Hyperpituitarism

Introduction
Background
Hyperpituitarism, or primary hypersecretion of pituitary hormones,
is rare in children. It typically results from a pituitary microadenoma.
The most frequently encountered adenoma in children is the
prolactinoma, followed by corticotropinoma and somatotropinoma.
Fewer than 20 cases of thyrotropinoma in children have been
reported, all with onset after age 11 years. Pediatric
gonadotropinoma has not been reported.
Hypersecretion of pituitary hormones secondary to macroadenomas
can interfere with other pituitary hormone functions, resulting in
target organ hormone deficiencies (hypogonadism, hypoadrenalism,
hypothyroidism). In some cases, long-standing hormonal
hypersecretion is accompanied by sufficient hyperplasia of the
pituitary to produce sellar enlargement.
Elevated pituitary hormone levels that result from primary endocrine
organ deficiency (eg, high circulating thyroid-stimulating hormone
[TSH] levels in primary hypothyroidism due to Hashimoto thyroiditis)
quickly suppress to reference range values upon replacement of the
active hormone. Most rarely, ectopic tumors can secrete pituitary
hormones. This article focuses on the endocrine manifestations of
pituitary adenomas in children.

Pathophysiology
Hypothalamic dysfunction clearly may promote tumor growth, but
overwhelming evidence indicates intrinsic pituicyte genetic
disruption leads to pituitary tumorigenesis. The monoclonal nature
of most pituitary adenomas, confirmed by X-inactivation studies,
implies their usual origin from a clonal event in a single cell. Most
pituitary adenomas are functional and secrete a hormone that
produces a characteristic clinical presentation. Nonfunctioning
pituitary adenomas are rare in children, accounting for only 3-6% of
all adenomas in 2 large series, whereas they comprise 30% of
adenomas in adults. In children, disruption of growth regulation
and/or sexual maturation is common, either because of hormone
hypersecretion or because of manifestations caused by local
compression by the tumor.
Prolactinoma

Overall, prolactinoma is the most common pituitary adenoma

encountered in childhood. Most pediatric cases occur in
adolescence, more commonly in females than males. Boys tend to
have larger tumors and higher serum prolactin (PRL) levels than
girls. Females with these tumors present with amenorrhea, and
males present with gynecomastia and hypogonadism. Prolactinomas
arise from acidophilic cells that are derived from the same lineage
as the somatotropes and thyrotropes. Hence, PRL-secreting
adenomas may also stain for and secrete growth hormone (GH) and,
occasionally, TSH.
Corticotropinoma (Cushing disease)
In children, corticotropinomas are the most common adenomas
observed before puberty, although they occur in people of all ages.
They increase in frequency in pubescent and postpubescent
children, with a female preponderance. First described by Harvey
Cushing in the early 1900s, Cushing disease specifically refers to an
adrenocorticotropic hormone (ACTH)producing pituitary adenoma
that stimulates excess cortisol secretion. Adenomas that cause
Cushing disease are significantly smaller than all other types of
adenomas at presentation. Children have clinical courses somewhat
different from adults. They most commonly present with weight gain
(usually not centripetal) and growth failure. As in adults, most
patients display an absence of the physiologic diurnal rhythm of
plasma cortisol and ACTH with increased urinary excretion of free
cortisol and 17-hydroxycorticosteroids (17-OHCS).
Somatotropinoma (gigantism)
GH-secreting adenomas are rare in childhood. Gigantism refers to
GH excess in childhood when open epiphysial plates allow for
excessive longitudinal growth. Most cases of gigantism result from
GH-secreting pituitary adenomas or hyperplasia. Although gigantism
typically occurs as an isolated disorder, it occasionally represents
one feature of other conditions (eg, multiple endocrine neoplasia
[MEN] type 1, McCune-Albright syndrome [MAS], neurofibromatosis,
tuberous sclerosis, Carney complex).
Mammosomatotrophs are the most common type of GH-secreting
cells in childhood gigantism; hence, GH-secreting adenomas often
stain for and secrete PRL (67% in one study). GH-secreting tumors in
pediatric patients are more likely to be locally invasive or aggressive
than those in adult patients. Activating mutations of the stimulatory
Gs alpha (Gsa) protein have been identified in the somatotrophs of
pituitary lesions in MAS and in as many as 40% of sporadic GHsecreting pituitary adenomas.
Thyrotropinoma

Very few cases of thyrotropinoma have been reported in children.

These adenomas may secrete excess PRL, GH, and alpha subunit in
addition to TSH. They are usually large because of their aggressive
features and because their diagnosis is often delayed. The clinical
presentation consists of signs and symptoms of hyperthyroidism,
visual symptoms, and headaches. Biochemical features include the
elevation of circulating free thyroxine (T4) and total triiodothyronine
(T3) levels but inappropriately unsuppressed TSH.

Frequency
United States
Although less common in children than in adults, pituitary adenomas
constitute 2.7% of supratentorial tumors in children and 3.6-6% of
all pituitary adenomas that are surgically treated. The average
annual incidence of pituitary adenomas presenting before age 20
years is estimated to be less than 0.1 per million children.

Mortality/Morbidity
Transsphenoidal pituitary surgery has emerged as the treatment of
choice for ACTH-secreting and GH-secreting adenomas.
Transsphenoidal surgery is indicated for prolactinomas that do not
respond to medical therapy. Transsphenoidal surgery is associated
with remarkably little morbidity and near zero mortality. A
permanent loss of pituitary function occurs infrequently. The
incidence of postoperative hypopituitarism is about 3% in patients
with microadenomas and slightly increases with the invasiveness of
the tumor.

Race
Race and ethnicity have not been reported as significant
contributing factors to hyperpituitarism.

Sex

In prolactinoma, the female-to-male ratio is 4.5:1.

In ACTH-releasing adenoma, the female-to-male ratio is 2:1.
In GH-releasing adenoma, the female-to-male ratio is 1:2.

Age

In children, ACTH-releasing adenomas are most prevalent in

the youngest group and decrease in frequency with advancing
age.
The incidence of prolactinomas increases with age; 93% occur
in children older than 12 years.

GH-releasing tumors have a fairly even distribution among the

various age groups.

Clinical
History
The clinical presentation of a pituitary adenoma primarily results
from the oversecreted hormone. The tumor mass itself may cause
headaches, visual changes due to optic nerve compression, or
hypopituitarism.

Excess prolactin
o The presentation of prolactinomas may vary, depending
on the age and sex of the child.
o Prepubertal children typically present with a
combination of headache, visual disturbance, and
growth failure.
o Pubertal females frequently present with symptoms of
pubertal arrest or hypogonadism (with or without
galactorrhea) due to suppression of gonadotropin
secretion or local compression of the pituitary.
o Pubertal males may present with headaches, visual
impairment, and pubertal arrest or growth failure.
Excess adrenocorticotropic hormone
o The most sensitive indicator of excess glucocorticoid
secretion in children is weight gain with concurrent
growth failure, which generally precedes other
manifestations.
o Patients commonly present with weight gain that tends
to be generalized rather than centripetal.
o Hirsutism and premature adrenarche may occur in
prepubertal children.
o Pubertal arrest, acne, fatigue, and depression are also
common.
o Snoring, poor sleep quality, deteriorating academic
performance (compared with prior school terms), or
other signs of obstructive sleep apnea (OSA) should
prompt a formal sleep study and consultation with a
pulmonologist.
Excess growth hormone
o The presentation of gigantism in a child is usually
dramatic, unlike the insidious onset of acromegaly in
adults.
o The cardinal clinical feature of gigantism is longitudinal
growth acceleration secondary to GH excess.
o Presentation depends on whether the epiphyseal growth
plate is open. Before epiphyseal fusion, accelerated
growth velocity is prominent. As epiphyseal fusion

approaches, the spectrum of symptoms resembles the

presentation in adults (eg, coarsening of facial features,
change in ring and shoe size).

Physical

Prolactinoma
o Hypogonadism, leading to pubertal arrest, pubertal
failure, or pubertal delay
o Menstrual abnormalities, including primary or secondary
amenorrhea
o Galactorrhea
o Short stature
o Gynecomastia
Cushing disease
o Cushingoid appearance, including a dorsal cervical fat
pad, moon facies, bruising, and striae. These features
are only observed in patients with advanced longstanding disease.
o Growth failure and short stature may be observed.
o Weight gain and obesity in children with Cushing
disease tends to be generalized rather than centripetal.
o Pubertal arrest, failure, or delay may occur.
o Amenorrhea may be noted.
o Hypertension may be present.
Gigantism: All growth parameters are affected, although not
necessarily symmetrically. GH excess over time is
characterized by progressive cosmetic disfigurement and
systemic organ manifestations.
o Tall stature
o Mild-to-moderate obesity (common)
o Macrocephaly, which may precede linear growth
o Exaggerated growth of the hands and feet with thick
fingers and toes
o Coarse facial features, including frontal bossing and
prognathism
o Hyperhidrosis
o Menstrual irregularities
o Peripheral neuropathies (eg, carpal tunnel syndrome)
o Cardiovascular disease: Prolonged GH excess can result
in cardiac hypertrophy, hypertension, and left
ventricular hypertrophy.
o Tumors: Although benign tumors, including uterine
myomas, prostatic hypertrophy, colon polyps, and skin
tags, may be frequently encountered in acromegaly, the
documentation of the overall prevalence of malignancies
in patients with acromegaly remains controversial.
o Endocrinopathies: Frequently associated
endocrinopathies include hypogonadism, diabetes,

decreased glucose tolerance, and

hyperprolactinemia. OSA has been reported in up to half
of patients with acromegaly, particularly those who are
obese or older than 50 years.

Causes
Hypothalamic dysfunction can promote tumor growth, but
overwhelming evidence points to intrinsic pituicyte genetic
disruption as the main underlying cause of pituitary tumorigenesis.
The monoclonal nature of most pituitary adenomas, confirmed with
X-inactivation studies, implies their origin from a clonal event in a
single cell. Most pituitary adenomas are functional, and clinical
presentation typically depends on the particular pituitary hormone
that is hypersecreted. Nonfunctioning pituitary adenomas are rare in
children, accounting for only 3-6% of all adenomas in 2 large series;
they comprise 30% of adenomas in adults.
Diabetes Insipidus
What is diabetes insipidus? Diabetes insipidus is a condition that
results from insufficient production of the antidiuretic hormone
(ADH), a hormone that helps the kidneys, and body, conserve the
correct amount of water. Diabetes insipidus may also occur when
the kidneys do not respond properly to normal levels of ADH. The
disease is actually categorized into two groups:

central diabetes insipidus - insufficient production or secretion

of ADH; usually a result of a problem in the brain or central
nervous system.
nephrogenic diabetes insipidus - lack of kidney response to
normal levels of ADH.

Normally, the antidiuretic hormone controls the kidneys' output of

urine. It is secreted by the pituitary gland to decrease the amount of
urine output so that dehydration does not occur. Diabetes insipidus,
however, causes excessive thirst and excessive production of very

diluted urine.
What causes diabetes insipidus? Diabetes
insipidus can be caused by several conditions, including the
following:

malfunctioning hypothalamus (that produces too little ADH)

malfunctioning pituitary gland (that fails to release ADH into
the bloodstream)
damage to hypothalamus or pituitary gland during surgery

brain injury
tumor
tuberculosis
blockage in the arteries leading to the brain
encephalitis - inflammation of the brain.
meningitis - inflammation of the meninges, the membranes
that cover the brain and spinal cord.
sarcoidosis - a rare inflammation of the lymph nodes and
other tissues throughout the body.
family heredity

What are the symptoms of diabetes insipidus?

The
following are the most common symptoms of diabetes insipidus.
However, each child may experience symptoms differently.

Symptoms may include:

excessive thirst
excessive urine production
dehydration
Infants with diabetes insipidus may also exhibit the following
symptoms:
irritability
poor feeding
failure to grow
high fevers
The symptoms of diabetes insipidus may resemble other problems
or medical conditions. Always consult your child's physician for a

diagnosis.
How is diabetes insipidus diagnosed?
In
addition to a complete medical history and physical examination,
including the child's daily fluid intake, dietary intake, and voiding
(bowel and bladder elimination) patterns, diagnostic procedures for
diabetes insipidus may include:
urine tests
blood tests
water deprivation test (to observe if dehydration occurs)
magnetic resonance imaging (MRI) - a diagnostic procedure
that uses a combination of large magnets, radiofrequencies,
and a computer to produce detailed images of organs and
structures within the body; to check for pituitary
abnormalities.

Treatment of diabetes insipidus:

If left untreated in children,
diabetes insipidus can lead to brain damage, impaired mental
function, mental retardation, hyperactivity, short attention span,
and/or restlessness. Treatment for diabetes insipidus depends on
what is causing the disease. Treating the cause usually treats the
diabetes insipidus. Specific treatment for diabetes insipidus will be

determined by your child's physician based on:

your child's age, overall health, and medical history
extent of the disease
your child's tolerance for specific medications, procedures, or
therapies
expectations for the course of the disease
your opinion or preference
Treatment may include modified antidiuretic hormone medications
(often taken as a nasal spray), or medications that stimulate the
production of the antidiuretic hormone. In addition, persons with
diabetes insipidus must maintain adequate fluid intake to
compensate for the excessive urinary output, and eat a low-sodium
diet. Although children with the
disease also need to drink
plenty of fluids, care should be taken to monitor sodium intake in
their fluids. Long-term outlook for children with diabetes insipidus.
Diabetes insipidus can be a temporary or a permanent condition,
depending on what is causing the disease. Children with central
diabetes insipidus, with proper management, can lead full, healthy
lives. Children with nephrogenic diabetes insipidus can also lead
relatively normal lives with proper medical care and management,
especially if the medical care is started early.
Precocious
Puberty

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Precocious puberty is onset of sexual maturation before age 8 in

girls or age 9 in boys. Diagnosis is by comparison with
population standards, x-ray of the left hand and wrist to assess
skeletal maturation and check for accelerated bone growth, and
measurement of serum levels of gonadotropins and gonadal and
adrenal steroids. Treatment depends on the cause.
The definition of precocious puberty depends on reliable
population standards for onset of puberty (ie, when pubertal
milestones occur); because onset seems to be occurring earlier
in the US, these standards are being reevaluated. Almost 8 to
10% of white girls, almost 30% of black girls, and an
intermediate percentage of Hispanic girls reach early puberty at
age 8. The lower limit of normal puberty may be 7 yr for white
girls and 6 yr for black girls. The mean age for early breast
development is about 10 yr for white girls and 9 yr for black girls
(range 8 to 13 yr). The mean age for pubic hair growth is 9 to
10.5 yr for both groups. These findings imply that guidelines for
evaluating disorders that cause precocious puberty can be
interpreted more leniently if children are otherwise healthy and
are not at risk of not reaching their full adult height potential.
In girls, the first pubertal milestone is typically breast
development (thelarche), followed soon after by appearance of
pubic hair (pubarche) and axillary hair and later by the first
menstrual period (menarche). In boys, the first pubertal
milestone is typically testicular growth, followed by penile
growth and appearance of pubic and axillary hair. In both sexes,
appearance of pubic and axillary hair is called adrenarche.

Precocious puberty can be divided into 2 types:

Gonadotropin-releasing hormone (GnRH)dependent

GnRH-independent

GnRH-dependent precocious puberty is 5 to 10 times more

frequent in girls; in boys, GnRH-dependent and GnRHindependent precocious puberty occur with similar frequency. In
GnRH-dependent precocious puberty, the hypothalamic-pituitary
axis is activated, resulting in enlargement and maturation of the
gonads, development of secondary sexual characteristics, and
oogenesis or spermatogenesis. In GnRH-independent precocious
puberty, secondary sexual characteristics result from high
circulating levels of estrogens or androgens, without activation
of the hypothalamic-pituitary axis.
Precocious puberty may also be classified by whether
gonadarche or adrenarche occurs. In girls, gonadarche includes
breast development, change in body habitus, growth of the
uterus, and eventually menarche. In boys, gonadarche includes
testicular enlargement; phallic growth; the initial appearance of
pubic, facial, and axillary hair; adult body odor; and facial skin
oiliness or acne. Adrenarche for both girls and boys involves the
development of body hair, body odor, and acne.
Premature appearance of only one specific pubertal milestone is
generally considered a benign variant of development.
Examples are precocious appearance of pubic and axillary hair
before age 8 in girls and age 9 in boys, and precocious onset of
breast development before age 8 in girls.
Etiology
GnRH-dependent precocious puberty: In most affected girls 4
yr, a specific cause cannot be identified. However, many girls <
4 yr have a CNS lesion. Most (60%) affected boys have an
identifiable underlying lesion. Such lesions include intracranial
tumors, especially of the hypothalamus (hamartoma, rarely
craniopharyngioma) or pineal gland region (teratoma,
pinealoma). Neurofibromatosis and a few other rare disorders
have also been linked to precocious puberty.
GnRH-independent precocious puberty: Follicular ovarian cysts
cause most cases; other causes include granulosa-theca cell
tumors, adrenal enzyme defects, and McCune-Albright
syndrome (a triad of follicular cysts, polyostotic fibrous
dysplasia, and caf-au-lait spots). Causes of GnRH-independent
precocious puberty in boys include certain enzyme defects,

familial male gonadotropin-independent precocity (due to an

activating mutation of the gene for luteinizing hormone [LH]
receptors), testosterone-producing testicular tumors, and
occasionally McCune-Albright syndrome.
Rarely in girls and boys, puberty results from pituitary
adenomas (hamartomas) that secrete gonadotropins.
Symptoms and Signs
In girls, breasts develop, and pubic hair, axillary hair, or both
appear. Girls may begin to menstruate. In boys, facial, axillary,
and pubic hair appears and the penis grows, with or without
enlargement of testes. Body odor, acne, and behavior changes
may develop in either sex. Height gain is initially rapid in both
sexes, but premature closure of the epiphyses results in short
adult stature. Ovarian or testicular enlargement occurs in
precocious puberty but is usually absent in isolated precocious
adrenarche.
Diagnosis

Bone age x-rays

Serum hormone measurement
Possibly pelvic ultrasound and brain MRI or CT

Diagnosis is clinical. X-rays of the left hand and wrist are done to
check for accelerated skeletal maturation as a result of sex
hormone effect. Unless history and examination suggest an
abnormality, no further evaluation is required for children with
pubertal milestones that are within 1 yr of population standards
or for girls and boys with precocious adrenarche and girls with
precocious thelarche, as long as x-rays confirm that skeletal
maturation is not accelerated.
When further evaluation is necessary, the following serum
hormones may be measured: -human chorionic gonadotropin,
estradiol Some Trade Names
ESTRADERM
ESTROGEL
VIVELLE
Click for Drug Monograph
, testosterone, dehydroepiandrosterone, 17hydroxyprogesterone, LH, follicle-stimulating hormone (FSH),
and prolactin. Pelvic and adrenal ultrasonography and MRI or CT
of the brain may be done.
A GnRH stimulation test (see Endocrine Disorders in Children:

Diagnosis) confirms a diagnosis of GnRH-independent

precocious puberty when gonadotropin responses to exogenous
GnRH are prepubertal in boys or girls with no tumor or other
obvious cause of early sexual development. If the response is
pubertal, CNS lesions must be excluded.
Treatment

GnRH agonist therapy (GnRH-dependant precocious

puberty)
Androgen or estrogen antagonist therapy (GnRHindependent precocious puberty)
Tumor excision as needed

If pubertal milestones are within 1 yr of population standards,

reassurance and regular reexamination are sufficient. Treatment
is not needed for premature adrenarche or thelarche, but
regular reexamination is warranted to check for later
development of precocious puberty. For GnRH-dependent
precocious puberty, pituitary LH and FSH secretion can be
suppressed until normal puberty begins with the GnRH agonist
leuprolide Some Trade Names
LUPRON
Click for Drug Monograph
acetate 0.2 to 0.3 mg/kg (minimum, 7.5 mg) IM q 4 wk.
Responses to treatment must be monitored, and drug dosages
modified accordingly.
In girls with McCune-Albright syndrome, testolactone Some
Trade Names
TESLAC
Click for Drug Monograph
, an aromatase inhibitor, reduces serum estradiol Some Trade
Names
ESTRADERM
ESTROGEL
VIVELLE
Click for Drug Monograph
and effectively treats affected girls; alternatively, tamoxifen
Some Trade Names
NOLVADEX
Click for Drug Monograph
, an estrogen antagonist, may be beneficial.
If GnRH-independent precocious puberty in boys is due to
familial male gonadotropin-independent precocity or McCuneAlbright syndrome, androgen antagonists (eg, spironolactone
Some Trade Names

ALDACTONE
Click for Drug Monograph
) ameliorate the effects of excess androgen. The antifungal drug
ketoconazole Some Trade Names
NIZORAL
Click for Drug Monograph
reduces testosterone in boys with familial male gonadotropinindependent precocity.
If GnRH-independent precocious puberty is due to a hormoneproducing tumor (eg, granulosa-theca cell tumors in girls,
testicular tumors in boys), such tumor should be excised.
However, girls require extended follow-up to check for
recurrence in the contralateral ovary
Hyperthyroidism
INTRODUCTION The clinical manifestations of hyperthyroidism in
children and adolescents are similar to those seen in adults. In
addition, the disorder has unique effects on growth and
development. The clinical features of hyperthyroidism are largely
independent of the cause. Although there are several potential
causes of hyperthyroidism in children, Graves' disease is by far the
most common etiology.
Graves' disease causes unique problems that are not related to the
high serum thyroid hormone concentrations. They include Graves'
ophthalmopathy and infiltrative dermopathy (localized or pretibial
myxedema). Graves' ophthalmopathy is common in children, but
less severe than in adults; dermopathy is almost never found in
children. Most patients with Graves' hyperthyroidism have a diffuse
goiter, but so do patients with other, less common causes of
hyperthyroidism, such as "Hashitoxicosis" (silent or painless
thyroiditis), subacute thyroiditis, or forms of non-autoimmune
hyperthyroidism (discussed below).
The clinical presentation and evaluation of children with
hyperthyroidism and thyrotoxicosis are discussed here. Treatment of
hyperthyroidism is discussed separately. Hyperthyroidism presenting
during the neonatal period is discussed separately. (See "Treatment
and prognosis of Graves' disease in children and adolescents" and
see "Evaluation and management of neonatal Graves' disease").
INCIDENCE Graves' hyperthyroidism occurs in approximately 0.02
percent (1:5000) of children, mostly in the 11- to 15-year age group
[1]. Girls are affected more commonly than boys, at a ratio of about

5:1. The ratio is considerably lower among younger children,

suggesting that estrogen secretion in some way affects the
occurrence of Graves' disease.
PATHOGENESIS The proximate cause of Graves' hyperthyroidism
in children and adolescents, as in adults, is thyrotropin (TSH)
receptor-stimulating antibodies (TRS-Ab), which activate the TSH
receptor. A population-based study of Danish twins suggested that
approximately 80 percent of the risk of Graves' disease is
attributable to genetic factors [2]. Graves' ophthalmopathy may
result from antibodies against a TSH receptor-like protein in
retroorbital connective tissue

Hashimoto's thyroiditis
The most common cause of hypothyroidism in children and
adolescents is Hashimoto's thyroiditis, an autoimmune disease.
Here, the body's own immune system attacks the thyroid gland and
interferes with the production of thyroid hormones. The onset of this
condition can occur at any age, and the diagnosis may be easily
overlooked for years, as the symptoms of hypothyroidism develop
very slowly. As the thyroid gland becomes increasingly underactive,
physical and mental changes will become more obvious.
Often the first sign is that the child's growth rate decreases
unexpectedly and skeletal development is delayed. The child may
also have an obvious swelling of the neck (goitre), as the thyroid
gland becomes inflamed. Other symptoms may emerge, such as
unusual tiredness or lethargy, dry itchy skin, increased sensitivity to
cold, weight gain or generalised swelling, poor concentration,
decreased energy, and constipation.
If hypothyroidism is suspected, a simple blood test is taken,
measuring the levels of thyroid hormone and thyroid stimulating
hormone (TSH), in the blood. The presence of thyroid antibodies
(anti-thyroperoxidase and anti-thyroglobulin) is also helpful in
confirming the diagnosis.
Treatment
The treatment for Hashimoto's thyroiditis in children and
adolescents is the same as in adults. Thyroid hormone replacement
is taken daily for life. The dosage of thyroid hormone needs to be
age-appropriate, as the body's demands for thyroid hormone vary
with age. Regular thyroid function tests will need to be assessed by
a doctor to ensure that normal hormone levels are maintained.
Side effects
For those children and adolescents being treated for
hypothyroidism, the results are mainly positive. The majority of their

symptoms will disappear, and the body's time for 'catch-up' growth
will begin. An increase in bone development will also occur.
However, in children who have had long-standing hypothyroidism,
ultimate height potential may be partly lost. As the child regains
normal thyroid function, behavioural problems may arise as their
physical and mental processes speed up. An increase in energy and
alertness may lead to a decreased attention span and a loss of
concentration, especially in school. Teachers should be made aware
of the child's condition, as well as treatment and possible changes in
behaviour. Over time, any problems with behaviour, or at school, will
resolve.

Graves' disease
The most common cause of hyperthyroidism in children and
adolescents is an autoimmune condition called Graves' disease. In
Graves' disease the body produces antibodies that stimulate the
thyroid gland uncontrollably, to make too much thyroid hormone.
Children can have similar symptoms to adults, although they are
less likely to complain about them. Initially the most prominent sign
of this condition may be that the child displays increased energy.
They may appear hyperactive and restless, be noisier in class, and
easily distracted. This may lead to poor academic performance, and
parent frustration. A child's hyperthyroidism may not be diagnosed
until more pronounced signs and symptoms appear. These include
an enlarged thyroid gland. Other symptoms include a fast pulse,
nervousness, heat intolerance, weight loss, accelerated growth rate,
shaky hands, muscle weakness, diarrhoea, and sleep and
behavioural disturbances. Thyroid eye disease is very rare in young
children.
Once a thyroid disorder is suspected, a simple blood test is
performed to measure the levels of thyroid hormones and thyroid
stimulating hormone (TSH) in the blood. The presence of thyroidstimulating antibodies may also be helpful in confirming the
diagnosis. If test results come back positive, then appropriate
treatment is commenced immediately.
Treatment
Treatment of hyperthyroidism in children initially involves the use of
antithyroid drugs, such as propylthiouracil (PTU) or carbimazole, and
if well tolerated, these may be continued for months or even years.
For some children, these drugs alone stabilise their condition, and
no further treatment is needed. For some, a period of 'block and
replace therapy' (antithyroid drugs as well as thyroxine) is useful.
For others, surgery or even radioactive iodine may be necessary,
depending on the severity of their thyroid disorder, or their response
to antithyroid drugs. Throughout a child's treatment, thyroid

hormone levels will need to be monitored regularly, along with their

clinical symptoms.
Side effects
In children and adolescents with Graves' disease, the main
difficulties usually occur before treatment is initiated. Once their
condition is under control, their physical and mental capabilities
return to normal. Antithyroid drugs can, however, occasionally stop
the production of white blood cells or platelets. Sore throats, mouth
ulcers, excessive bruising or skin rashes can indicate this. Patients
should stop taking their medication and see their doctor
immediately or attend the casualty department at their local
hospital to test whether their blood cells or platelets are normal. Of
course, these symptoms are common and it is most likely that they
are not due to the antithyroid drugs. However, the only safe action
is to stop the medication until after the result of the blood test.

Parent involvement
Parent involvement is vital for children and adolescents receiving
treatment for their thyroid disorder. They will need to supervise the
taking of medication on a daily basis, and carefully monitor their
child's progress. They will also need to be aware of the signs and
symptoms of under- or over-medicating, so they can work with their
doctor to obtain the right level of medication.
As children grow, it is important for parents to keep close track of
their child's thyroid hormone levels, as periodic changes in dosage
will occur with changes in age. Doctors often recommend that a
child have blood tests at least every 3 to 6 months. Some children
may have a tendency to neglect their medication regimen, and this
may lead to symptoms reappearing.
Thyroid disorders can run in families, so it is important to let your
doctor know of your family background. If close family members
have either hypothyroidism or hyperthyroidism, then it would be
wise to keep a close eye on children in the family. Girls tend to be
especially prone to developing thyroid problems, due to hormonal
changes throughout their life.
In summary, the signs and symptoms of thyroid disease are similar
in children, adolescents, and adults. However, there are a few key
differences that relate to growth, development and behaviour. If
children are treated early and appropriately, with regular
monitoring, they will grow and develop normally, and enjoy life as a
child.

Hyperparathyroidism

What is hyperparathyroidism? Hyperparathyroidism is caused by

overactive parathyroid glands. Overactive parathyroid glands
produce high levels of parathyroid hormones, which, in turn, results
in increased levels of calcium in the blood stream. The excess
calcium released by the bones leads to osteoporosis and
osteomalacia (both bone-weakening diseases). Another result of
hyperparathyroidism is kidney stones, because of high levels of
calcium excreted into the urine by the kidneys. Hyperparathyroidism
is quit rare in children. What causes hyperparathyroidism? Causes of
hyperparathyroidism include benign (non-cancerous) tumors on the
parathyroid glands or enlargement of the parathyroid glands. What
are symptoms of hyperparathyroidism? According to a recent study,
children with hyperparathyroidism experience more severe
symptoms than adults. The following are the most common
symptoms of hyperparathyroidism in children. However, each child
may experience symptoms differently. Symptoms may include:
kidney pain (due to the presence of kidney stones)
diminished bone density that causes bone pain
aches and pains
abdominal pain
nausea
vomiting
fatigue
excessive urination
confusion
muscle weakness
The symptoms of hyperparathyroidism may resemble other
conditions or medical problems. Always consult your child's

physician for a diagnosis.

How is hyperparathyroidism
diagnosed? In addition to a complete medical history and physical
examination, diagnostic procedures for hyperparathyroidism may
include:
bone x-rays - a diagnostic test which uses invisible
electromagnetic energy beams to produce images of internal
tissues, bones, and organs onto film.
laboratory tests (to measure calcium and parathyroid
hormone levels)
Treatment for hyperparathyroidism: Specific treatment for
hyperparathyroidism will be determined by your child's physician

based on:
your child's age, overall health, and medical history

extent of the disease

your child's tolerance for specific medications, procedures, or
therapies
expectations for the course of the disease
your opinion or preference

Treatment may include removal of parathyroid tissue.

Overactive Adrenal Glands

(Cushing's Syndrome)
What are overactive adrenal glands?
When adrenal glands produce excessive amounts of certain
hormones, they are called overactive. Symptoms and treatment
depend on which hormones are being overproduced, including the
following:

androgenic steroids (androgen hormones) - an overproduction

of androgenic steroids (such as testosterone) can lead to
exaggerated male characteristics in both men and women,
such as excess hair on the face and body, baldness, acne,
deeper voice, and increased muscle mass. If a female fetus is
exposed to high levels of androgens early in pregnancy, her
genitals may develop abnormally. Young boys who experience
high levels of androgen levels may grow faster, but bones may
also mature faster and stop growing too soon.
corticosteroids - an overproduction of corticosteroids can lead
to Cushing's syndrome (see below).

aldosterone - an overproduction of the aldosterone hormone

can lead to high blood pressure and to those symptoms
associated with low levels of potassium (i.e., weakness,
muscle aches, spasms, and, sometimes, paralysis.)
The symptoms of overactive adrenal glands may resemble other
problems or medical conditions. Always consult your child's
physician for a diagnosis.

How are overactive adrenal glands diagnosed?

In addition to a complete medical history and physical examination,
diagnostic procedures for overactive adrenal glands may include:

specific blood tests (to measure levels of hormones)

urine tests (to measure levels of hormones)

Treatment of overactive adrenal glands:

your child's age, overall health, and medical history

extent of the disease
your child's tolerance for specific medications, procedures, or
therapies
expectations for the course of the disease

your opinion or preference

Treatment may include surgical removal of growths on the adrenal
gland(s), or the adrenal gland(s) itself. Medications that block the
excessive production of certain hormones may also be administered.

What is Cushing's syndrome?

Cushing's syndrome is a myriad of abnormalities that are the result
of hypersecretion of corticosteroids by the adrenal cortex. An
overproduction of cortisol, the hormone that controls the adrenal
gland, by the pituitary gland, which stimulates the adrenal glands to
produce corticosteroids, may be one cause. In addition, certain lung
cancers and other tumors outside the pituitary gland may produce
corticotropins. Other causes include benign (non-cancerous) or
cancerous tumors on the adrenal glands. Cushing's syndrome is rare
in children and more commonly seen in adults.
What are the symptoms of Cushing's syndrome?
The following are the most common symptoms of Cushing's
syndrome. However, each child may experience symptoms
differently. Children and adolescents with Cushing's syndrome
primarily experience weight gain, growth retardation, and
hypertension (high blood pressure). Symptoms may include:

upper body obesity

round or moon-shaped face
increased fat around neck
thinning arms and legs
fragile and thin skin
darkened pigmentation of the skin
acne
bruising
stretch marks on abdomen, thighs, buttocks, arms, and
breasts
bone and muscle weakness
severe fatigue
high blood sugar
irritability and anxiety
excessive hair growth in females
irregular or stopped menstrual cycles in females

reduced sex drive and fertility in males

The symptoms of Cushing's syndrome may resemble other

conditions or medical problems. Always consult your child's

physician for a diagnosis.
How is Cushing's syndrome diagnosed?
In addition to a complete medical history and physical examination,
diagnostic procedures for Cushing's syndrome may include:

x-ray - a diagnostic test which uses invisible electromagnetic

energy beams to produce images of internal tissues, bones,
and organs onto film.
24-hour urinary test (urine is collected over a 24-hour period
to measure for corticosteroid hormones)
computerized tomography scan (Also called a CT or CAT scan.)
- a diagnostic imaging procedure that uses a combination of xrays and computer technology to produce cross-sectional
images (often called slices), both horizontally and vertically, of
the body. A CT scan shows detailed images of any part of the
body, including the bones, muscles, fat, and organs. CT scans
are more detailed than general x-rays.
magnetic resonance imaging (MRI) - a diagnostic procedure
that uses a combination of large magnets, radiofrequencies,
and a computer to produce detailed images of organs and
structures within the body.
dexamethasone suppression test (to differentiate whether the
excess production of corticotropins are from the pituitary
gland or tumors elsewhere)

corticotropin-releasing hormone (CRH) stimulation test (to

differentiate whether the cause is a pituitary tumor or an
adrenal tumor)
Treatment for Cushing's syndrome:

Specific treatment for Cushing's syndrome will be determined by

your child's physician based on:

your child's age, overall health, and medical history

the extent of the disease
your child's tolerance for specific medications, procedures, or
therapies
expectations for the course of the disease

your opinion or preference

Treatment for Cushing's syndrome depends on its cause. Surgery
may be needed to remove tumors of the adrenal glands.

Addison's disease

Addison's disease (chronic adrenal insufficiency) is a rare and

progressive disorder that affects between one and six in every
100,000 people. It affects people of both sexes and all ages.
The human body has two adrenal glands, one on top of each kidney.
These glands form part of the endocrine system, which works with
the nervous system and the immune system to help the body cope
with different events and stresses. Addison's disease is caused by
the inability of the adrenal glands to make sufficient amounts of
regulating hormones.
Adrenaline is the most well known of the hormones that are
secreted by the adrenal glands, in the adrenal medulla (the central
part of the gland). The adrenal cortex (the outer part) also produces
important hormones, the corticosteroids. They include cortisol,
aldosterone and supplementary sex hormones. In a person with
Addison's disease, only the adrenal cortex is affected. The person
cannot produce enough glucocorticoid or cortisol and, occasionally,
also fails to produce sufficient mineralocorticoid or aldosterone.
Causes
Most cases of Addison's disease are caused by an autoimmune
response that attacks and damages the adrenal glands over time.
Other causes include:

Infection
Cancer
Surgical removal of particular tumours in the adrenal or
pituitary glands or the hypothalamus.

Symptoms
The symptoms of Addison's disease can include any or all of the
following:
Loss of appetite and weight.
Nausea, vomiting or diarrhoea.
Muscle weakness.
Chronic, worsening fatigue.
Low blood pressure.
Salt cravings.
Dehydration.
Hypoglycaemia, or low blood sugar levels (especially in
children).
Increased pigmentation of the skin, particularly around scars
and bony areas.
Irregular or no menstrual periods in women.
Mood swings, mental confusion or loss of consciousness.

These symptoms can develop quickly (especially in children and

teenagers), or progress slowly for 20 years or more. Many
symptoms can mimic other diseases, so diagnosis can be delayed.
The hormone cortisol
Cortisol is produced by the outer layer of the adrenal gland, called
the adrenal cortex. The quantities of cortisol released by the adrenal
glands are closely monitored by the master gland of the endocrine
system, the pituitary, which is located in the brain. The workings of
the pituitary are governed by another brain structure, the
hypothalamus. When cortisol levels are too low, the pituitary
secretes the stimulating hormone adrenocorticotropin (ACTH).
Conversely, high levels of cortisol prompt the pituitary to decrease
ACTH secretion, which slows cortisol production.
Cortisol plays many vital roles and is essential to many body
functions because it:
Works with adrenaline to help the body manage physical and
emotional stress.
Converts protein into glucose to boost flagging blood sugar
levels.
Works in tandem with the hormone insulin to maintain
constant blood sugar levels.
Reduces inflammation.
Helps the body maintain a constant blood pressure.
Helps the workings of the immune system.
The hormone aldosterone
Aldosterone is a mineralocorticoid, also produced by the adrenal
cortex. The amount of aldosterone in the body is monitored by the
kidneys, which secrete hormones to increase or decrease
aldosterone production. Aldosterone regulates electrolytes (such as
sodium and potassium) in the blood. This helps to maintain blood
pressure and heart function. If too much sodium is excreted by the
kidneys, a considerable amount of body fluid is also lost. This
reduces blood volume and drops blood pressure. Too much or too
little potassium can affect the way the heart functions.
Primary adrenal insufficiency
Addison's disease can occur gradually, and is defined when
approximately 90 per cent of the adrenal gland(s) is damaged. This
is known as primary adrenal insufficiency. Around seven out of 10
cases of Addison's disease are caused by an autoimmune response,
where the body's own immune cells attack and destroy the adrenal
glands. In some cases, other glands of the endocrine system are
affected by an autoimmune response, in a condition called
polyendocrine deficiency syndrome.
Polyendocrine deficiency syndrome

There are two types of this disorder and both types tend to run in
families:
Type I - is more common in children. Symptoms include
underactive parathyroid, pernicious anaemia, recurring
candida infections, chronic active hepatitis and slow sexual
development.
Type II - (Schmidt's syndrome) is more common in younger
adults. Symptoms include underactive thyroid, diabetes
mellitus and slow sexual development.
Other conditions related to primary Addison's disease are:
Adrenomyeloneuropathy (AMN) - which can occur in some
adults. It affects the spine, and is degenerative over time.
Adrenoleukodystrophy (ALD) - which occurs (rarely) in
some children (one in 100,000), especially males. It can cause
brain damage and can be fatal. Survivors often develop AMN.
Treatment for primary Addison's disease is with glucocorticoid and
mineralocorticoid replacement for life.
Secondary adrenal insufficiency
Sometimes, Addison's disease is caused by the pituitary gland's
inability to produce sufficient amounts of ACTH, which means the
adrenal glands aren't prompted to secrete cortisol. This is known as
secondary adrenal insufficiency. Causes may include:
Some medications - inflammatory disorders, such as
rheumatoid arthritis and asthma, are often treated with
prolonged or high dose steroids (glucocorticoid replacements).
If the dose is suddenly stopped, or not reduced by appropriate
tapering measures, the pituitary gland may respond by failing
to produce enough ACTH. This situation can sometimes be
reversed.
Cushing's disease - a benign tumour of the pituitary gland
that produces ACTH. This results in too much cortisol being
produced. Treatment requires surgical removal of the tumour
and, in some cases, removal of damaged adrenal gland(s).
Other causes - infections, reduced blood flow, radiotherapy
and some neurosurgery can damage the pituitary gland or
hypothalamus, and decrease ability to produce ACTH.
Treatment for secondary Addison's disease is with glucocorticoid
replacement only.
Addisonian crisis
A sudden, acute worsening of symptoms is known as an Addisonian
crisis. It can be caused by:
Extreme stress - an accident, excessive heat or physical
exertion.

Severe illness - especially dehydration from vomiting or

diarrhoea.
Sudden shock - for example, the death of a significant
person.

The symptoms of Addisonian crisis include:

Violent pain in the abdomen, back and legs.
Nausea, vomiting or diarrhoea.
Low blood pressure, low blood sugar, high potassium, low
sodium and a rapid heart rate.
Possible mental confusion and loss of consciousness.
Prompt emergency hospital treatment must be sought, including
intravenous fluids, increased steroid medication and saline. Many
Addisonians wear a medical alert bracelet or pendant with
information and identification, and carry a hydrocortisone injectable
for use in emergencies. They will still need hospitalisation and
ongoing monitoring.
If untreated, an Addisonian crisis can be fatal.
Diagnostic tools
Diagnosis of Addison's disease may involve:
Complete detailed family history, with special attention to any
other endocrine disorders.
Biochemical tests, which measure cortisol levels before and
after a challenge injection of synthetic ACTH, known as a
'short synacthen test'. A 'long synacthen test' is done over
several days in hospital. Synacthen tests will indicate the
person's baseline level of cortisol production and their
response to an increased need for cortisol in the body. An
Addisonian may show a flat or reduced response.
Blood electrolyte and plasma renin tests will indicate if there is
a need for mineralocorticoid replacement.
Anti-adrenal antibody test. If the result is positive, primary
Addison's disease is definitively diagnosed. However, even if
these antibodies do not exist, the person may still have
Addison's disease.
X-rays, ultrasounds and CAT scans of the abdominal region to
check for visual signs of damage and the size of adrenal
glands.
Treatment options
Treatment aims to bolster or replace insufficient or absent steroid
components. Glucocorticoid replacement is essential for primary
and secondary Addisonian patients, and must be taken for life.
Treatment should:
Be tailored to each person over the course of their life.

Be altered, in consultation with a doctor, during illness or

other stressful events.
Allow for the different needs of children and young adults.

Where to get help

Your doctor
Endocrinologist
Australian Addison's Disease Association Tel. (02) 6652 4761
Things to remember
Addison's disease is a progressive disorder, characterised by
the inability of the adrenal glands to produce sufficient
hormones.
Causes can include infection, damage, and an autoimmune
response that prompts the immune system to attack and
destroy the adrenal glands.
Treatment includes steroid replacement therapy that must be
managed for life.
An Addisonian crisis can be fatal unless treated quickly and
appropriately.

IDDM is a polygenic disorder. The major locus is HLA (human

leukocyte antigen) region short arm of chromosome 6. This locus is
referred to as IDDM.

Environmental factors they are relatively low in numbers.

Viral infection in-utero is consistent with observation that
incidence of IDDM increased in children with congenital
rubella. IgM antibodies against Coxsackies virus have been
found in 25-30% of new cases, suggesting recent infection.

Dietary factors - a positive association between IDDM, high

protein intake and frequency of consumption of foods
containing nitrosamine is seen in close control studies.

Pathogenesis
1. Auto-immunity islets of newly diagnosed persons show
histological picture of marked mononuclear cell infiltration
around islets.
2. Islets cell antibodies (ICA) they are present in 80% cases
of children at the time of diagnosis. Long term follow up has
shown that family members with ICA are at increased risk of
progression to DM.
3. B cell destruction this process is slow with patchy
histological appearance in newly diagnosed persons. Clinical

onset of diabetes does not occur until 90% of cells have been
destroyed.
Clinically - children with complaints of polyuria, intense thirst,
nocturia, polyphagia, weight loss, weakness, lassitude, leg cramps
and leg cramps. Some children have a stormy onset and seek
medical aid for first time with symptoms of ketoacidosis, such as
persistent enuresis, abdominal pain, vomiting, dehydration,
prostration, drowsiness and even coma. Characteristic features of
IDDM include:

Severe insulin deficiency.

Abrupt onset of severe symptoms.
Tendency to ketoacidosis.
Dependence on exogenous insulin to sustain life.

Complications of diabetes in Children:

Acute: ketoacidosis, coma and lactic acidosis.

Sub-acute: infection either bacterial or fungal involving skin
mucosa, soft tissue, lungs (tuberculosis) and urinary tract
infection.
Chronic: arteriosclerosis, retinopathy, polyneuropathy,
diabetic neuropathy, delayed development of secondary
sexual characters.

Diagnosis through urine sugar and blood sugar level examination

and oral glucose tolerance test.
Management main line management includes diet and insulin.

Aims of managing diabetes in children:

1. To maintain ideal body weight essential to preserve optimal
insulin sensitivity.
2. To maintain long term nutritional balance for normal growth
and development in children.
3. To time meal and snacks to prevent wide swings in BSL
especially because these persons have to be managed with
insulin.
4. To maintain BSL and avoid complications.
Total calorie intake should be according to ideal body weight (IBW)
of child, calculated as IBW (in kgs) = (height in cms -100) x 0.9
Children need baseline calories of 1000, plus 100 calories (for girls)
and 125 calories (for boys) per year of age up to 12 yrs.
Distribution of total calories into various nutrients is:

Carbohydrate 60 to 65% of total calories

Proteins-15 to 20% of total calories
Fats-15 to 25% of total calories

Carbohydrates supply 4 cal/gm of cereals, roots and pulses rich in

complex carbohydrates are preferred and diet with low glycaemic
index are preferred.
Proteins most amino acids are glucogenic. They decrease
glucagon secretion as well. It supplies 4 cal per gram. Its intake
must be restricted in diabetic nephropathy.
Fats supply 9 cal per gram. It must not exceed 20% of total calorie
intake.

Gynecomastia
Programs related to this topic

Reproductive Endocrine
Practice
Breast Clinic

Adolescent/Young Adult Medical

Practice

What is gynecomastia?

Gynecomastia is a condition in which above average amounts of

firm breast tissue form in males. The breast tissue is usually less
than 2 inches across and is located directly under either one nipple
or both nipples.
How common is gynecomastia?

Gynecomastia is not unusual or abnormal in adolescent boys.

Temporary breast enlargement often happens during adolescence
when there are hormonal changes.
What causes gynecomastia?

Gynecomastia is usually caused by changes in hormones during

puberty or as part of aging, possibly by changes in the balance of
the two hormones, estrogen and testosterone.
In rare cases, gynecomastia can be caused by prescription drugs,
over-the-counter medicines, illegal drugs (such as marijuana and
steroids) or tumors.
Gynecomastia can also be caused by certain genetic disorders and
conditions (such as Klinefelter Syndrome).

Is gynecomastia physically harmful?

Gynecomastia is not physically harmful, although it can occasionally

indicate more serious underlying conditions. Occasionally, males
with gynecomastia experience tenderness that can be treated with
medications. Males with gynecomastia usually experience
psychological and social issues rather than physical problems.
What are the psychological effects of gynecomastia?

Gynecomastia can have a major emotional impact on males and can

include feelings of shame, embarrassment and depression. Males
with gynecomastia often hide their chests in public or withdraw
socially and avoid discussing their concerns with parents and peers.
What is the treatment for gynecomastia?

In most cases, no treatment is needed for gynecomastia. In 90

percent of teenage boys, gynecomastia goes away in less than three
years. A physician should still monitor the condition every few
months.
For the remaining 10 percent of males who continue to have
gynecomastia, treating the underlying cause may improve the
condition. If medications are causing gynecomastia, they may be
stopped or changed. In overweight males, weight loss sometimes
helps remedy gynecomastia. An evaluation by an experienced
plastic surgeon is often suggested because cosmetic surgery can
surgically remove the breast tissue. Some males choose to live with
the condition.

Amenorrhea
What is amenorrhea?
Amenorrhea is a menstrual condition characterized by absent
menstrual periods for more than three monthly menstrual cycles.
Amenorrhea may be classified as primary or secondary.

primary amenorrhea - from the beginning and usually lifelong;

menstruation never begins at puberty.

secondary amenorrhea - due to some physical cause and

usually of later onset; a condition in which menstrual periods
which were at one time normal and regular become increasing
abnormal and irregular or absent.
What causes amenorrhea?

There are several possible causes of amenorrhea, including the

following:

pregnancy - Females no longer ovulate when they are

pregnant, thus, menstruation ceases temporarily.
ovulation abnormality - Ovulation abnormalities are usually
the cause of very irregular or frequently missed menstrual
periods.
birth defect, anatomical abnormality, or other medical
condition - If a young woman has not started to menstruate by
the age of 16, a birth defect, anatomical abnormality, or other
medical condition may be suspected.
eating disorder - Females with anorexia nervosa (or simply
anorexia) and/or bulimia nervosa (or simply bulimia) often
experience amenorrhea as a result of maintaining a body
weight that would be too low to sustain a pregnancy. As a
result, as a form of protection for the body, the reproductive
system "shuts down" because it is severely malnourished.
over-exercise or strenuous exercise - Many young female
athletes in training experience absent menstrual cycles due to
low body fat content.
thyroid disorder - In many cases, an underactive thyroid gland
(a condition called hypothyroidism in which the thyroid gland
is producing insufficient amounts of the thyroid hormone) or
an overactive thyroid gland (a condition called
hyperthyroidism in which the thyroid gland secretes too much
thyroid hormone - resulting in too much thyroid hormone in
the bloodstream and overactivity of the body's metabolism) is
responsible for the absent menstrual cycles.

obesity - Females who are obese often experience amenorrhea

as a result of excess fat cells interfering with the process of
ovulation.
How is amenorrhea diagnosed?

Diagnosis begins with a gynecologist evaluating a female's medical

history and a complete physical examination including a pelvic
examination. A diagnosis of amenorrhea can only be certain when
the physician rules out other menstrual disorders, medical
conditions, or medications that may be causing or aggravating the
condition. In addition, a diagnosis of amenorrhea requires that a
female has missed at least three consecutive menstrual cycles,
without being pregnant. Young women who have not had their first
menstrual period by the age of 15 should be evaluated promptly, as
making an early diagnosis and starting treatment as soon as
possible is very important.
Treatment for amenorrhea:
Specific treatment for amenorrhea will be determined by your
physician based on:

your age, overall health, and medical history

extent of the condition
cause of the condition (primary or secondary)
your tolerance for specific medications, procedures, or
therapies
expectations for the course of the condition

your opinion or preference

Treatment for amenorrhea may include:

progesterone supplements (hormone treatment)

oral contraceptives (ovulation inhibitors)

dietary modifications (to include increased caloric and fat

intake)
In most cases, physicians will induce menstruation in non-pregnant
females who have missed two or more consecutive menstrual
periods, because of the danger posed to the uterus if the nonfertilized egg and endometrium lining are not expelled. Without this
monthly expulsion, the risk of uterine cancer increases.

Causes of Secondary amenorrhea in children

1. 3?-hydroxysteroid dehydrogenase deficiency
A ver rare form of congenital adrenal hyperplasia involving a
deficiency of 3?-hydroxysteroid dehydrogenase which results
in reduced production of adrenal steroids (mineralocorticoids,
sex steroids and glucocorticoids). The disorder can occur in
classical...read more
2. Adrenal Cancer
A malignant cancer that develops in the adrenal gland. The
tumor may be nonfunctioning (does not produce hormones) or
functioning in which case excessive levels of hormones can
cause a variety of symptoms depending on which hormone is
involved. Adrenal ho...read more
3. Anorexia Nervosa
A disorder where a distorted sense of body image leads to
self-starvation to the point of death in some cases....read
more
4. Chiari-Frommel syndrome
A rare condition where galactorrhea and amenorrhea
continues for an abnormal length of time (generally longer
than 6 months) after giving birth....read more
5. Cushing's syndrome
A rare syndrome where excessive secretion of corticosteroids
by the adrenal cortex leads to a variety of symptoms.
Hormone-secreting adrenal or pituitary tumors are often the

cause of the excessive corticosteroid secretion....read more

6. Emotional stress
A condition which occurs when a person is under stress
affecting their emotions...read more
7. Hyperprolactinemia
High levels of prolactin in the blood....read more
8. Hyperthyroidism - Teratogenic Agent
There is strong evidence to indicate that the development of
hyperthyroidism during pregnancy may have a teratogenic
effect on the fetus. A teratogen is a substance that can cause
birth defects. The likelihood and severity of defects may be
affected by th...read more
9. Lactotroph adenoma
A benign pituitary tumor that secretes excessive prolactin
which can affect the functioning of the reproductive system testes and ovaries. The tumor may also grow large enough to
compress adjacent structures such as the eye nerves....read
more
10. Obesity
An increase in the body weight greater than that required for
normal function that is characterised by the accumulation of
excessive fats

Teen Health Conditions and

Diagnoses

Dysmenorrhea
What is dysmenorrhea?
Dysmenorrhea is a menstrual condition characterized by severe and
frequent menstrual cramps and pain associated with menstruation.
Dysmenorrhea may be classified as primary or secondary.

Primary Dysmenorrhea is classified as recurrent, crampy,

lower abdominal pain that occurs during menstruation in the
absence of other medical problems. The pain usually occurs
form days 1-2 before onset of menses to days 2-3 of

menstruation. It is the most common gynecologic complaint in

adolescent females.
Secondary Dysmenorrhea is painful menstruation caused by a
gynecologic abnormality. This is more common in adults in
their fourth and fifth decades of life.

What causes dysmenorrhea?

In primary dysmenorrhea, the cause is over production of
prostaglandin a hormone like compound found in the body. This
compound increases monthly during the menstrual cycle and causes
contraction of the muscles in the uterus resulting in pain. In some
people this compound affects the gastrointestinal tract causing
symptoms such as nausea and vomiting.

What are the symptoms?

The most common symptoms of dysmenorrhea are:

Cramping in the lower abdomen

Pain in lower abdomen
Low back pain
Pain radiating down the legs

Other symptoms that may be present include:

Nausea
Vomiting
Diarrhea
Fatigue
Weakness
Fainting
Headaches

How is dysmenorrhea treated?

Treatment is based on many factors and is best if determined with
your health care provider. There are non-pharmacological
treatments that perform well in the control of dysmenorrhea.
These treatments include:

Heat via a heating pad or bathing

Abdominal massage
Regular exercise

Pharmacologic treatments that can achieve pain relief include:

Non-steroidal anti-inflammatory drugs (NSAIDs)

Tylenol
Oral contraceptive pills
Long-acting hormonal contraceptives

Dysmenorrhea is a very common gynecological condition. A good

treatment plan can help achieve optimal pain relief during monthly
menstrual cycles. Coordination with a health care provider can help
determine if other problems exist and to find the most effective
treatment options available.