Adolescence Syndrome Overview
Adolescence Syndromes (Puberty syndromes) are usually caused by problems with the glands that contain such hormones that are responsible for puberty.
Hormones cause puberty, the mechanism by which a child’s body transforms into an adult body. These issues may cause puberty to begin sooner or later than normal. Depending on the circumstances, the late or early onset of puberty does not necessitate medication. Puberty timing, on the other hand, is critical because it affects a child’s development and height, as well as emotional well-being.
Symptoms of adolescence syndrome may include;
- Symptoms of puberty syndrome include:
- Acne and body odor in girls under the age of eight and boys under the age of nine
- Breast growth in girls under the age of eight
- Changes in facial hair and voice in boys under the age of nine
- Growth spurt in girls under the age of eight or boys under the age of nine
- By the age of 13, there has been no growth of breasts.
- By the age of 15, there is no menstruation (period).
- By the age of 14, there is no testicle or penis development (child also may be shorter than other children of his age)
- Pubic or underarm hair in girls under the age of eight or boys under the age of nine
- Development of the testicles and penis in boys under the age of nine
Clinical Terms for Treatments Procedure
- Congenital(birth defect) adrenal hyperplasia
- The delayed puberty
- Genetic disorders that disrupt puberty, such as Turner syndrome, Klinefelter syndrome, and more
- The Kallmann syndrome
- The Mc Cune Albright syndrome
- The Precocious(early) puberty
We’ll discuss those medical terms after this summary part in this article.
- Hormone therapy
- Pubertal blockers
- Sometimes surgical treatment
The Precocious Puberty
When a child’s body starts to change into that of an adult (puberty) too soon, this is referred to as precocious puberty. Precocious puberty occurs when puberty starts before the age of eight in girls and before the age of nine in boys.
Puberty is characterized by rapid bone and muscle growth, changes in body shape and size, and the enhancement of the body’s capacity to reproduce.
The causes of precocious puberty are often unknown. In rare cases, precocious puberty may be caused by diseases, hormone disturbances, cancers, brain defects, or accidents. Medication to postpone further growth is often used in the treatment of precocious puberty.
Precocious puberty common symptoms include the appearance of the following well before age of eight in girls and before the age of nine in boys.
- Menstruation in girls
- Breast growth in girls
- Underarm and pubic hair
- Acne problem
- Body odor (adult)
- Fast growth
To understand the cause of precocious puberty in some kids, it’s important to understand what causes puberty to begin in the first place. The brain initiates the process by producing a hormone known as gonadotropin-releasing hormone (GnRH).
Once this hormone enters the pituitary gland, a small bean-shaped gland at the base of your brain, it causes more hormones to be produced in the ovaries for females (estrogen) and the testicles for males (testosterone).
Estrogen plays a role in the production of female sexual characteristics. Testosterone is in control of the production and growth of male sexual characteristics.
This phase starts earlier in certain children depending on whether they have central or peripheral precocious puberty.
Central Precocious Puberty
The cause of this form of precocious puberty is sometimes unknown.
The puberty process begins too soon in central precocious puberty. Otherwise, the pattern and sequence of the steps in the process are natural. There is no underlying medical disorder and no known cause of early puberty in the majority of kids with this disease.
Central precocious puberty can cause by some rare medical conditions. These may include;
- Brain tumor or spinal cord tumor
- Congenital brain defects
- Brain or spinal cord injury
- The Mc Cune Albright syndrome
- Congenital adrenal hyperplasia
Peripheral precocious puberty
This form of precocious puberty is caused by the presence of estrogen or testosterone in your child’s body.
Peripheral precocious puberty is less common and happens without the presence of the hormone in your brain (GnRH) that usually causes the start of puberty. The cause is instead the release of estrogen or testosterone into the body as a result of issues with the ovaries, testicles, adrenal glands, or pituitary gland.
Some existing medical condition may lead to peripheral precocious puberty such as;
- Adrenal gland or pituitary gland tumor
- The Mc Cune Albright syndrome
- Administration of external estrogen and progesterone
- An ovarian cyst(in girls)
- An ovarian tumor(in girls)
- Germ cell tumor(in boys)
- Gonadotropin independent familial sexual precocity
Complications of Precocious Puberty
Children with precocious puberty can develop quickly and be taller than their peers at first. However, since their bones mature faster than average, they often stop developing earlier than normal. As a result, they may be shorter than normal as adults. Early treatment of precocious puberty, especially in very young children, may help them grow taller than they would otherwise.
Girls and boys who reach puberty earlier than their peers can be highly self-conscious about the changes taking place in their bodies. This can have an effect on self-esteem and raise the likelihood of depression or drug abuse.
- Girls are much more likely than boys to experience precocious puberty.
- Precocious puberty tends to affect African-American children more often than other races.
- Children who are substantially overweight are more likely to have precocious puberty.
- Administration of estrogen or testosterone cream or ointment, or other hormone-containing substances (such as an adult’s prescription or dietary supplements), may increase your child’s risk of developing precocious puberty.
- Precocious puberty can be a complication of Mc Cune Albright syndrome or congenital adrenal hyperplasia, both of which involve irregular male hormone development (androgens). Precocious puberty can be associated with hypothyroidism in rare cases.
- Radiation therapy for cancers, leukemia, or other diseases may raise the risk of precocious puberty.
Some risk factors for precocious puberty, such as gender and ethnicity, are unavoidable. There are, however, measures you can do to minimize your child’s risk of experiencing precocious puberty, such as:
Keeping your child away from potential estrogen and testosterone sources, such as prescription drugs for adults in the home or nutritional supplements containing estrogen or testosterone.
Encourage your child to keep a healthy weight.
Congenital adrenal hyperplasia is a hereditary disease caused by gene mutations that code for enzymes involved in the production of steroid hormones in the adrenal glands. The most common enzyme malfunction, 21-hydroxylase deficiency, causes the adrenal glands to produce excessive quantities of male hormones.
Sign and Symptoms
During growth, a foetus with congenital adrenal hyperplasia will contain an excess of male hormones. If the foetus is female, the external genitalia may be virilized (they may seem more masculine), and the female baby may be born with ambiguous genitalia (from the appearance of the external genitalia it is unclear if the baby is male or female sex). Since both boys and girls with congenital adrenal hyperplasia have a cortisol deficit, they are likely to introduce to an adrenal crisis in the first few days or weeks of life unless treated with steroid replacement.
The healthy child turns off the release of sex steroid hormones during childhood. If the baby has untreated congenital adrenal hyperplasia, their adrenal glands may contain elevated amounts of male hormones such as testosterone. This would result in rapid progress in both boys and girls, as well as virilization (the acquisition of male characteristics) in girls. Adrenaline androgens can cause early or precocious puberty, with pubic hair development, body odor, and penis or clitoris enlargement at a younger age than would normally be anticipated. This can result in early bone fusion. As a result, both boys and girls with poorly regulated congenital adrenal hyperplasia will experience rapid growth in infancy and will be tall as a child but short as an adult.
If masculine hormones are not regulated in adulthood, a woman may become virilized, and both men and women may experience a variety of health issues, including infertility and an increased risk of developing obesity and hypertension as a result of excessive steroid use. Any people with mild types of congenital adrenal hyperplasia may be diagnosed later in life, either in childhood or in adulthood.
Congenital adrenal hyperplasia is caused by mutations in the gene that codes for one of several enzymes involved in the production of steroid hormones in the adrenal glands. The enzyme 21-hydroxylase, which is a central regulator in the synthesis of the stress hormone cortisol, is the most commonly affected. The enzyme defect in the adrenal may also affect the development of the hormone aldosterone, which is responsible for salt retention in the body, in approximately two-thirds of affected individuals.
Single mutations in the gene encoding 21-hydroxylase are extremely common, affecting 1 in every 50 people in the general population. Congenital adrenal hyperplasia, on the other hand, is a recessive disease, which means that you must inherit a mutation in the gene from both parents in order to acquire the condition. As a result, one in every 12,000 babies will be born with congenital adrenal hyperplasia.
In patients with congenital adrenal hyperplasia, the body detects a deficiency of cortisol and attempts to stimulate the adrenal glands to produce adequate levels. However, due to an enzyme deficiency, the adrenal glands are unable to generate cortisol and instead produce an excess of precursor steroids. These precursor steroids are mostly androgenic, which means they are similar to the male hormone testosterone. Male hormone imbalance results in the growth of male characteristics and precocious (early) puberty.
Patients with congenital adrenal hyperplasia are normally required to take steroid medication for the rest of their lives. Current therapies attempt to replicate natural biology as much as possible, but they are not without flaws. Most patients with congenital adrenal hyperplasia will attain a normal adult height but will be a little shorter than would have been expected if they did not have the condition if they are well treated during childhood. Fertility is limited in some patients, but there are more options for assisting patients in achieving fertility. In older girls with ambiguous genitalia, reconstruction genital surgery can be needed. Maintaining the proper steroid balance during adulthood is critical to avoiding the risks of osteoporosis, obesity, and hypertension.
Despite the fact that congenital adrenal hyperplasia is a lifelong disease, it can be very effectively managed with the correct balance of steroid treatment, and patients can live full and active lives.
Diagnosis and Treatment
Congenital adrenal hyperplasia is typically diagnosed around the time of birth, either by a newborn screening examination, which is performed in some countries but not in the UK, or by symptomatology. Congenital adrenal hyperplasia is often suspected in female infants born with ambiguous genitalia. If the baby has an adrenal crisis in the first few weeks of life, the diagnosis will be accelerated. Children with milder forms (particularly boys) are often diagnosed with signs of early puberty between the ages of two and four.
The treatment targets for congenital adrenal hyperplasia are to replace the defective steroid hormone cortisol as well as to normalize the excessive male hormone secretion. This is accomplished by administering steroid hormone therapy, usually in the form of hydrocortisone in childhood and a number of steroids in adulthood. The treatment’s aim is to optimize growth and development during childhood while also maintaining fertility and health in adulthood. Steroids are commonly administered to children in the form of tablets three times a day. Hydrocortisone is used in adults in conjunction with other longer-acting steroids such as prednisolone and dexamethasone. To achieve natural salt balance in patients lacking aldosterone development, fludrocortisone must be replaced.
The specific care given to each patient will differ based on the nature of their condition and the specific genetic disorder’>genetic mutation they have. Patients should consult their doctor if they have any questions about their prescription.
Delayed puberty occurs when a teen experiences these physical changes later than the normal age range. For females, this means no breast growth before the age of 13 and no menstrual cycles before the age of 16. For boys, this means no testicular enlargement by the age of 14.
Some teenagers are “late bloomers,” meaning they begin puberty later than other children their age. The most common cause of delayed puberty is becoming a late bloomer. It is not affected by a medical condition and normally does not need medication. Late bloomers will finally catch up to their peers and begin puberty on their own.
Kallmann Syndrome can also be the cause of other forms of delayed puberty. This disorder is characterized by a loss of smell as well as low levels of luteinizing and follicle-stimulating hormones.
Girls will not begin having periods because their uterus and vagina do not grow properly. They may either have an excess of a hormone called prolactin, or they may have a disorder known as polycystic ovary syndrome (PCOS).
Your teen’s wellbeing and medications will be discussed with your doctor. The doctor may also want to know if your child has noticed any puberty symptoms or if there is a family history of delayed puberty. Your child will undergo a physical examination as well as blood testing to determine hormone levels. The doctor will examine your child’s development by measuring his or her height and weight, as well as taking an X-ray of the hand to see if his or her bones are growing more slowly than normal. A doctor might be able to detect puberty symptoms that you or your teen have missed. Some teenagers need a brain scan (such as an MRI) to rule out pituitary gland issues. A sonogram may be needed for girls to determine if their uterus and ovaries are developing normally.
If your doctor does not detect a medical condition, your child is unlikely to need medication and will finally begin evolving on his or her own. Your doctor will continue to monitor your child’s development as he or she approaches puberty.
If your adolescent does have a medical issue, your doctor can refer you to a pediatric endocrinologist, who specializes in growth and puberty.
Doctors will also prescribe short-term hormone therapy to help teenagers begin growing. Girls are given estrogen pills or skin patches, while boys are given testosterone injections. If a teen is unable to produce normal quantities of estrogen or testosterone, they can need long-term hormone therapy.
When To Consult Doctor
Your child’s delayed puberty is unlikely to need medication. However, if you or your teen are worried, you should consult a doctor, particularly if your child began to grow but then abruptly stopped. If your child should be tested for medical conditions, your family doctor or pediatrician will advise you. Often, what teenagers need is hope that they can catch up to their peers.
Kallmann syndrome is characterized by sluggish or absent puberty as well as a poor sense of smell.
This condition is a type of hypogonadotropic hypogonadism, which is caused by a lack of output of certain hormones that regulate sexual development. These hormones are typically produced in the hypothalamus, a region of the brain. Males with hypogonadotropic hypogonadism also have a tiny penis (micropenis) and undescended testes (cryptorchidism). Most sufferers do not develop secondary sexual characteristics during puberty, such as facial healthy hair and voice differentiation in males, the start of menstrual periods (menstruation) and breast growth in girls, and a growth spurt in both genders. Most affected men and women are still unable to have children naturally until they receive care (infertile).
The sense of smell is either impaired (hyposmia) or entirely absent in Kallmann syndrome (anosmia). This separates Kallmann syndrome from the majority of other forms of hypogonadotropic hypogonadism, which do not impair the sense of smell. Many people with Kallmann syndrome are unaware that they are unable to detect odors before testing reveals the issue.
Supplemental signs and symptoms of Kallmann syndrome may occur. These include a failure to produce one kidney, bone anomalies in the fingers or toes, a cleft lip with or without an opening in the roof of the mouth, irregular eye movements, hearing loss, and tooth growth abnormalities. Some people with this condition have a condition known as bimanual synkinesis, in which the movements of one hand are mirrored by the movements of the other. Bimanual synkinesis can make it difficult to perform tasks that enable the hands to move independently, such as playing an instrument.
Kallmann syndrome has been linked to changes in over 20 genes. Mutations in the ANOS1, CHD7, FGF8, FGFR1, PROK2 or PROKR2 genes are among the most common causes of the disease. Affected individuals may have mutations in more than one of these genes. Researchers have also discovered mutations in other genes that may lead to the development and symptoms of Kallmann syndrome but are unlikely to trigger the disease on their own.
The genes linked to Kallmann syndrome are involved in the formation of specific areas of the brain before birth. While some of their basic roles are unknown, these genes tend to be involved in the development and movement (migration) of a group of nerve cells specialized in processing the sense of smell (olfactory neurons). These nerve cells originate in the developing nose and then migrate together to the olfactory bulb, a structure in the front of the brain essential for odor perception. According to research, the genes linked to Kallmann syndrome are also involved in the migration of neurons that contain a hormone known as gonadotropin-releasing hormone (GnRH). GnRH-producing neurons, including olfactory neurons, move from the developing nose to the front of the brain. GnRH regulates the production of many hormones that influence sexual development before and during puberty. These hormones are essential for the proper functioning of the ovaries in women and the testes in men.
Mutations in genes linked to Kallmann syndrome appear to interrupt the movement of olfactory nerve cells and GnRH-producing nerve cells in the developing brain. A person’s sense of smell will be diminished or absent if olfactory nerve cells do not extend to the olfactory bulb. Misplacement of GnRH-producing neurons in the brain inhibits the formation of other sex hormones, interfering with normal sexual growth and causing hypogonadotropic hypogonadism. It is unknown how gene mutations cause the other signs and symptoms of Kallmann syndrome. Since the symptoms of this disorder differ from person to person, additional genetic and environmental factors are likely to play a role in its development.
Mutations in identified genes account for approximately 30% of all Kallmann syndrome cases. The cause of the disorder is unclear in cases where there is no mutation in one of the established genes. Researchers are on the lookout for additional genetic changes that may be causing this disease.
McCune Albright syndrome
McCune-Albright syndrome is a bone, skin, and hormone-producing (endocrine) tissue condition.
Polyostotic fibrous dysplasia is a disorder in which people with McCune-Albright syndrome develop areas of irregular scar-like (fibrous) tissue in their bones. Polyostotic means that irregular areas (lesions) can occur in several bones; however, they are often limited to one side of the body. Fractures, uneven development, and deformity can result from the replacement of bone with fibrous tissue. As lesions develop in the bones of the skull and jaw, they can cause irregular (asymmetric) facial development. Long bone asymmetry can also occur; irregular development of leg bones can cause limping. Abnormal spine curvature is also possible. Bone lesions may become cancerous, but this occurs in less than 1% of McCune-Albright syndrome patients.
Aside from bone defects, affected people typically have light brown patches of skin known as café-au-lait spots, which may be present from birth. The irregular boundaries of McCune-Albright syndrome’s café-au-lait spots are often compared to a map of Maine’s coast. Café-au-lait spots in other disorders, on the other hand, have smooth boundaries that are compared to the California coast. The café-au-lait spots in McCune-Albright syndrome, like bone lesions, can occur on only one side of the body.
Girls with McCune-Albright syndrome can experience puberty at a young age. By the age of two, these girls frequently have menstrual bleeding. Excess estrogen, a female sex hormone, released by cysts that form in one of the ovaries, is thought to be the cause of this early onset of menstruation. Boys with McCune-Albright syndrome can experience early puberty in a minority of cases.
People with McCune-Albright syndrome may also experience other endocrine issues. The thyroid gland, a butterfly-shaped organ located at the base of the neck, may swell (a condition known as goiter) or grow masses known as nodules. Around half of those affected produce too much thyroid hormone (hyperthyroidism), which causes a rapid heart rate, high blood pressure, weight loss, tremors, sweating, and other symptoms. The pituitary gland (a structure at the base of the brain that produces a variety of hormones) can produce excessive amounts of growth hormone. Excess growth hormone may cause acromegaly, a disorder marked by large hands and feet, arthritis, and distinct facial features that are often defined as “coarse.” Excess growth hormone secretion may also result in increased fibrous dysplasia in the bones, most notably in the skull. Cushing syndrome, characterized by an excess of the hormone cortisol released by the adrenal glands, which are small glands located on top of each kidney, occurs in a small number of affected individuals. Cushing syndrome is characterized by weight gain in the face and upper body, delayed development in infants, frail skin, weakness, and other health issues. Cushing syndrome exists only in people with McCune-Albright syndrome before the age of two.
McCune-Albright syndrome may also cause problems in other organs and structures, such as noncancerous (benign) gastrointestinal growths called polyps and other anomalies.
A mutation in the GNAS gene causes McCune-Albright syndrome. The GNAS gene codes for one component of a protein complex known as a guanine nucleotide-binding protein, or G protein.
G proteins, through a process known as signal transduction, activate a complex network of signaling pathways that ultimately affect many cell functions by regulating hormone activity. The protein formed by the GNAS gene aids in the activation of an enzyme known as adenylate cyclase. McCune-Albright syndrome is caused by GNAS gene mutations that produce a G protein that causes the adenylate cyclase enzyme to be continuously triggered (constitutively activated). Constitutive activation of the adenylate cyclase enzyme results in the overproduction of many hormones, resulting in irregular bone growth and other McCune-Albright syndrome signs and symptoms.
Adolescence Syndrome Summary
Adolescence Syndrome is a term that describes irregular adolescent interactions caused by sensitivity and dysfunction.
Support your child in this situation. This is the best thing you can do in this condition.