GH and Precocious Puberty
Here we will discuss GH and the effects on precocious puberty. To fully understand this we must first dive into details as to what Precocious puberty is.
What is precocious puberty?
Precocious puberty is when there is any sign of a secondary sexual characteristic in boys younger than 9 years old and girls younger than 7½ or 8 years old. In the United States, precocious puberty affects about 1% to 2% of boys. However, in most of these children, early puberty is a variation of the norm, and there is no medical problem. Many children with signs of precocious or delayed puberty have other relatives who had precocious or delayed puberty. Just as there are differences in the age of onset, there are differences in the duration of puberty in each child.
Near the end of puberty growth in stature stops. Because the bones of children with precocious puberty mature and stop growing earlier than normal, these children may be shorter than expected as adults. Precocious puberty can also cause emotional and social problems in boys who are sexually more mature than their peers.
Signs of precocious puberty
Precocious Puberty in Girls
- Early Breast development
- Early Vaginal bleeding
Precocious Puberty in Boys
- Growth of testicles and penis
- Facial hair
- Thickening of voice
Precocious Puberty in
- Pubic or armpit hair
- Rapid growth or “stretch”
- Adult body odor
What are the causes of precocious puberty?
Many types of precocious puberty are simply variants of normal growth. For example, breast development in girls and pubic or armpit hair in boys of both sexes, without other puberty symptoms, usually do not indicate an underlying medical problem.
Two main types of precocious puberty are abnormal. The first is called central precocious puberty and the second is peripheral precocious puberty.
puberty Central precocious puberty (CPP) occurs when the hypothalamus releases GnRH and triggers puberty very early. In most girls with CPP, there is no underlying medical problem. In men, the disorder is less common and is more likely to be related to a medical problem. Such problems include a tumor, brain trauma (such as a blow to the head, brain surgery, or radiation treatment to the head), or inflammation (such as meningitis).
puberty Peripheral precocious puberty (PPP) is less common than CPP. It is the result of premature production of sex hormones due to problems with the ovaries, testicles, or adrenal glands. Another cause can be external exposure to sex hormones (such as coming into contact with estrogen or testosterone cream).
Is there a way to diagnose P.PC.?
Of course, there are ways to diagnose precocious puberty, your child’s docto,r in this case, a pediatric endocrinologist will determine which is the way to diagnose it but we will tell you more or less what are the ways to diagnose it and they are the following.
- Radiographs to assess bone age
- Determination of serum hormone concentration
- Possibly pelvic ultrasound and brain MRI
The diagnosis of precocious puberty is clinical. Radiographs of the left hand and wrist are taken to investigate accelerated skeletal maturation secondary to the effect of sex hormones. Unless history and physical examination suggest an abnormality, no further evaluation is required in children with pubertal patterns that are within one year of population standards. Girls and boys with isolated premature adrenoceptors and girls with premature thelarche also do not require further evaluation as long as radiographs confirm that there is no acceleration of skeletal maturation.
When a further evaluation is necessary, blood tests should be chosen according to the characteristics present. For patients who have primarily androgenic effects, the most useful initial tests include measurements of total testosterone, dehydroepiandrosterone sulfate, 17-hydroxyprogesterone, and luteinizing hormone (LH); everything should be measured using high sensitivity assays designed for pediatric patients. For patients showing only estrogen effects, the most useful screening tests for girls include ultrasensitive LH and follicle-stimulating hormone (FSH), and estradiol, and, for boys, LH, FSH, beta-human chorionic gonadotropin, and estradiol. Pelvic and adrenal ultrasound may be helpful if either steroid levels are elevated, and MRI of the brain may be done to rule out intracranial abnormalities in younger patients or men with central precocious puberty.
A GnRH stimulation test may be considered to confirm GnRH-dependent precocious puberty when initial tests are inconclusive. Previously, a 1-hour stimulation test with the GnRH agonist gonadorelin was used, but because gonadorelin is no longer available, other GnRH agonists are used, such as leuprolide. Leuprolide acetate 10–20 mcg/kg is given subcutaneously, and LH, FSH, testosterone (in boys), and estradiol (in girls) are measured at 0, 1, and 2 hours. At 24 h post leuprolide, estradiol and testosterone can be measured to improve the sensitivity of the test. In GnRH-dependent precocious puberty, gonadotropin responses are pubertal. In GnRH-independent precocious puberty, gonadotropin responses to leuprolide are prepubertal.
Genetic testing may be considered in familial cases of GnRH-dependent precocious puberty, but this remains controversial.
What is the treatment for precocious puberty?
The treatment will be the one indicated by your child’s doctor but an idea of
- Treatment with GnRH agonists (GnRH-dependent precocious puberty)
- Treatment with androgen or estrogen antagonists (precocious puberty independent of GnRH)
- Tumor resection as needed
If pubertal patterns are within established population standards within 1 year, reassurance and regular examinations are sufficient. Treatment of adrenochemia or thelarch is not necessary, but regular reexploration is warranted to monitor for the later onset of precocious puberty. In GnRH-dependent precocious puberty, pituitary secretion of LH and FSH can be inhibited with GnRH agonists, including leuprolide acetate 7.5 to 15 mg IM every 4 weeks, 11.25 mg, or 30 mg IM every 12 weeks , or 45 mg every 24 weeks, triptorelin 22.5 mg every 6 months, or histrelin implants (changed annually). Responses to treatment should be monitored and drug dosage modified accordingly. Treatment can continue until the age of 11 years in girls and the age of 12 years in boys.
In girls with McCune-Albright syndrome, aromatase inhibitors, such as letrozole and anastrazole, have been used with varying degrees of success in reducing estradiol.
If GnRH-independent precocious puberty in males is due to gonadotropin-independent familial male precocity or McCune-Albright syndrome, androgen antagonists (eg, spironolactone) enhance the effects of androgen excess. The antifungal ketoconazole reduces testosterone in men with gonadotropin-independent familial male precocity.
If GnRH-independent precocious puberty is due to a hormone-producing tumor (eg, granulosa-theca cell tumors in girls, testicular tumors in boys), it should be resected. However, girls require prolonged follow-up to detect recurrences in the contralateral ovary.