- MRI to rule out CNS pathology
Final diagnosis: Central precocious puberty likely due to early activation of hyp
This case discusses a 7-year-old boy presenting with early signs of puberty over the past 5-6 months. Laboratory tests showed elevated levels of testosterone, LH, and FSH, confirming precocious puberty. A GnRH stimulation test showed an LH spike, indicating central precocious puberty. The patient was diagnosed with idiopathic central precocious puberty and prescribed injections of Decapeptyl to delay further pubertal progression until age 11 in order to avoid short adult stature. The document discusses evaluation and management of precocious puberty.
Precocious puberty is an early onset of sexual maturation, usually defined as beginning before age 8 in girls and age 9 in boys. It can be caused by genetic factors or physical abnormalities affecting the hypothalamus or other parts of the hormonal system. Symptoms in girls include breast development and menstruation, while boys experience genital growth and facial hair. Treatment aims to stop further sexual development using drugs that block hormone production.
This document discusses precocious puberty, which is defined as the development of secondary sex characteristics before age 8 in girls and 9 in boys. There are two types: central precocious puberty caused by early activation of the hypothalamic-pituitary axis, and peripheral precocious puberty caused by elevated sex steroid levels independent of gonadotropins. Imaging depends on gender and lab results, and may include MRI of the brain in boys with central precocious puberty or ovarian/testicular ultrasound in peripheral precocious puberty cases. Common causes discussed include hypothalamic hamartomas, ovarian cysts, Leydig cell tumors, and congenital adrenal hyperplasia.
Puberty disorders can involve either precocious or delayed puberty. Precocious puberty is defined as the onset of puberty before age 8 in girls or age 9 in boys. It can be central, involving premature activation of the hypothalamic-pituitary-gonadal axis, or peripheral. Central precocious puberty is more common in girls. Delayed puberty involves the lack of signs of puberty starting by certain ages. The most common cause is constitutional delay of growth and puberty, but it can also be caused by hypothalamic-pituitary defects or gonadal failure. Investigation is usually needed to determine the underlying cause.
1) Precocious puberty is the onset of secondary sexual characteristics before age 8 in girls and age 9 in boys. It can be caused by premature activation of the hypothalamic-pituitary-gonadal axis (central) or premature sex hormone secretion from other sources like the adrenal glands (peripheral).
2) Treatment involves suppressing sex hormone production using GnRH analogues to stop further sexual development and rapid growth. This helps preserve final adult height.
3) Pubertal development is assessed using the Tanner stages, which evaluate breast/genital development and pubic hair growth. Precocious puberty disrupts the normal timing and progression of these stages.
This document provides an overview of precocious puberty, including its definition, classification, and causes. Precocious puberty is defined as the onset of puberty more than 2 standard deviations earlier than normal. The mean age of pubertal onset is 10.5 years for girls and 11.5 years for boys, with 1 standard deviation being approximately 1 year. Precocious puberty can be classified as benign/non-progressive variants, central precocious puberty, or peripheral precocious puberty. Benign variants include premature thelarche, premature adrenarche, and isolated premature menarche.
1) Puberty is the process of physical maturation from child to adult, triggered by hormonal changes. It involves growth, development of secondary sex characteristics, and reproductive ability.
2) The timing of puberty is influenced by genetics as well as environmental factors like nutrition and geography. It typically occurs between ages 8-13 in girls and 9-14 in boys.
3) Precocious puberty describes the onset of puberty before age 8 in girls and age 9 in boys. It can be caused by genetic conditions, brain abnormalities, or tumors and requires medical evaluation and sometimes treatment to delay puberty.
Female sexual orientation and pubertal onsetTeresa Levy
This article examines the relationship between female sexual orientation and pubertal onset. The researchers hypothesized that lesbians would have a later, more masculine age of pubertal onset compared to heterosexual women based on theories that both sexual orientation and pubertal timing are influenced by prenatal androgens. They studied samples of community volunteers and discordant twins but found no significant differences in pubertal onset between homosexual and heterosexual women, contrary to their hypothesis.
Radiation Protection in Paediatric Interventional CardiologyÜlger Ahmet
Children are more sensitive to radiation than adults. Exposure parameters are often not adjusted for pediatric patients, which can result in larger and unnecessary radiation doses for children. Unique considerations for radiation safety in pediatric patients include adjusting exposure factors based on patient size and anatomy. Radiation dose should be carefully managed and minimized for pediatric interventional procedures.
The document discusses the endocrine basis of normal pubertal development. It describes how puberty is regulated by the hypothalamic-pituitary-gonadal axis and the hormonal interactions involved in pubertal development in boys and girls. It also discusses adrenarche and the role of growth hormone in puberty. Key points include:
1) Puberty results from increased GnRH pulsatility from the hypothalamus, which activates the HPG axis.
2) Gonadotropins stimulate sex hormone production from the gonads, leading to secondary sex characteristics and gamete production.
3) Adrenarche involves increased adrenal androgen production starting in mid-childhood
Precocious puberty refers to the early onset of sexual maturation before 8 years in girls and 9 years in boys. It can be classified as true precocious puberty, which is GnRH-dependent, or pseudoprecocious puberty, which is GnRH-independent. Evaluation involves physical exam, lab tests, imaging and bone age assessment. Treatment depends on the type but may include GnRH analogues to suppress early puberty.
Precocious puberty can be caused by central or peripheral conditions. Central precocious puberty is gonadotropin dependent and caused by organic brain lesions or idiopathically. Peripheral precocious puberty is gonadotropin independent and caused by conditions like McCune-Albright syndrome or adrenal tumors. Hypothyroidism can also cause precocious puberty by elevating TSH levels and interacting with FSH receptors. Evaluation involves assessing pubertal progression, growth, hormonal levels, and imaging. Treatment depends on the underlying cause, and may involve surgery, medication like GnRH agonists, or treating the primary condition in cases of hypothyroidism.
Precocious puberty refers to the onset of puberty before age 8 in girls and age 9 in boys. It can be caused by central activation of the hypothalamic-pituitary-gonadal axis or peripheral problems affecting the ovaries, testes or adrenal glands. Treatment typically involves suppressing early hormone production through GnRH analogues to delay puberty and allow for normal adult height. Parents can help children cope by educating them about the changes, monitoring for emotional impacts, and offering praise and support through participation in other activities rather than focusing on appearance.
This document provides an overview of paediatric endocrinology for adult endocrinologists. It discusses various growth and puberty related conditions seen in paediatric endocrinology practice including short stature, precocious and delayed puberty, congenital hypothyroidism, and growth hormone deficiency. It also covers approaches to evaluating growth using height measurements and bone age assessments. Case examples are presented to illustrate various conditions.
This document provides information on evaluating and treating delayed puberty. It defines delayed puberty and discusses the main causes, which include constitutional delay of puberty, hypogonadotropic hypogonadism, and hypergonadotropic hypogonadism. Evaluation involves assessing medical history, physical exam including Tanner staging, lab tests of hormone levels, bone age, and imaging if needed. Treatment depends on the underlying cause, and may include observation, sex hormone therapy, or treating any underlying medical conditions.
This document discusses delayed puberty in children. It begins by defining normal puberty and factors that can affect the timing of puberty. It then defines delayed puberty and describes the main types as hypogonadotropic hypogonadism, characterized by low gonadotropins, and hypergonadotropic hypogonadism, characterized by high gonadotropins. The document outlines the evaluation and management of delayed puberty, including history, physical exam, laboratory tests, and treatment approaches depending on the underlying cause. Treatment may involve hormone replacement therapy, addressing underlying medical conditions, or observation in cases of constitutional delay.
This document discusses precocious puberty, including central precocious puberty and peripheral precocious puberty. Central precocious puberty is the early activation of the hypothalamic-pituitary-gonadal axis, leading to the onset of secondary sexual characteristics before age 8 in girls and 9 in boys. Peripheral precocious puberty is caused by external sex hormones and may be isosexual or heterosexual. McCune-Albright syndrome is a rare cause of peripheral precocious puberty associated with patchy skin pigmentation and fibrous dysplasia. Treatment for central precocious puberty involves suppressing puberty with GnRH agonists to help increase adult height potential.
Precocious puberty is when sexual and physical maturation occurs earlier than normal. It can begin as early as age 6-7 in girls and before age 9 in boys. This is caused by the early release of hormones from the hypothalamus and pituitary gland. Treatment aims to stop further sexual development and rapid growth to allow children to reach their full adult height. Medications that block sex hormones are commonly used, and can help reverse physical changes and return behavior to age-appropriate levels. Precocious puberty affects girls more often than boys and carries health risks if not properly treated.
Disorders of pubertal development can involve delayed, premature, or arrested puberty. The document discusses the normal physiology of puberty and various conditions that cause abnormalities in pubertal development, including central precocious puberty, peripheral precocious puberty, premature adrenarche, constitutional delay of growth and puberty, and pubertal arrest. Evaluation and management of disorders of pubertal development involves assessment of signs of puberty, auxiliary investigations, and potential treatments depending on the underlying cause.
Precocious puberty refers to the onset of sexual maturation before age 8 in girls and age 9 in boys. Common signs in girls include breast development, pubic hair growth, growth spurts, and menstruation. In boys, signs are enlargement of the testes or penis, pubic hair growth, growth spurts, and voice deepening. The causes can include brain injuries, infections, thyroid issues, or primary sex organ abnormalities. Treatment involves lowering sex hormone levels with medications like LHRH to stop further sexual development. Supporting the child emotionally is also important.
Additional important history:
- Family history of precocious or early puberty
- Developmental milestones
- Medications/supplements
Examination:
- Bone age X-ray
- Pelvic/abdominal ultrasound
- MRI brain
Differential diagnosis:
- Central precocious puberty
- Peripheral precocious puberty (e.g. McCune-Albright syndrome)
- Pseudoprecocious puberty
Investigations:
- LH, FSH, estradiol
- Chromosome analysis
- MRI to rule out CNS pathology
Final diagnosis: Central precocious puberty likely due to early activation of hyp
This case discusses a 7-year-old boy presenting with early signs of puberty over the past 5-6 months. Laboratory tests showed elevated levels of testosterone, LH, and FSH, confirming precocious puberty. A GnRH stimulation test showed an LH spike, indicating central precocious puberty. The patient was diagnosed with idiopathic central precocious puberty and prescribed injections of Decapeptyl to delay further pubertal progression until age 11 in order to avoid short adult stature. The document discusses evaluation and management of precocious puberty.
Precocious puberty is an early onset of sexual maturation, usually defined as beginning before age 8 in girls and age 9 in boys. It can be caused by genetic factors or physical abnormalities affecting the hypothalamus or other parts of the hormonal system. Symptoms in girls include breast development and menstruation, while boys experience genital growth and facial hair. Treatment aims to stop further sexual development using drugs that block hormone production.
This document discusses precocious puberty, which is defined as the development of secondary sex characteristics before age 8 in girls and 9 in boys. There are two types: central precocious puberty caused by early activation of the hypothalamic-pituitary axis, and peripheral precocious puberty caused by elevated sex steroid levels independent of gonadotropins. Imaging depends on gender and lab results, and may include MRI of the brain in boys with central precocious puberty or ovarian/testicular ultrasound in peripheral precocious puberty cases. Common causes discussed include hypothalamic hamartomas, ovarian cysts, Leydig cell tumors, and congenital adrenal hyperplasia.
Puberty disorders can involve either precocious or delayed puberty. Precocious puberty is defined as the onset of puberty before age 8 in girls or age 9 in boys. It can be central, involving premature activation of the hypothalamic-pituitary-gonadal axis, or peripheral. Central precocious puberty is more common in girls. Delayed puberty involves the lack of signs of puberty starting by certain ages. The most common cause is constitutional delay of growth and puberty, but it can also be caused by hypothalamic-pituitary defects or gonadal failure. Investigation is usually needed to determine the underlying cause.
1) Precocious puberty is the onset of secondary sexual characteristics before age 8 in girls and age 9 in boys. It can be caused by premature activation of the hypothalamic-pituitary-gonadal axis (central) or premature sex hormone secretion from other sources like the adrenal glands (peripheral).
2) Treatment involves suppressing sex hormone production using GnRH analogues to stop further sexual development and rapid growth. This helps preserve final adult height.
3) Pubertal development is assessed using the Tanner stages, which evaluate breast/genital development and pubic hair growth. Precocious puberty disrupts the normal timing and progression of these stages.
This document provides an overview of precocious puberty, including its definition, classification, and causes. Precocious puberty is defined as the onset of puberty more than 2 standard deviations earlier than normal. The mean age of pubertal onset is 10.5 years for girls and 11.5 years for boys, with 1 standard deviation being approximately 1 year. Precocious puberty can be classified as benign/non-progressive variants, central precocious puberty, or peripheral precocious puberty. Benign variants include premature thelarche, premature adrenarche, and isolated premature menarche.
1) Puberty is the process of physical maturation from child to adult, triggered by hormonal changes. It involves growth, development of secondary sex characteristics, and reproductive ability.
2) The timing of puberty is influenced by genetics as well as environmental factors like nutrition and geography. It typically occurs between ages 8-13 in girls and 9-14 in boys.
3) Precocious puberty describes the onset of puberty before age 8 in girls and age 9 in boys. It can be caused by genetic conditions, brain abnormalities, or tumors and requires medical evaluation and sometimes treatment to delay puberty.
Female sexual orientation and pubertal onsetTeresa Levy
This article examines the relationship between female sexual orientation and pubertal onset. The researchers hypothesized that lesbians would have a later, more masculine age of pubertal onset compared to heterosexual women based on theories that both sexual orientation and pubertal timing are influenced by prenatal androgens. They studied samples of community volunteers and discordant twins but found no significant differences in pubertal onset between homosexual and heterosexual women, contrary to their hypothesis.
Radiation Protection in Paediatric Interventional CardiologyÜlger Ahmet
Children are more sensitive to radiation than adults. Exposure parameters are often not adjusted for pediatric patients, which can result in larger and unnecessary radiation doses for children. Unique considerations for radiation safety in pediatric patients include adjusting exposure factors based on patient size and anatomy. Radiation dose should be carefully managed and minimized for pediatric interventional procedures.
The document discusses the endocrine basis of normal pubertal development. It describes how puberty is regulated by the hypothalamic-pituitary-gonadal axis and the hormonal interactions involved in pubertal development in boys and girls. It also discusses adrenarche and the role of growth hormone in puberty. Key points include:
1) Puberty results from increased GnRH pulsatility from the hypothalamus, which activates the HPG axis.
2) Gonadotropins stimulate sex hormone production from the gonads, leading to secondary sex characteristics and gamete production.
3) Adrenarche involves increased adrenal androgen production starting in mid-childhood
The document discusses the normal physiological process of puberty in humans. It describes the prepubertal period and the three changes that occur: adrenarche, decreasing repression of the hypothalamic-pituitary system, and gradual amplification of the interaction between GnRH and gonadotropins. It also discusses the stages of pubertal development, timing of puberty which is influenced mostly by genetics, and average ages for the different Tanner stages of breast and pubic hair development.
This document defines pre-pubertal bleeding and outlines its causes and approaches to management. It discusses the developmental anatomy and physiology of the genital tract in infants/toddlers, preschoolers, and older children. Common causes of pre-pubertal bleeding include vulvovaginitis, urethral prolapse, lichen sclerosus, foreign bodies, trauma, precocious puberty, and rare tumors. A thorough history, physical exam, and investigations are needed to evaluate the bleeding and identify its cause, which is often a local genital tract lesion but could occasionally be a serious condition like cancer. Careful diagnosis is important for successful treatment.
Puberty is the physiological transition from childhood to reproductive maturity associated with growth spurts and development of primary and secondary sexual characteristics between ages 8-14. It is controlled by the hypothalamic-pituitary-gonadal axis, which stimulates sex hormone secretion and profound biological changes. Precocious or delayed puberty may have underlying pathological causes that require investigation through assessments of medical history, examinations, blood tests, and imaging to diagnose conditions and guide management.
This document summarizes various causes of vaginal itching and discharge and their treatments. It discusses yeast, bacterial vaginosis, trichomoniasis, contact dermatitis, pubic lice, HPV, and several types of vulvar dystrophy as potential causes. Topical and oral antifungal agents are recommended for treating yeast. Flagyl, clindamycin, or amoxicillin can treat bacterial vaginosis. Flagyl is used to treat trichomoniasis. Further evaluation including wet mounts, cultures or biopsies may be needed to diagnose other conditions.
The document discusses several diseases that can affect the vulva, including Bartholin's gland cysts and abscesses, Herpes vulvitis, Molluscum contagiosum, HPV warts, Tinea cruris, lichen sclerosis, Paget's disease, vulvar hematoma, primary syphilis, condyloma lata, chancroid, lymphogranuloma venereum, and granuloma inguinale. For each condition, it describes symptoms, diagnosis, and treatment options.
Vaginal discharge is the most common gynecologic complaint encountered. It can be caused by normal physiologic changes, disturbances in vaginal flora, infections like bacterial vaginosis (BV), yeast infections, trichomoniasis, or less commonly sexually transmitted diseases or other issues. A full history and physical exam including diagnostic tests like pH checks and microscopy of discharge can determine the cause. Common causes like BV, yeast, and trichomoniasis are treated with antibiotics or antifungals, while less common issues may require further testing or management.
The document discusses several topics related to puberty in girls and boys:
- It describes some of the physical changes girls experience during puberty like breast development between ages 8-13 and that breasts usually continue growing until ages 17-18.
- It explains that girls are born with all the eggs they will ever have and ovaries typically release one egg per month through ovulation.
- Periods usually last 3-7 days and occur about once a month, though cycles can vary between 21-35 days.
- For boys, puberty brings body growth, voice changes, and new hair growth typically between ages 9-14, though everyone develops at their own pace.
The document describes the anatomy of the pelvic floor, urogenital diaphragm, and perineum. It discusses the levator ani muscles that form the pelvic floor and their functions in supporting pelvic organs and assisting in childbirth. It describes the urogenital diaphragm deep to the pelvic floor and the perineal spaces and triangles below. The document then discusses perineal tears that can occur during childbirth, their degrees of severity, symptoms, repair techniques, and complications if left untreated.
Central precocious puberty (CPP) is the early activation of the hypothalamic-pituitary-gonadal axis, leading to premature sexual maturation. Peripheral precocious puberty (PPP) involves the appearance of secondary sex characteristics without activation of the HPG axis, instead caused by direct sex steroid production. Evaluation of precocious puberty involves determining which pubertal changes are present to classify it as CPP or PPP, followed by laboratory tests and imaging studies to identify potential underlying causes.
This document discusses precocious puberty, including its definition, types, epidemiology, evaluation, and treatment. Precocious puberty is defined as the onset of puberty before age 8 in girls and age 9 in boys. It can be central, originating from the brain, or peripheral, originating from the gonads or adrenal glands. Evaluation involves medical history, physical exam, labs, imaging, and bone age assessment. Treatment is aimed at delaying further pubertal progression using GnRH analogs.
This document summarizes a review article about the lifecycle of polycystic ovary syndrome (PCOS) from early life through menopause. It finds that:
1) Daughters of women with PCOS show signs of an increased follicle count and mild metabolic abnormalities from infancy, suggesting early genetic and environmental influences.
2) PCOS is often diagnosed in puberty with the onset of hyperandrogenism and menstrual irregularities.
3) During the reproductive years, features of PCOS such as androgen levels and ovarian volume decrease over time, though cardiovascular risks persist after menopause for women who had PCOS.
1) The document presents a clinical review of precocious puberty, discussing the timing, classification, and management. Precocious puberty can be gonadotropin dependent (central) or independent (peripheral) and may be complete or incomplete.
2) Central precocious puberty results from premature activation of the hypothalamic-pituitary-gonadal axis. Gonadotropin-releasing hormone analogs are the mainstay of treatment to slow pubertal progression.
3) Evaluation involves medical history, physical exam, bone age assessment and hormonal/imaging tests to identify underlying causes and differentiate central from peripheral precocious puberty.
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Recent Trends in Pubertal Timing and Current Management of Precocious Puberty in Girls
1. Recent Trends in Pubertal Timing and Current Management of
Precocious Puberty in Girls.
2. Review Article
Recent trends in pubertal timing and current management of
precocious puberty in girls
Anjana Hulse*
Consultant Pediatric Endocrinologist, Apollo Hospitals, Bangalore, India
a r t i c l e i n f o
Article history:
Received 28 April 2013
Accepted 15 May 2013
Available online 6 June 2013
Keywords:
Precocious puberty
GnRHa therapy
Early puberty
a b s t r a c t
Precocious puberty is defined as development of pubertal signs at a younger age than the
accepted lower limits for the onset of puberty. Precocious puberty can be classified as
gonadotropin dependent (central or true) and gonadotropin independent (peripheral or
pseudo). Commonest etiology in girls is idiopathic gonadotropin dependent precocious
puberty. Recently, timing of onset of puberty in girls has gained considerable interest
among the professionals and general public. Recent data suggests a decrease in the age of
onset of puberty in girls over the past 2e3 decades which may be attributable to increased
incidence of obesity, improved nutrition and other environmental factors.
Precocious puberty in girls warrants prompt evaluation and early initiation of treatment
to optimize adult height potential and to minimize psychosocial stress to the child.
Treatment is directed at the primary cause. Gonadotropin releasing hormone analog
(GnRHa) is the treatment of choice for gonadotropin dependent precocious puberty. GnRHa
are effective in preventing pubertal progression clinically as well as biochemically. A va-
riety of GnRHa preparations are available and the details are mentioned in the text.
Copyright ª 2013, Indraprastha Medical Corporation Ltd. All rights reserved.
1. Introduction
Precocious puberty is defined as the development of pubertal
signs at a younger age than the accepted lower limits for the
onset of puberty. In girls, breast development before the age of
8 years, appearance of sexual pubic hair before the age of 8
years or beginning menses before the age of 9.5 years is
traditionally considered as precocious puberty. This is
accompanied by rapid growth rate, advanced skeletal matu-
ration and increased levels of gonadotropins and/or sex
steroids.
Precocious puberty can be classified as gonadotropin
dependent (central or true) and gonadotropin independent
(peripheral or pseudo). Central precocious puberty (CPP) is due
to premature activation of hypothalamoepituitaryegonadal
(HPG) axis. There is no activation of HPG axis in peripheral
precocious puberty (PPP). Even though organic lesions of the
central nervous system (CNS) are occasionally the cause of
precocious puberty, in the vast majority of the girls, CPP is
idiopathic. The source of sex steroid in PPP is endogenous as in
ovarian cysts or tumors; or adrenal as in adrenal tumors or
CAH; or exogenous such as ingestion of estrogen containing
* TF3, Dhanush Paradise, 10th Cross, 5th Main, Vijaya Bank Layout, Behind IIM-B, Bangalore 76, India. Tel.: þ91 (0) 80 26304050, þ91 (0)
9591382502 (mobile).
E-mail address: anmhulse@gmail.com.
Available online at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/apme
a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 1 3 4 e1 3 7
0976-0016/$ e see front matter Copyright ª 2013, Indraprastha Medical Corporation Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.apme.2013.05.010
3. pills or other endocrine disruptors (ED) present in food or
cosmetics.
2. Recent trends in pubertal timing
CPP is 10 times (female to male ratio varies from 3:1 to 23:1)
more common in girls than in boys.1,2
During the past 2e3
decades the timing of onset of puberty in girls has been a topic
of debate among pediatric endocrinologists. European data
have shown a sharp decline in age at menarche from 17 years
in the early 19th century to about 13 years in mid 20th cen-
tury.3
In the past 25 years a decrement of 2.5e4 months in age
at menarche has been noticed in both Europe and United
States.4e6
In contrast to menarche, age at onset of breast
development seem to have declined markedly from a mean
age of 11 years to less than 10 years during the past 2 decades.7
Although these findings were reported by two American
studies in 1990s similar findings were confirmed in Europe 15
years later.4,7,8
These studies prompted (LWPES) to recom-
mend a lower age limit for evaluation of precocious puberty in
girls from 8 years to 7 years.9
These recommendations were
based mainly on Pediatric Research in Office Settings network
(PROS)/National Health and Nutrition Examination Survey
(NHANES III) study where only girls up to the age of 12 years
were included. Moreover, NHANES study mainly relied on vi-
sual grading of breast development which may not be the
appropriate way to assess puberty in obese individuals. The
proposal of lowering of the age for evaluation of precocious
puberty in girls by LWPES was criticized by many experts.
More recently Copenhagen Puberty Study reported 12 months
decline in mean age at onset of puberty in Danish girls.4
Further studies clearly suggest a secular trend toward earlier
onset of breast development where as age at menarche has
changed only marginally. However, extrapolation from these
cross sectional findings may not be appropriate to redefine the
age limit for evaluation of precocious puberty and may lead to
possible misdiagnosis of potentially treatable underlying pa-
thology in about 5e10% girls.10
Therefore, cut off values for
age at which diagnostic evaluation is needed should not be
lowered.
Rapid change in pubertal timing in the recent years is a
pointer toward environmental influence on puberty in chil-
dren. Recent increase in the incidence of childhood obesity
has also contributed to early onset of puberty in girls. Genetic
factors, fetal nutrition and physical activity also play a role.
Catch up growth following early fetal or post natal under
nutrition may also be associated with early puberty.11
3. Evaluation of precocious puberty in girls
More than 90% of the girls with precocious puberty have
gonadotropin releasing hormone (GnRH) dependent preco-
cious puberty. Diagnostic evaluation is based on the devel-
opment of physical pubertal changes and laboratory testing
that are consistent with progressive changes of HPG axis
activation. Documentation of history, physical examination
findings and assessing hormonal status make important part
of evaluation. History taking should include growth patterns
since birth, age of onset of physical changes, past medical,
family and psychosocial history. Possibility of exposure to
exogenous hormones should be explored. Past history of CNS
infection, tumors, chemo or radiotherapy should be elicited.
Gelastic seizures may occur with CNS hamartomas. Physical
examination should include careful assessment of growth,
growth velocity, BMI, Tanner staging and systemic examina-
tion including fundus examination. Visualization of vaginal
mucosa to look for the evidence of estrogenization should be
included as a part of the examination.
Initial hormonal evaluation should include assessment of
bone age hormonal assays including luteinizing hormone
(LH), follicle stimulating hormone (FSH), estradiol (E2) and
where indicated dehydroepiandrostenedione (DHEAS) and
thyroid function tests. LH measurements are most valuable
for diagnosing precocious puberty. Pre-pubertal LH levels are
less than 0.1 IU/L. Basal LH level greater than 0.2 IU/L may
have 100% sensitivity and specificity for boys, but there 50% of
the girls in Tanner stage II breast development may have pre-
pubertal LH levels.12
Because of the variations in basal levels
and overlap between pre-pubertal and early pubertal hor-
monal levels, GnRH/GnRHa stimulation test is considered as
the gold standard to confirm the diagnosis of GnRH dependent
precocious puberty. However, there is a lot of debate about the
cut off values of LH and FSH for diagnosis of puberty following
stimulation with GnRH/GnRHa. Moreover, GnRH stimulation
test has low sensitivity, though it is highly specific for con-
firming precocious puberty.13
Conventionally, a peak LH value
more than 4.2e5 IU/L or a greater stimulated peak of LH/FSH is
considered as pubertal response. Peak levels of gonadotropins
are obtained 30 min after GnRH stimulation and 60 min after
GnRHa such as Leuprolide injection.14
Sensitive assays with
pediatric norms should be used.
Pelvic ultrasound in girls determines the ovarian and
uterine size. Uterine length, transverse diameter, endometrial
thickness, ratio of fundus to cervix, ovarian size and volume,
number of follicles and size of the biggest follicle should be
measured. Cut off values for uterine length is considered to be
about 4 cm and fundus to cervix ratio of more than 2:1 is
suggestive of pubertal status. Presence of endometrial echo is
highly specific but less sensitive.15
Cut off for pubertal ovarian
volume is about 1e3 ml.16
MRI of the CNS is usually done to
identify CNS lesions, though this investigation can be omitted
in older girls presenting with typical features of true central
precocious puberty.
4. Treatment
Early treatment of precocious puberty is utmost important. If
untreated, precocious puberty may lead to early epiphyseal
fusion and compromised final height.17,18
In addition early
puberty/menarche can cause significant psychological stress
in young girls.19
Treatment of precocious puberty is directed at
the primary cause.
GnRHa is the treatment of choice for GnRH dependent
precocious puberty. GnRHa suppresses the episodic secretion
of gonadotropins by continued occupation of the GnRH re-
ceptors on the pituitary gonadotropes with high level of
GnRHa. Girls with onset of progressive central precocious
a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 1 3 4 e1 3 7 135
4. puberty before the age of 6 years benefit the most in terms of
height from GnRHa therapy. A variety of GnRHa formulations
are available (monthly and depot preparations for intramus-
cular use; intranasal and sub-cutaneous injections).
Commonly used GnRHa include Goserelin, Buserelin, Leu-
prolide, Triptorelin and Histrelin. GnRHa are expensive and
this may be a limiting factor for its use for patients from lower
socioeconomic status in developing countries. For most chil-
dren, monthly injections in a dose of 0.3 mg/kg/28 days
adequately suppress the gonadotropins. Occasionally more
frequent injections may be required. Depot preparations (3
monthly) also have been tried and shown to be equally effi-
cacious and is useful when compliance in an issue.20
But
larger randomized trials are required to confirm the effec-
tiveness and safety of depot preparations. The choice of
therapy depends on local availability, physician as well as
patient or parents’ choice. GnRHa are generally well tolerated.
Hot flushes, headaches and sterile abscess have been
described in the literature but the incidence is very low.
Anaphylaxis is extremely rare. Vaginal bleeding may occur
after the first injection but, should cease with subsequent
doses. Some pediatric endocrinologists suggest measurement
of stimulated LH and E 2 levels to assess the efficacy of
treatment. However there is no consensus on routine use of
this. Decline in growth velocity and bone age advancement
should occur during treatment. Progression of breast devel-
opment or other pubertal signs (not pubic hair) suggests fail-
ure of treatment and calls for re-evaluation of the patient.
Discontinuation of GnRHa at a chronological age of 11 years
and at a bone age of 12 years has been associated with
maximum adult height.21
Timing of cessation of therapy de-
pends on the parents’ and the child’s wish and also physi-
cian’s assessment. In one study menses began at a mean of 16
months after stopping the treatment with GnRHa.21
Currently
available data does not suggest impairment of gonadal func-
tion in long term after stopping GnRHa therapy.21
Weight gain
and reduction in bone mineral density in children treated with
GnRHa have been mentioned, but these findings are not
objectively supported by the studies.21
GnRHa therapy is also used for hypothalamic hamartoma.
Treatment of PPP is directed against the cause and could be
sometimes challenging. CNS tumors, ectopic gonadotropin
producing gonadal and adrenal tumors require surgery, radio
or chemotherapy. Adrenal suppression in CAH and thyroxine
replacement in hypothyroidism is required. Where there is
autonomous gonadal steroid suppression such as McCune-
eAlbright syndrome aromatase inhibitors or ketoconazole
have been used to reduce the effect of sex steroids.
5. Newer therapies
Histrelin implant has been tried in girls with CPP in some
centers. There was no difference in terms of final height
achievement in children treated with implant or long acting
GnRHa. Menarche occurred sooner after removal of the
implant.22e25
However, long term studies are still awaited.
Orally acting GnRHa are also under development and poten-
tially could be used to treat children with central precocious
puberty in future. Adjunctive therapy with growth hormone
or oxandrolone have been tried, but are not routinely advo-
cated yet.
6. Conclusion
Population based studies have shown a shift towards earlier
mean age at the onset of breast development in girls in the
past two to three decades. These studies have not confirmed
rapid progression of entire sequence of puberty including
menarche. Even then, to avoid overlooking a small subset of
children with rapidly progressive puberty and to avoid
missing the pathological causes of puberty, lowering the
normal age for the evaluation of precocious puberty is not
advisable.
Treatment with GnRHa is reversible, safe and effective for
CPP in girls. Treatment of PPP sometimes is challenging. Long
term studies looking at the use of depot GnRHa preparations
for CPP and newer routes of administration such as implants
are needed. Cost of the treatment is also a limiting factor for
use of GnRHa for treatment of precocious puberty in devel-
oping countries like India.
Conflicts of interest
The author has none to declare.
r e f e r e n c e s
1. Teilmann G, Pedersen CB, Jensen TK, Skakkebaek NE, Juul A.
Prevalence and incidence of precocious pubertal
development in Denmark: an epidemiologic study based on
national registries. Pediatrics. 2005;116:1323e1328.
2. Berberoglu M. Precocious puberty and normal variant
puberty: definition, etiology, diagnosis and current
management. J Clin Res Pediatr Endocrinol. 2009;1:164e174.
3. Tanner JM. Trend towards earlier menarche in London, Oslo,
Copenhagen, the Netherlands and Hungary. Nature.
1973;243:95e96.
4. Aksglaede L, Sorensen K, Petersen JH, Skakkebaek NE, Juul A.
Recent decline in age at breast development: the Copenhagen
Puberty Study. Pediatrics. 2009;123:e932ee939.
5. Rubin C, Maisonet M, Kieszak S, et al. Timing of maturation
and predictors of menarche in girls enrolled in a
contemporary British cohort. Paediatr Perinat Epidemiol.
2009;23:492e504.
6. Anderson SE, Dallal GE, Must A. Relative weight and race
influence average age at menarche: results from two
nationally representative surveys of US girls studied 25 years
apart. Pediatrics. 2003;111:844e850.
7. Herman-Giddens ME, Slora EJ, Wasserman RC, et al.
Secondary sexual characteristics and menses in young girls
seen in office practice: a study from the Pediatric Research in
Office Settings Network. Pediatrics. 1997;99:505e512.
8. Karpati AM, Rubin CH, Kieszak SM, Marcus M, Troiano RP.
Stature and pubertal stage assessment in American boys: the
1988e1994 Third National Health and Nutrition Examination
Survey. J Adolesc Health. 2002;30:205e212.
9. Kaplowitz PB, Oberfield SE. Reexamination of the age limit for
defining when puberty is precocious in girls in the United
States: implications for evaluation and treatment. Drug and
a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 1 3 4 e1 3 7136
5. Therapeutics and Executive Committees of the Lawson
Wilkins Pediatric Endocrine Society. Pediatrics.
1999;104:936e941.
10. Sorensen K, Mouritsen A, Aksglaede L, Hagen CP,
Mogensen SS, Juul A. Recent secular trends in pubertal
timing: implications for evaluation and diagnosis of
precocious puberty. Horm Res Paediatr. 2012;77(3):137e145.
11. Proos L, Gustafsson J. Is early puberty triggered by catch-up
growth following undernutrition? Int J Environ Res Public
Health. 2012 May;9(5):1791e1809.
12. Resende EA, Lara BH, Reis JD, Ferreira BP, Pereira GA,
Borges MF. Assessment of basal and gonadotropin-releasing
hormone-stimulated gonadotropins by
immunochemiluminometric and immunofluorometric
assays in normal children. J Clin Endocrinol Metab.
2007;92(4):1424e1429.
13. Kılıc¸ A, Durmus‚ MS, Unuvar E, et al. Clinical and laboratory
characteristics of children referred for early puberty:
preponderance in 7e8 years of age. J Clin Res Pediatr Endocrinol.
2012 December;4(4):208e212.
14. Pescovitz OH, Hench KD, Barnes KM, Loriaux DL, Cutler Jr GB.
Premature thelarche and central precocious puberty: the
relationship between clinical presentation and the
gonadotropin response to luteinizing hormone-releasing
hormone. J Clin Endocrinol Metab. 1988;67:474e479.
15. de Vries L, Horev G, Schwartz M, Phillip M. Ultrasonographic
and clinical parameters for early differentiation between
precocious puberty and premature thelarche. Eur J Endocrinol.
2006;154(6):891e898.
16. Battaglia C, Mancini F, Regnani G, Persico N, Iughetti L,
De Aloysio D. Pelvic ultrasound and color Doppler findings in
different isosexual precocities. Ultrasound Obstet Gynecol.
2003;22(3):277e283.
17. Kauli R, Galatzer A, Kornreich L, Lazar L, Pertzelan A, Laron Z.
Final height of girls with central precocious puberty,
untreated versus treated with cyproterone acetate or GnRH
analogue. A comparative study with re-evaluation of
predictions by the BayleyePinneau method. Horm Res.
1997;47:54e61.
18. Brauner R, Adan L, Maiandry A, Zantleifer D. Adult height in
girls with idiopathic true precocious puberty. J Clin Endocrinol
Metab. 1994;79:415e420.
19. Ehrhardt AA, Meyer-Bahlburg HFL. Idiopathic precocious
puberty in girls: long-term effects on adolescent behavior.
Acta Endocrinol Suppl (Copenh). 1986;279:247e253.
20. Badaru A, Wilson DM, Bachrach LK, et al. Sequential
comparisons of one-month and three-month depot
leuprolide regimens in central precocious puberty. J Clin
Endocrinol Metab. 2006;91(5):1862e1867.
21. Carel JC, Eugster EA, Rogol A, Ghizzoni L, Palmert MR.
Consensus statement on the use of gonadotropin-releasing
hormone analogs in children. Pediatrics. 2009;123:e752.
22. Eugster EA, Clarke W, Kletter GB, et al. Efficacy and safety of
histrelin subdermal implant in children with central
precocious puberty: a multicenter trial. J Clin Endocrinol Metab.
2007;92(5):1697e1704.
23. Hirsch HJ, Gillis D, Strich D, et al. The histrelin implant: a
novel treatment for central precocious puberty. Pediatrics.
2005;116(6).
24. Gillis D, Karavani G, Hirsch HJ, Strich D. Time to menarche
and final height after histrelin implant treatment for central
precocious puberty. J Pediatr 2013 Feb 26; http://dx.doi.org/
10.1016/j.jpeds.2013.01.021. pii: S0022e3476(13)00045-0.
[Epub ahead of print].
25. Kappy MS, Ganong CS. Advances in the treatment of
precocious puberty. Adv Pediatr. 1994;41:223e261.
a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 1 3 4 e1 3 7 137