Whileboys with a constitutional delay of puberty eventually have normal activation of the hypothalamic-pituitary-gonadal axis, their sexual immaturity and relative short stature may contribute to psychosocial problems. Androgen therapy, commonly given as a four-month course of testosterone injections, provides a boost in physical growth and maturity. In addition to constitutional delay of puberty, obesity and growth hormone deficiency may cause delayed puberty. Kaplowitz conducted a retrospective study to compare responses to testosterone therapy in boys with delayed puberty from constitutional delay, obesity and possible gonadotropin deficiency.
All of the boys were 14 years of age or older when they received testosterone injections. Twenty-three had constitutional delay of puberty and were of short stature, six had obesity and were of normal stature, five had hypopituitarism and growth hormone deficiency and two had isolated gonadotropin deficiency. They were prepubertal or in early puberty according to both physical characteristics and serum testosterone levels, which were less than 40 ng per dL (1.4 nmol per L). All received a course of testosterone enanthate injections, 100 mg intramuscularly, once a month for four months.
Testosterone therapy resulted in an increase in height and weight velocity in the 23 boys with constitutional pubertal delay. Penis and testicular size also increased during treatment. The six obese boys also had an increase in penis and testicular growth. The five boys with growth hormone deficiency received growth hormone replacement in addition to testosterone injections. Two of these boys had severe gonadotropin deficiency and did not demonstrate increased maturation rates. In two boys, testicular size increased, although not as rapidly as in boys with constitutional delay of puberty.
The author concludes that monitoring the response to testosterone injections in boys with delayed puberty helps to differentiate constitutional delay of puberty from gonadotropin deficiency in boys with delayed puberty. Since a rapid growth rate requires increased androgen and growth hormone production, the response to testosterone augmentation in the boys with constitutional delayed puberty excluded the possibility of growth hormone deficiency. In the obese boys, progression of maturation may have occurred after testosterone injections because of the inhibitory effects of androgens on leptin levels, which are presumed to be inceased in obese adolescent boys. After age 10, as testosterone and gonadotropin levels increase, serum leptin levels normally decline to levels found in boys five to six years of age, suggesting that increasing testosterone levels may inhibit leptin production. The author also believes that a lack of response to four testosterone injections may be useful in identifying boys who require long-term therapy because of gonadotropin deficiency.
In an accompanying editorial, Saenger and Sandberg note that testosterone therapy in boys with delayed maturation may help increase the velocity of maturation, but there is insufficient documentation to show that the psychosocial stress from delayed maturation is severe enough to warrant intervention with testosterone injections. Most of these children have a healthy adaptation, and treatment decisions should be weighed carefully. The authors believe the psychosocial benefit of treating constitutional delay of puberty may be overstated.
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Male hypogonadism is a condition in which the body doesn't produce enough of the hormone that plays a key role in masculine growth and development during puberty (testosterone) or enough sperm or both.
If the body doesn't produce enough testosterone during fetal development, the result may be impaired growth of the external sex organs. Depending on when hypogonadism develops and how much testosterone is present, a child who is genetically male may be born with:
Either type of hypogonadism can be caused by an inherited (congenital) trait or something that happens later in life (acquired), such as an injury or an infection. At times, primary and secondary hypogonadism occur together.
Klinefelter syndrome. This condition results from a congenital abnormality of the sex chromosomes, X and Y. A male normally has one X and one Y chromosome. In Klinefelter syndrome, two or more X chromosomes are present in addition to one Y chromosome.
The Y chromosome contains the genetic material that determines the sex of a child and related development. The extra X chromosome that occurs in Klinefelter syndrome causes abnormal development of the testicles, which in turn results in underproduction of testosterone.
Undescended testicles. Before birth, the testicles develop inside the abdomen and normally move down into their permanent place in the scrotum. Sometimes one or both of the testicles aren't descended at birth.
This condition often corrects itself within the first few years of life without treatment. If not corrected in early childhood, it can lead to malfunction of the testicles and reduced production of testosterone.
Cancer treatment. Chemotherapy or radiation therapy for the treatment of cancer can interfere with testosterone and sperm production. The effects of both treatments often are temporary, but permanent infertility may occur.
In secondary hypogonadism, the testicles are normal but don't function properly due to a problem with the pituitary or hypothalamus. A number of conditions can cause secondary hypogonadism, including:
Pituitary disorders. An abnormality in the pituitary gland can impair the release of hormones from the pituitary gland to the testicles, affecting normal testosterone production. A pituitary tumor or other type of brain tumor located near the pituitary gland may cause testosterone or other hormone deficiencies.
Later, hair will grow under the arms and in the beard area. And that first crack in the voice is a sign that the voice is changing and will get deeper. Some males get some breast growth (called gynecomastia). It usually goes away in 6 to 18 months.
Their body shape begins to change as their shoulders broaden and they gain weight and muscle. A growth spurt usually happens between ages 12 and 15. By age 16, most males have stopped growing, but their muscles will continue to develop.
For most females, the first physical change of puberty is breast development. It starts with small, firm, tender lumps (called buds) under one or both nipples. The breasts will get larger over the next year or two. Dark, coarse, curly hair will appear on the labia (the folds of skin surrounding the vagina). Later, more hair will grow in the pubic area and under the arms.
Just as those hormones change the way your body looks on the outside, they also change how you feel on the inside. While your body is adjusting to all the new hormones, so is your mind. During puberty, you might feel confused or have strong emotions that you've never had before. You may feel anxious about how your changing body looks. You might feel get upset or lose your temper more than usual.
Even though everyone goes through puberty, we all go through it a little differently. Some of your friends might have gotten curves, but you haven't yet. Maybe your best friend's voice has changed, and you think you still sound like a kid. But eventually everyone catches up, and the differences will even out.
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Precocious puberty is when children's bodies begin to change into adult bodies too soon. This change is known as puberty. Most of the time, puberty occurs after age 8 in girls and after age 9 in boys. However, Black, Hispanic, and Native American children might naturally reach puberty earlier. Precocious puberty is when puberty begins too early for the child who's going through it.
The cause of precocious puberty often can't be found. Rarely, certain conditions, such as infections, hormone issues, tumors, brain issues or injuries, may cause precocious puberty. Treatment for precocious puberty usually includes medicines to delay puberty.
To understand the causes of precocious puberty in some children, it's helpful to know what happens at puberty. The brain starts the process by making a hormone called gonadotropin-releasing hormone (GnRH).
When this hormone reaches the small, bean-shaped gland at the base of the brain, called the pituitary gland, it leads to more estrogen in the ovaries and more testosterone in the testicles. Estrogen makes female sex traits. Testosterone makes male sex traits.
With this type of precocious puberty, the hormone in the brain (GnRH) that typically causes puberty to start isn't involved. Instead, the cause is the release of estrogen or testosterone into the body. A problem with the ovaries, testicles, adrenal glands or pituitary gland causes the hormone release.
Testosterone is responsible for the development of primary sexual development, which includes testicular descent, spermatogenesis, enlargement of the penis and testes, and increasing libido. The testes usually begin the descent into the scrotum around 7 months of gestation, when the testes begin secreting reasonable quantities of testosterone. If a male child is born with undescended but normal testes that do not descend by 4 to 6 months of age, administration of testosterone can help the testes descend through the inguinal canals. [2]
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