endocrine&metab disorders

8/20/2019 Endocrine&Metab Disorders

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Hyperpituitarism•

IntroductionBackground

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 theprolactinoma, followed by corticotropinoma and somatotropinoma.Fewer than 20 cases of thyrotropinoma in children have beenreported, all with onset after age years. !ediatricgonadotropinoma has not been reported.

Hypersecretion of pituitary hormones secondary to macroadenomascan interfere with other pituitary hormone functions, resulting intarget organ hormone de"ciencies #hypogonadism, hypoadrenalism,hypothyroidism$. In some cases, long%standing hormonalhypersecretion is accompanied by su&cient hyperplasia of thepituitary to produce sellar enlargement.

'levated pituitary hormone levels that result from primary endocrineorgan de"ciency #eg, high circulating thyroid%stimulating hormone(T)H* levels in primary hypothyroidism due to Hashimoto thyroiditis$quic+ly suppress to reference range values upon replacement of theactive hormone. ost rarely, ectopic tumors can secrete pituitaryhormones. This article focuses on the endocrine manifestations ofpituitary adenomas in children.

Pathophysiology

Hypothalamic dysfunction clearly may promote tumor growth, butoverwhelming evidence indicates intrinsic pituicyte geneticdisruption leads to pituitary tumorigenesis. The monoclonal nature

of most pituitary adenomas, con"rmed by -%inactivation studies,implies their usual origin from a clonal event in a single cell. ostpituitary adenomas are functional and secrete a hormone thatproduces a characteristic clinical presentation. onfunctioningpituitary adenomas are rare in children, accounting for only /%1 ofall adenomas in 2 large series, whereas they comprise /01 ofadenomas in adults. In children, disruption of growth regulationandor se3ual maturation is common, either because of hormonehypersecretion or because of manifestations caused by localcompression by the tumor.

Prolactinoma

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4verall, prolactinoma is the most common pituitary adenomaencountered in childhood. ost pediatric cases occur inadolescence, more commonly in females than males. 5oys tend tohave larger tumors and higher serum prolactin #!67$ levels thangirls. Females with these tumors present with amenorrhea, and

males present with gynecomastia and hypogonadism. !rolactinomasarise from acidophilic cells that are derived from the same lineageas the somatotropes and thyrotropes. Hence, !67%secretingadenomas may also stain for and secrete growth hormone #8H$ and,occasionally, T)H.

Corticotropinoma (Cushing disease)

In children, corticotropinomas are the most common adenomasobserved before puberty, although they occur in people of all ages.

They increase in frequency in pubescent and postpubescentchildren, with a female preponderance. First described by Harvey9ushing in the early :00s, 9ushing disease speci"cally refers to anadrenocorticotropic hormone #;9TH$1 in one study$. 8H%secreting tumors inpediatric patients are more li+ely to be locally invasive or aggressivethan those in adult patients. ;ctivating mutations of the stimulatory8s alpha #8sa$ protein have been identi"ed in the somatotrophs ofpituitary lesions in ;) and in as many as @01 of sporadic 8H%secreting pituitary adenomas.

Thyrotropinoma

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Aery few cases of thyrotropinoma have been reported in children. These adenomas may secrete e3cess !67, 8H, and alpha subunit inaddition to T)H. They are usually large because of their aggressivefeatures and because their diagnosis is often delayed. The clinicalpresentation consists of signs and symptoms of hyperthyroidism,

visual symptoms, and headaches. 5iochemical features include theelevation of circulating free thyro3ine #T@$ and total triiodothyronine#T/$ levels but inappropriately unsuppressed T)H.

Frequency

United States

;lthough less common in children than in adults, pituitary adenomasconstitute 2.>1 of supratentorial tumors in children and /.%1 of

all pituitary adenomas that are surgically treated. The averageannual incidence of pituitary adenomas presenting before age 20years is estimated to be less than 0. per million children.

ortality!or"idity

Transsphenoidal pituitary surgery has emerged as the treatment ofchoice for ;9TH%secreting and 8H%secreting adenomas.

Transsphenoidal surgery is indicated for prolactinomas that do notrespond to medical therapy. Transsphenoidal surgery is associatedwith remar+ably little morbidity and near Bero mortality. ;

permanent loss of pituitary function occurs infrequently. Theincidence of postoperative hypopituitarism is about /1 in patientswith microadenomas and slightly increases with the invasiveness ofthe tumor.

#ace

6ace and ethnicity have not been reported as signi"cantcontributing factors to hyperpituitarism.

Se$

• In prolactinoma, the female%to%male ratio is @.CD.• In ;9TH%releasing adenoma, the female%to%male ratio is 2D.• In 8H%releasing adenoma, the female%to%male ratio is D2.

%ge

• In children, ;9TH%releasing adenomas are most prevalent inthe youngest group and decrease in frequency with advancingage.

• The incidence of prolactinomas increases with age? :/1 occurin children older than 2 years.

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• 8H%releasing tumors have a fairly even distribution among thevarious age groups.

Clinical

History

The clinical presentation of a pituitary adenoma primarily resultsfrom the oversecreted hormone. The tumor mass itself may causeheadaches, visual changes due to optic nerve compression, orhypopituitarism.

• '3cess prolactino The presentation of prolactinomas may vary, depending

on the age and se3 of the child.

o !repubertal children typically present with acombination of headache, visual disturbance, andgrowth failure.

o !ubertal females frequently present with symptoms ofpubertal arrest or hypogonadism #with or withoutgalactorrhea$ due to suppression of gonadotropinsecretion or local compression of the pituitary.

o !ubertal males may present with headaches, visualimpairment, and pubertal arrest or growth failure.

• '3cess adrenocorticotropic hormoneo The most sensitive indicator of e3cess glucocorticoid

secretion in children is weight gain with concurrentgrowth failure, which generally precedes othermanifestations.

o !atients commonly present with weight gain that tendsto be generaliBed rather than centripetal.

o Hirsutism and premature adrenarche may occur inprepubertal children.

o !ubertal arrest, acne, fatigue, and depression are alsocommon.

o )noring, poor sleep quality, deteriorating academic

performance #compared with prior school terms$, orother signs of obstructive sleep apnea #4);$ shouldprompt a formal sleep study and consultation with apulmonologist.

• '3cess growth hormoneo The presentation of gigantism in a child is usually

dramatic, unli+e the insidious onset of acromegaly inadults.

o The cardinal clinical feature of gigantism is longitudinalgrowth acceleration secondary to 8H e3cess.

o !resentation depends on whether the epiphyseal growth

plate is open. 5efore epiphyseal fusion, acceleratedgrowth velocity is prominent. ;s epiphyseal fusion

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approaches, the spectrum of symptoms resembles thepresentation in adults #eg, coarsening of facial features,change in ring and shoe siBe$.

Physical

• !rolactinomao Hypogonadism, leading to pubertal arrest, pubertal

failure, or pubertal delayo enstrual abnormalities, including primary or secondary

amenorrheao 8alactorrheao )hort statureo 8ynecomastia

• 9ushing diseaseo

9ushingoid appearance, including a dorsal cervical fatpad, moon facies, bruising, and striae. These featuresare only observed in patients with advanced long%standing disease.

o 8rowth failure and short stature may be observed.o Eeight gain and obesity in children with 9ushing

disease tends to be generaliBed rather than centripetal.o !ubertal arrest, failure, or delay may occur.o ;menorrhea may be noted.o Hypertension may be present.

• 8igantismD ;ll growth parameters are a=ected, although not

necessarily symmetrically. 8H e3cess over time ischaracteriBed by progressive cosmetic dis"gurement andsystemic organ manifestations.

o Tall statureo ild%to%moderate obesity #common$o acrocephaly, which may precede linear growtho '3aggerated growth of the hands and feet with thic+

"ngers and toeso 9oarse facial features, including frontal bossing and

prognathismo Hyperhidrosiso enstrual irregularitieso !eripheral neuropathies #eg, carpal tunnel syndrome$o 9ardiovascular diseaseD !rolonged 8H e3cess can result

in cardiac hypertrophy, hypertension, and leftventricular hypertrophy.

o TumorsD ;lthough benign tumors, including uterinemyomas, prostatic hypertrophy, colon polyps, and s+intags, may be frequently encountered in acromegaly, thedocumentation of the overall prevalence of malignanciesin patients with acromegaly remains controversial.

o 'ndocrinopathiesD Frequently associatedendocrinopathies include hypogonadism, diabetes,

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decreased glucose tolerance, andhyperprolactinemia. 4); has been reported in up to half of patients with acromegaly, particularly those who areobese or older than C0 years.

Causes

Hypothalamic dysfunction can promote tumor growth, butoverwhelming evidence points to intrinsic pituicyte geneticdisruption as the main underlying cause of pituitary tumorigenesis.

The monoclonal nature of most pituitary adenomas, con"rmed with-%inactivation studies, implies their origin from a clonal event in asingle cell. ost pituitary adenomas are functional, and clinicalpresentation typically depends on the particular pituitary hormonethat is hypersecreted. onfunctioning pituitary adenomas are rare in

children, accounting for only /%1 of all adenomas in 2 large series?they comprise /01 of adenomas in adults.

Diabetes Insipidus

Ehat is diabetes insipidus Giabetes insipidus is a condition thatresults from insu&cient production of the antidiuretic hormone#;GH$, a hormone that helps the +idneys, and body, conserve thecorrect amount of water. Giabetes insipidus may also occur whenthe +idneys do not respond properly to normal levels of ;GH. Thedisease is actually categoriBed into two groupsD

• central diabetes insipidus % insu&cient production or secretionof ;GH? usually a result of a problem in the brain or centralnervous system.

nephrogenic diabetes insipidus % lac+ of +idney response tonormal levels of ;GH.

ormally, the antidiuretic hormone controls the +idneys output ofurine. It is secreted by the pituitary gland to decrease the amount of

urine output so that dehydration does not occur. Giabetes insipidus,however, causes e3cessive thirst and e3cessive production of very

diluted urine. Ehat causes diabetes insipidus Giabetesinsipidus can be caused by several conditions, including thefollowingD

• malfunctioning hypothalamus #that produces too little ;GH$• malfunctioning pituitary gland #that fails to release ;GH into

the bloodstream$• damage to hypothalamus or pituitary gland during surgery


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• brain inury• tumor• tuberculosis• bloc+age in the arteries leading to the brain• encephalitis % inJammation of the brain.• meningitis % inJammation of the meninges, the membranes

that cover the brain and spinal cord.• sarcoidosis % a rare inJammation of the lymph nodes and

other tissues throughout the body.• family heredity

Ehat are the symptoms of diabetes insipidus Thefollowing are the most common symptoms of diabetes insipidus.

However, each child may e3perience symptoms di=erently.

)ymptoms may includeD• e3cessive thirst• e3cessive urine production• dehydration

Infants with diabetes insipidus may also e3hibit the followingsymptomsD

• irritability• poor feeding• failure to grow• high fevers

The symptoms of diabetes insipidus may resemble other problemsor medical conditions. ;lways consult your childs physician for a

diagnosis. How is diabetes insipidus diagnosed Inaddition to a complete medical history and physical e3amination,including the childs daily Juid inta+e, dietary inta+e, and voiding#bowel and bladder elimination$ patterns, diagnostic procedures fordiabetes insipidus may includeD

• urine tests• blood tests• water deprivation test #to observe if dehydration occurs$• magnetic resonance imaging #6I$ % 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 chec+ for pituitaryabnormalities.


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Treatment of diabetes insipidusD If left untreated in children,diabetes insipidus can lead to brain damage, impaired mental

function, mental retardation, hyperactivity, short attention span,andor restlessness. Treatment for diabetes insipidus depends onwhat is causing the disease. Treating the cause usually treats thediabetes insipidus. )peci"c treatment for diabetes insipidus will be

determined by your childs physician based onD• your childs age, overall health, and medical history• e3tent of the disease• your childs tolerance for speci"c medications, procedures, or

therapies• e3pectations for the course of the disease• your opinion or preference

Treatment may include modi"ed antidiuretic hormone medications#often ta+en as a nasal spray$, or medications that stimulate theproduction of the antidiuretic hormone. In addition, persons withdiabetes insipidus must maintain adequate Juid inta+e tocompensate for the e3cessive urinary output, and eat a low%sodiumdiet. ;lthough children with the disease also need to drin+plenty of Juids, care should be ta+en to monitor sodium inta+e in

their Juids. 7ong%term outloo+ for children with diabetes insipidus.

Giabetes insipidus can be a temporary or a permanent condition,depending on what is causing the disease. 9hildren with centraldiabetes insipidus, with proper management, can lead full, healthylives. 9hildren with nephrogenic diabetes insipidus can also leadrelatively normal lives with proper medical care and management,especially if the medical care is started early.

5uy the5oo+ !G;Gownload

!recocious!uberty

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!recocious puberty is onset of se3ual maturation before age L ingirls or age : in boys. Giagnosis is by comparison withpopulation standards, 3%ray of the left hand and wrist to assesss+eletal maturation and chec+ for accelerated bone growth, andmeasurement of serum levels of gonadotropins and gonadal andadrenal steroids. Treatment depends on the cause.

The de"nition of precocious puberty depends on reliable

population standards for onset of puberty #ie, when pubertalmilestones occur$? because onset seems to be occurring earlierin the K), these standards are being reevaluated. ;lmost L to01 of white girls, almost /01 of blac+ girls, and anintermediate percentage of Hispanic girls reach early puberty atage L. The lower limit of normal puberty may be > yr for whitegirls and yr for blac+ girls. The mean age for early breastdevelopment is about 0 yr for white girls and : yr for blac+ girls#range L to / yr$. The mean age for pubic hair growth is : to0.C yr for both groups. These "ndings imply that guidelines for

evaluating disorders that cause precocious puberty can beinterpreted more leniently if children are otherwise healthy andare not at ris+ of not reaching their full adult height potential.

In girls, the "rst pubertal milestone is typically breastdevelopment #thelarche$, followed soon after by appearance ofpubic hair #pubarche$ and a3illary hair and later by the "rstmenstrual period #menarche$. In boys, the "rst pubertalmilestone is typically testicular growth, followed by penilegrowth and appearance of pubic and a3illary hair. In both se3es,appearance of pubic and a3illary hair is called adrenarche.

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!recocious puberty can be divided into 2 typesD

• 8onadotropin%releasing hormone #8n6H$


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familial male gonadotropin%independent precocity #due to anactivating mutation of the gene for luteiniBing hormone (7H*receptors$, testosterone%producing testicular tumors, andoccasionally c9une%;lbright syndrome.

6arely in girls and boys, puberty results from pituitaryadenomas #hamartomas$ that secrete gonadotropins.

)ymptoms and )igns

In girls, breasts develop, and pubic hair, a3illary hair, or bothappear. 8irls may begin to menstruate. In boys, facial, a3illary,and pubic hair appears and the penis grows, with or withoutenlargement of testes. 5ody odor, acne, and behavior changesmay develop in either se3. Height gain is initially rapid in bothse3es, but premature closure of the epiphyses results in shortadult stature. 4varian or testicular enlargement occurs inprecocious puberty but is usually absent in isolated precociousadrenarche.

Giagnosis

• 5one age 3%rays• )erum hormone measurement• !ossibly pelvic ultrasound and brain 6I or 9T

Giagnosis is clinical. -%rays of the left hand and wrist are done tochec+ for accelerated s+eletal maturation as a result of se3hormone e=ect. Knless history and e3amination suggest anabnormality, no further evaluation is required for children withpubertal milestones that are within yr of population standardsor for girls and boys with precocious adrenarche and girls withprecocious thelarche, as long as 3%rays con"rm that s+eletalmaturation is not accelerated.

Ehen further evaluation is necessary, the following serum

hormones may be measuredD P%human chorionic gonadotropin,estradiol )ome Trade ames')T6;G'6')T648'7AIA'77'9lic+ for Grug onograph , testosterone, dehydroepiandrosterone, >%hydro3yprogesterone, 7H, follicle%stimulating hormone #F)H$,and prolactin. !elvic and adrenal ultrasonography and 6I or 9Tof the brain may be done.

; 8n6H stimulation test #see 'ndocrine Gisorders in 9hildrenD

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Giagnosis$ con"rms a diagnosis of 8n6H%independentprecocious puberty when gonadotropin responses to e3ogenous8n6H are prepubertal in boys or girls with no tumor or otherobvious cause of early se3ual development. If the response is

pubertal, 9) lesions must be e3cluded.

Treatment

• 8n6H agonist therapy #8n6H%dependant precociouspuberty$

• ;ndrogen or estrogen antagonist therapy #8n6H%independent precocious puberty$

• Tumor e3cision as needed

If pubertal milestones are within yr of population standards,reassurance and regular ree3amination are su&cient. Treatmentis not needed for premature adrenarche or thelarche, butregular ree3amination is warranted to chec+ for laterdevelopment of precocious puberty. For 8n6H%dependentprecocious puberty, pituitary 7H and F)H secretion can besuppressed until normal puberty begins with the 8n6H agonistleuprolide )ome Trade ames7K!649lic+ for Grug onograph acetate 0.2 to 0./ mg+g #minimum, >.C mg$ I q @ w+.

6esponses to treatment must be monitored, and drug dosagesmodi"ed accordingly.

In girls with c9une%;lbright syndrome, testolactone )ome Trade ames T')7;99lic+ for Grug onograph , an aromatase inhibitor, reduces serum estradiol )ome Tradeames')T6;G'6')T648'7

AIA'77'9lic+ for Grug onograph and e=ectively treats a=ected girls? alternatively, tamo3ifen)ome Trade ames47A;G'-9lic+ for Grug onograph , an estrogen antagonist, may be bene"cial.

If 8n6H%independent precocious puberty in boys is due tofamilial male gonadotropin%independent precocity or c9une%

;lbright syndrome, androgen antagonists #eg, spironolactone)ome Trade ames

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;7G;9T4'9lic+ for Grug onograph $ ameliorate the e=ects of e3cess androgen. The antifungal drug+etoconaBole )ome Trade ames

IQ46;79lic+ for Grug onograph reduces testosterone in boys with familial male gonadotropin%independent precocity.

If 8n6H%independent precocious puberty is due to a hormone%producing tumor #eg, granulosa%theca cell tumors in girls,testicular tumors in boys$, such tumor should be e3cised.However, girls require e3tended follow%up to chec+ forrecurrence in the contralateral ovary

Hyperthyroidism

IT64GK9TI4 R The clinical manifestations of hyperthyroidism inchildren and adolescents are similar to those seen in adults. Inaddition, the disorder has unique e=ects on growth anddevelopment. The clinical features of hyperthyroidism are largelyindependent of the cause. ;lthough there are several potentialcauses of hyperthyroidism in children, 8raves disease is by far the

most common etiology.

8raves disease causes unique problems that are not related to thehigh serum thyroid hormone concentrations. They include 8ravesophthalmopathy and in"ltrative dermopathy #localiBed or pretibialmy3edema$. 8raves ophthalmopathy is common in children, butless severe than in adults? dermopathy is almost never found inchildren. ost patients with 8raves hyperthyroidism have a di=usegoiter, but so do patients with other, less common causes ofhyperthyroidism, such as SHashito3icosisS #silent or painlessthyroiditis$, subacute thyroiditis, or forms of non%autoimmune

hyperthyroidism #discussed below$.

The clinical presentation and evaluation of children withhyperthyroidism and thyroto3icosis are discussed here. Treatment of hyperthyroidism is discussed separately. Hyperthyroidism presentingduring the neonatal period is discussed separately. #)ee STreatmentand prognosis of 8raves disease in children and adolescentsS andsee S'valuation and management of neonatal 8raves diseaseS$.

I9IG'9' R 8raves hyperthyroidism occurs in appro3imately 0.02

percent #DC000$ of children, mostly in the % to C%year age group(*. 8irls are a=ected more commonly than boys, at a ratio of about

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CD. The ratio is considerably lower among younger children,suggesting that estrogen secretion in some way a=ects theoccurrence of 8raves disease.

!;TH48'')I) R The pro3imate cause of 8raves hyperthyroidism

in children and adolescents, as in adults, is thyrotropin #T)H$receptor%stimulating antibodies #T6)%;b$, which activate the T)Hreceptor. ; population%based study of Ganish twins suggested thatappro3imately L0 percent of the ris+ of 8raves disease isattributable to genetic factors (2*. 8raves ophthalmopathy mayresult from antibodies against a T)H receptor%li+e protein inretroorbital connective tissue

Hashimoto&s thyroiditis

The most common cause of hypothyroidism in children andadolescents is Hashimotos thyroiditis, an autoimmune disease.Here, the bodys own immune system attac+s the thyroid gland andinterferes with the production of thyroid hormones. The onset of thiscondition can occur at any age, and the diagnosis may be easilyoverloo+ed for years, as the symptoms of hypothyroidism developvery slowly. ;s the thyroid gland becomes increasingly underactive,physical and mental changes will become more obvious.

4ften the "rst sign is that the childs growth rate decreasesune3pectedly and s+eletal development is delayed. The child may

also have an obvious swelling of the nec+ #goitre$, as the thyroidgland becomes inJamed. 4ther symptoms may emerge, such asunusual tiredness or lethargy, dry itchy s+in, increased sensitivity tocold, weight gain or generalised swelling, poor concentration,decreased energy, and constipation.

If hypothyroidism is suspected, a simple blood test is ta+en,measuring the levels of thyroid hormone and thyroid stimulatinghormone #T)H$, in the blood. The presence of thyroid antibodies#anti%thyropero3idase and anti%thyroglobulin$ is also helpful in

con"rming the diagnosis.

Treatment The treatment for Hashimotos thyroiditis in children andadolescents is the same as in adults. Thyroid hormone replacementis ta+en daily for life. The dosage of thyroid hormone needs to beage%appropriate, as the bodys demands for thyroid hormone varywith age. 6egular thyroid function tests will need to be assessed bya doctor to ensure that normal hormone levels are maintained.

Side e'ects

For those children and adolescents being treated forhypothyroidism, the results are mainly positive. The maority of their

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symptoms will disappear, and the bodys time for catch%up growthwill begin. ;n increase in bone development will also occur.However, in children who have had long%standing hypothyroidism,ultimate height potential may be partly lost. ;s the child regainsnormal thyroid function, behavioural problems may arise as their

physical and mental processes speed up. ;n increase in energy andalertness may lead to a decreased attention span and a loss ofconcentration, especially in school. Teachers should be made awareof the childs condition, as well as treatment and possible changes inbehaviour. 4ver time, any problems with behaviour, or at school, willresolve.

raes& disease

The most common cause of hyperthyroidism in children and

adolescents is an autoimmune condition called 8raves disease. In8raves disease the body produces antibodies that stimulate thethyroid gland uncontrollably, to ma+e too much thyroid hormone.9hildren can have similar symptoms to adults, although they areless li+ely to complain about them. Initially the most prominent signof this condition may be that the child displays increased energy.

They may appear hyperactive and restless, be noisier in class, andeasily distracted. This may lead to poor academic performance, andparent frustration. ; childs hyperthyroidism may not be diagnoseduntil more pronounced signs and symptoms appear. These includean enlarged thyroid gland. 4ther symptoms include a fast pulse,

nervousness, heat intolerance, weight loss, accelerated growth rate,sha+y hands, muscle wea+ness, diarrhoea, and sleep andbehavioural disturbances. Thyroid eye disease is very rare in youngchildren.

4nce a thyroid disorder is suspected, a simple blood test isperformed to measure the levels of thyroid hormones and thyroidstimulating hormone #T)H$ in the blood. The presence of thyroid%stimulating antibodies may also be helpful in con"rming thediagnosis. If test results come bac+ positive, then appropriate

treatment is commenced immediately.

Treatment Treatment of hyperthyroidism in children initially involves the use ofantithyroid drugs, such as propylthiouracil #!TK$ or carbimaBole, andif well tolerated, these may be continued for months or even years.For some children, these drugs alone stabilise their condition, andno further treatment is needed. For some, a period of bloc+ andreplace therapy #antithyroid drugs as well as thyro3ine$ 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 childs treatment, thyroid


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hormone levels will need to be monitored regularly, along with theirclinical symptoms.

Side e'ectsIn children and adolescents with 8raves disease, the main

di&culties usually occur before treatment is initiated. 4nce theircondition is under control, their physical and mental capabilitiesreturn to normal. ;ntithyroid drugs can, however, occasionally stopthe production of white blood cells or platelets. )ore throats, mouthulcers, e3cessive bruising or s+in rashes can indicate this. !atientsshould stop ta+ing their medication and see their doctorimmediately or attend the casualty department at their localhospital to test whether their blood cells or platelets are normal. 4fcourse, these symptoms are common and it is most li+ely that theyare not due to the antithyroid drugs. However, the only safe actionis to stop the medication until after the result of the blood test.

Parent inolement

!arent involvement is vital for children and adolescents receivingtreatment for their thyroid disorder. They will need to supervise theta+ing of medication on a daily basis, and carefully monitor theirchilds progress. They will also need to be aware of the signs andsymptoms of under% or over%medicating, so they can wor+ with theirdoctor to obtain the right level of medication.

;s children grow, it is important for parents to +eep close trac+ oftheir childs thyroid hormone levels, as periodic changes in dosagewill occur with changes in age. Goctors often recommend that achild have blood tests at least every / to months. )ome childrenmay have a tendency to neglect their medication regimen, and thismay lead to symptoms reappearing.

Thyroid disorders can run in families, so it is important to let yourdoctor +now of your family bac+ground. If close family membershave either hypothyroidism or hyperthyroidism, then it would be

wise to +eep a close eye on children in the family. 8irls tend to beespecially prone to developing thyroid problems, due to hormonalchanges throughout their life.

In summary, the signs and symptoms of thyroid disease are similarin children, adolescents, and adults. However, there are a few +eydi=erences that relate to growth, development and behaviour. Ifchildren are treated early and appropriately, with regularmonitoring, they will grow and develop normally, and enoy life as achild.

Hyperparathyroidism


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Ehat is hyperparathyroidism Hyperparathyroidism is caused byoveractive parathyroid glands. 4veractive parathyroid glandsproduce high levels of parathyroid hormones, which, in turn, resultsin increased levels of calcium in the blood stream. The e3cess

calcium released by the bones leads to osteoporosis andosteomalacia #both bone%wea+ening diseases$. ;nother result ofhyperparathyroidism is +idney stones, because of high levels ofcalcium e3creted into the urine by the +idneys. Hyperparathyroidismis quit rare in children. Ehat causes hyperparathyroidism 9auses of hyperparathyroidism include benign #non%cancerous$ tumors on theparathyroid glands or enlargement of the parathyroid glands. Ehatare symptoms of hyperparathyroidism ;ccording to a recent study,children with hyperparathyroidism e3perience more severesymptoms than adults. The following are the most commonsymptoms of hyperparathyroidism in children. However, each childmay e3perience symptoms di=erently. )ymptoms may includeD

• +idney pain #due to the presence of +idney stones$• diminished bone density that causes bone pain• aches and pains• abdominal pain• nausea• vomiting• fatigue• e3cessive urination• confusion

• muscle wea+ness

The symptoms of hyperparathyroidism may resemble otherconditions or medical problems. ;lways consult your childs

physician for a diagnosis. How is hyperparathyroidismdiagnosed In addition to a complete medical history and physicale3amination, diagnostic procedures for hyperparathyroidism mayincludeD

• bone 3%rays % a diagnostic test which uses invisibleelectromagnetic energy beams to produce images of internaltissues, bones, and organs onto "lm.

• laboratory tests #to measure calcium and parathyroidhormone levels$

Treatment for hyperparathyroidismD )peci"c treatment forhyperparathyroidism will be determined by your childs physician

based onD• your childs age, overall health, and medical history


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• e3tent of the disease• your childs tolerance for speci"c medications, procedures, or

therapies• e3pectations for the course of the disease• your opinion or preference

Treatment may include removal of parathyroid tissue.

*eractie %drenal lands(Cushing&s Syndrome)Ehat are overactive adrenal glands

Ehen adrenal glands produce e3cessive amounts of certain

hormones, they are called overactive. )ymptoms and treatmentdepend on which hormones are being overproduced, including thefollowingD

• androgenic steroids #androgen hormones$ % an overproductionof androgenic steroids #such as testosterone$ can lead toe3aggerated male characteristics in both men and women,such as e3cess hair on the face and body, baldness, acne,deeper voice, and increased muscle mass. If a female fetus ise3posed to high levels of androgens early in pregnancy, hergenitals may develop abnormally. oung boys who e3perience

high levels of androgen levels may grow faster, but bones mayalso mature faster and stop growing too soon.

• corticosteroids % an overproduction of corticosteroids can leadto 9ushings syndrome #see below$.

• aldosterone % an overproduction of the aldosterone hormonecan lead to high blood pressure and to those symptomsassociated with low levels of potassium #i.e., wea+ness,muscle aches, spasms, and, sometimes, paralysis.$

The symptoms of overactive adrenal glands may resemble otherproblems or medical conditions. ;lways consult your childs

physician for a diagnosis.

How are overactive adrenal glands diagnosed

In addition to a complete medical history and physical e3amination,diagnostic procedures for overactive adrenal glands may includeD

• speci"c blood tests #to measure levels of hormones$

• urine tests #to measure levels of hormones$

Treatment of overactive adrenal glandsD


19/33

• your childs age, overall health, and medical history• e3tent of the disease• your childs tolerance for speci"c medications, procedures, or

therapies• e3pectations for the course of the disease

• your opinion or preference Treatment may include surgical removal of growths on the adrenalgland#s$, or the adrenal gland#s$ itself. edications that bloc+ thee3cessive production of certain hormones may also be administered.

Ehat is 9ushings syndrome

9ushings syndrome is a myriad of abnormalities that are the resultof hypersecretion of corticosteroids by the adrenal corte3. ;noverproduction of cortisol, the hormone that controls the adrenal

gland, by the pituitary gland, which stimulates the adrenal glands toproduce corticosteroids, may be one cause. In addition, certain lungcancers and other tumors outside the pituitary gland may producecorticotropins. 4ther causes include benign #non%cancerous$ orcancerous tumors on the adrenal glands. 9ushings syndrome is rarein children and more commonly seen in adults.

Ehat are the symptoms of 9ushings syndrome

The following are the most common symptoms of 9ushingssyndrome. However, each child may e3perience symptomsdi=erently. 9hildren and adolescents with 9ushings syndromeprimarily e3perience weight gain, growth retardation, andhypertension #high blood pressure$. )ymptoms may includeD

• upper body obesity• round or moon%shaped face• increased fat around nec+• thinning arms and legs• fragile and thin s+in• dar+ened pigmentation of the s+in•

acne• bruising• stretch mar+s on abdomen, thighs, buttoc+s, arms, and

breasts• bone and muscle wea+ness• severe fatigue• high blood sugar• irritability and an3iety• e3cessive hair growth in females• irregular or stopped menstrual cycles in females

• reduced se3 drive and fertility in males The symptoms of 9ushings syndrome may resemble other


20/33

conditions or medical problems. ;lways consult your childsphysician for a diagnosis.

How is 9ushings syndrome diagnosed

In addition to a complete medical history and physical e3amination,diagnostic procedures for 9ushings syndrome may includeD

• 3%ray % a diagnostic test which uses invisible electromagneticenergy beams to produce images of internal tissues, bones,and organs onto "lm.

• 2@%hour urinary test #urine is collected over a 2@%hour periodto measure for corticosteroid hormones$

• computeriBed tomography scan #;lso called a 9T or 9;T scan.$% a diagnostic imaging procedure that uses a combination of 3%rays and computer technology to produce cross%sectional

images #often called slices$, both horiBontally and vertically, of the body. ; 9T scan shows detailed images of any part of thebody, including the bones, muscles, fat, and organs. 9T scansare more detailed than general 3%rays.

• magnetic resonance imaging #6I$ % a diagnostic procedurethat uses a combination of large magnets, radiofrequencies,and a computer to produce detailed images of organs andstructures within the body.

• de3amethasone suppression test #to di=erentiate whether thee3cess production of corticotropins are from the pituitarygland or tumors elsewhere$

• corticotropin%releasing hormone #96H$ stimulation test #todi=erentiate whether the cause is a pituitary tumor or anadrenal tumor$

Treatment for 9ushings syndromeD

)peci"c treatment for 9ushings syndrome will be determined byyour childs physician based onD

• your childs age, overall health, and medical history• the e3tent of the disease• your childs tolerance for speci"c medications, procedures, or

therapies• e3pectations for the course of the disease

• your opinion or preference Treatment for 9ushings syndrome depends on its cause. )urgerymay be needed to remove tumors of the adrenal glands.

%ddison&s disease


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;ddisons disease #chronic adrenal insu&ciency$ is a rare andprogressive disorder that a=ects between one and si3 in every00,000 people. It a=ects people of both se3es and all ages.

The human body has two adrenal glands, one on top of each +idney. These glands form part of the endocrine system, which wor+s withthe nervous system and the immune system to help the body copewith di=erent events and stresses. ;ddisons disease is caused bythe inability of the adrenal glands to ma+e su&cient amounts ofregulating hormones.

;drenaline is the most well +nown of the hormones that aresecreted by the adrenal glands, in the adrenal medulla #the centralpart of the gland$. The adrenal corte3 #the outer part$ also producesimportant hormones, the corticosteroids. They include cortisol,aldosterone and supplementary se3 hormones. In a person with;ddisons disease, only the adrenal corte3 is a=ected. The personcannot produce enough glucocorticoid or cortisol and, occasionally,also fails to produce su&cient mineralocorticoid or aldosterone.

Causesost cases of ;ddisons disease are caused by an autoimmuneresponse that attac+s and damages the adrenal glands over time.4ther causes includeD

• Infection• 9ancer• )urgical removal of particular tumours in the adrenal or

pituitary glands or the hypothalamus.

Symptoms The symptoms of ;ddisons disease can include any or all of thefollowingD

• 7oss of appetite and weight.• ausea, vomiting or diarrhoea.• uscle wea+ness.• 9hronic, worsening fatigue.• 7ow blood pressure.• )alt cravings.• Gehydration.• Hypoglycaemia, or low blood sugar levels #especially in

children$.• Increased pigmentation of the s+in, particularly around scars

and bony areas.• Irregular or no menstrual periods in women.•

ood swings, mental confusion or loss of consciousness.


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These symptoms can develop quic+ly #especially in children andteenagers$, or progress slowly for 20 years or more. anysymptoms can mimic other diseases, so diagnosis can be delayed.

The hormone cortisol

9ortisol is produced by the outer layer of the adrenal gland, calledthe adrenal corte3. The quantities of cortisol released by the adrenalglands are closely monitored by the master gland of the endocrinesystem, the pituitary, which is located in the brain. The wor+ings ofthe pituitary are governed by another brain structure, thehypothalamus. Ehen cortisol levels are too low, the pituitarysecretes the stimulating hormone adrenocorticotropin #;9TH$.9onversely, high levels of cortisol prompt the pituitary to decrease;9TH secretion, which slows cortisol production.

9ortisol plays many vital roles and is essential to many bodyfunctions because itD

• Eor+s with adrenaline to help the body manage physical andemotional stress.

• 9onverts protein into glucose to boost Jagging blood sugarlevels.

• Eor+s in tandem with the hormone insulin to maintainconstant blood sugar levels.

• 6educes inJammation.• Helps the body maintain a constant blood pressure.• Helps the wor+ings of the immune system.

The hormone aldosterone;ldosterone is a mineralocorticoid, also produced by the adrenalcorte3. The amount of aldosterone in the body is monitored by the+idneys, which secrete hormones to increase or decreasealdosterone production. ;ldosterone regulates electrolytes #such assodium and potassium$ in the blood. This helps to maintain bloodpressure and heart function. If too much sodium is e3creted by the+idneys, a considerable amount of body Juid is also lost. Thisreduces blood volume and drops blood pressure. Too much or toolittle potassium can a=ect the way the heart functions.

Primary adrenal insu+ciency;ddisons disease can occur gradually, and is de"ned whenappro3imately :0 per cent of the adrenal gland#s$ is damaged. Thisis +nown as primary adrenal insu&ciency. ;round seven out of 0cases of ;ddisons disease are caused by an autoimmune response,where the bodys own immune cells attac+ and destroy the adrenalglands. In some cases, other glands of the endocrine system area=ected by an autoimmune response, in a condition calledpolyendocrine de"ciency syndrome.

Polyendocrine de,ciency syndrome


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There are two types of this disorder and both types tend to run infamiliesD

• Type I % is more common in children. )ymptoms includeunderactive parathyroid, pernicious anaemia, recurringcandida infections, chronic active hepatitis and slow se3ual

development.• Type II % #)chmidts syndrome$ is more common in younger

adults. )ymptoms include underactive thyroid, diabetesmellitus and slow se3ual development.

4ther conditions related to primary ;ddisons disease areD• %drenomyeloneuropathy (%-) % which can occur in some

adults. It a=ects the spine, and is degenerative over time.• %drenoleukodystrophy (%./) % which occurs #rarely$ in

some children #one in 00,000$, especially males. It can causebrain damage and can be fatal. )urvivors often develop ;.

Treatment for primary ;ddisons disease is with glucocorticoid andmineralocorticoid replacement for life.

Secondary adrenal insu+ciency)ometimes, ;ddisons disease is caused by the pituitary glandsinability to produce su&cient amounts of ;9TH, which means theadrenal glands arent prompted to secrete cortisol. This is +nown assecondary adrenal insu&ciency. 9auses may includeD

• Some medications % inJammatory disorders, such as

rheumatoid arthritis and asthma, are often treated withprolonged or high dose steroids #glucocorticoid replacements$.If the dose is suddenly stopped, or not reduced by appropriatetapering measures, the pituitary gland may respond by failingto produce enough ;9TH. This situation can sometimes bereversed.

• Cushing&s disease % a benign tumour of the pituitary glandthat produces ;9TH. This results in too much cortisol beingproduced. Treatment requires surgical removal of the tumourand, in some cases, removal of damaged adrenal gland#s$.

• *ther causes % infections, reduced blood Jow, radiotherapy

and some neurosurgery can damage the pituitary gland orhypothalamus, and decrease ability to produce ;9TH.

Treatment for secondary ;ddisons disease is with glucocorticoidreplacement only.

%ddisonian crisis; sudden, acute worsening of symptoms is +nown as an ;ddisoniancrisis. It can be caused byD

• 0$treme stress % an accident, e3cessive heat or physical

e3ertion.


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• Seere illness % especially dehydration from vomiting ordiarrhoea.

• Sudden shock % for e3ample, the death of a signi"cantperson.

The symptoms of ;ddisonian crisis includeD• Aiolent pain in the abdomen, bac+ and legs.• ausea, vomiting or diarrhoea.• 7ow blood pressure, low blood sugar, high potassium, low

sodium and a rapid heart rate.• !ossible mental confusion and loss of consciousness.

!rompt emergency hospital treatment must be sought, includingintravenous Juids, increased steroid medication and saline. any;ddisonians wear a medical alert bracelet or pendant withinformation and identi"cation, and carry a hydrocortisone inectablefor use in emergencies. They will still need hospitalisation andongoing monitoring.

If untreated, an ;ddisonian crisis can be fatal.

/iagnostic toolsGiagnosis of ;ddisons disease may involveD

• 9omplete detailed family history, with special attention to anyother endocrine disorders.

• 5iochemical tests, which measure cortisol levels before and

after a challenge inection of synthetic ;9TH, +nown as ashort synacthen test. ; long synacthen test is done overseveral days in hospital. )ynacthen tests will indicate thepersons baseline level of cortisol production and theirresponse to an increased need for cortisol in the body. ;n;ddisonian may show a Jat or reduced response.

• 5lood electrolyte and plasma renin tests will indicate if there isa need for mineralocorticoid replacement.

• ;nti%adrenal antibody test. If the result is positive, primary;ddisons disease is de"nitively diagnosed. However, even ifthese antibodies do not e3ist, the person may still have

;ddisons disease.• -%rays, ultrasounds and 9;T scans of the abdominal region to

chec+ for visual signs of damage and the siBe of adrenalglands.

Treatment options Treatment aims to bolster or replace insu&cient or absent steroidcomponents. 8lucocorticoid replacement is essential for primaryand secondary ;ddisonian patients, and must be ta+en for life.

Treatment shouldD•

5e tailored to each person over the course of their life.


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• 5e altered, in consultation with a doctor, during illness orother stressful events.

• ;llow for the di=erent needs of children and young adults.

1here to get help • our doctor• 'ndocrinologist• ;ustralian ;ddisons Gisease ;ssociation Tel. #02$ C2 @>

Things to remem"er • ;ddisons disease is a progressive disorder, characterised by

the inability of the adrenal glands to produce su&cienthormones.

• 9auses can include infection, damage, and an autoimmuneresponse that prompts the immune system to attac+ anddestroy the adrenal glands.

• Treatment includes steroid replacement therapy that must bemanaged for life.

• ;n ;ddisonian crisis can be fatal unless treated quic+ly andappropriately.

•

IGG is a polygenic disorder. The maor locus is H7; #humanleu+ocyte antigen$ region short arm of chromosome . This locus isreferred to as IGG.

• 0nironmental 2actors < they are relatively low in numbers.Airal infection in%utero is consistent with observation thatincidence of IGG increased in children with congenitalrubella. Ig antibodies against 9o3sac+ieUs virus have beenfound in 2C%/01 of new cases, suggesting recent infection.

• /ietary 2actors % a positive association between IGG, highprotein inta+e and frequency of consumption of foodscontaining nitrosamine is seen in close control studies.

Pathogenesis

1. %uto3immunity < islets of newly diagnosed persons showhistological picture of mar+ed mononuclear cell in"ltrationaround islets.

2. Islets cell anti"odies #I9;$ < they are present in L01 casesof children at the time of diagnosis. 7ong term follow up hasshown that family members with I9; are at increased ris+ ofprogression to G.

3. B cell destruction < this process is slow with patchy

histological appearance in newly diagnosed persons. 9linical


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onset of diabetes does not occur until :01 of cells have beendestroyed.

Clinically % children with complaints of polyuria, intense thirst,nocturia, polyphagia, weight loss, wea+ness, lassitude, leg cramps

and leg cramps. )ome children have a stormy onset and see+medical aid for "rst time with symptoms of +etoacidosis, such aspersistent enuresis, abdominal pain, vomiting, dehydration,prostration, drowsiness and even coma. 9haracteristic features ofIGG includeD

• )evere insulin de"ciency.• ;brupt onset of severe symptoms.• Tendency to +etoacidosis.• Gependence on e3ogenous insulin to sustain life.

Complications o2 dia"etes in Children4

• ;cuteD +etoacidosis, coma and lactic acidosis.• )ub%acuteD infection either bacterial or fungal involving s+in

mucosa, soft tissue, lungs #tuberculosis$ and urinary tractinfection.

• 9hronicD arteriosclerosis, retinopathy, polyneuropathy,diabetic neuropathy, delayed development of secondaryse3ual characters.

/iagnosis < through urine sugar and blood sugar level e3aminationand oral glucose tolerance test.anagement < main line management includes diet and insulin.

%ims o2 managing dia"etes in children4

. To maintain ideal body weight essential to preserve optimalinsulin sensitivity.

2. To maintain long term nutritional balance for normal growthand development in children.

/. To time meal and snac+s to prevent wide swings in 5)7especially because these persons have to be managed withinsulin.

@. To maintain 5)7 and avoid complications.

Total calorie inta+e should be according to ideal body weight #I5E$of child, calculated as I5E #in +gs$ V #height in cms %00$ 3 0.:

9hildren need baseline calories of 000, plus 00 calories #for girls$and 2C calories #for boys$ per year of age up to 2 yrs.

Gistribution of total calories into various nutrients isD

http://www.tandurust.com/weight-loss-diet/how-much-should-i-weigh.htmlhttp://www.tandurust.com/weight-loss-diet/how-much-should-i-weigh.html


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• 9arbohydrate < 0 to C1 of total calories• !roteins%C to 201 of total calories• Fats%C to 2C1 of total calories

Car"ohydrates supply @ calgm of cereals, roots and pulses rich in

comple3 carbohydrates are preferred and diet with low glycaemicinde3 are preferred.Proteins < most amino acids are glucogenic. They decreaseglucagon secretion as well. It supplies @ cal per gram. Its inta+emust be restricted in diabetic nephropathy.Fats supply : cal per gram. It must not e3ceed 201 of total calorieinta+e.

ynecomastia

!rograms related to this topic

6eproductive 'ndocrine!ractice

;dolescentoung ;dult edical!ractice

5reast 9linic

1hat is gynecomastia5

8ynecomastia is a condition in which above average amounts of"rm breast tissue form in males. The breast tissue is usually lessthan 2 inches across and is located directly under either one nippleor both nipples.

Ho6 common is gynecomastia5

8ynecomastia is not unusual or abnormal in adolescent boys. Temporary breast enlargement often happens during adolescencewhen there are hormonal changes.

1hat causes gynecomastia5

8ynecomastia is usually caused by changes in hormones duringpuberty or as part of aging, possibly by changes in the balance ofthe two hormones, estrogen and testosterone.

In rare cases, gynecomastia can be caused by prescription drugs,over%the%counter medicines, illegal drugs #such as mariuana andsteroids$ or tumors.

8ynecomastia can also be caused by certain genetic disorders andconditions #such as Wlinefelter )yndrome$.

http://www.childrenshospital.org/clinicalservices/Site1906/mainpageS1906P0.htmlhttp://www.childrenshospital.org/clinicalservices/Site1906/mainpageS1906P0.htmlhttp://www.childrenshospital.org/clinicalservices/Site1847/mainpageS1847P0.htmlhttp://www.childrenshospital.org/clinicalservices/Site1847/mainpageS1847P0.htmlhttp://www.childrenshospital.org/clinicalservices/Site2284/mainpageS2284P0.htmlhttp://www.childrenshospital.org/clinicalservices/Site1906/mainpageS1906P0.htmlhttp://www.childrenshospital.org/clinicalservices/Site1906/mainpageS1906P0.htmlhttp://www.childrenshospital.org/clinicalservices/Site1847/mainpageS1847P0.htmlhttp://www.childrenshospital.org/clinicalservices/Site1847/mainpageS1847P0.htmlhttp://www.childrenshospital.org/clinicalservices/Site2284/mainpageS2284P0.html


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Is gynecomastia physically harm2ul5

8ynecomastia is not physically harmful, although it can occasionallyindicate more serious underlying conditions. 4ccasionally, maleswith gynecomastia e3perience tenderness that can be treated with

medications. ales with gynecomastia usually e3periencepsychological and social issues rather than physical problems.

1hat are the psychological e'ects o2 gynecomastia5

8ynecomastia can have a maor emotional impact on males and caninclude feelings of shame, embarrassment and depression. aleswith gynecomastia often hide their chests in public or withdrawsocially and avoid discussing their concerns with parents and peers.

1hat is the treatment 2or gynecomastia5

In most cases, no treatment is needed for gynecomastia. In :0percent of teenage boys, gynecomastia goes away in less than threeyears. ; physician should still monitor the condition every fewmonths.

For the remaining 0 percent of males who continue to havegynecomastia, treating the underlying cause may improve thecondition. If medications are causing gynecomastia, they may bestopped or changed. In overweight males, weight loss sometimeshelps remedy gynecomastia. ;n evaluation by an e3perienced

plastic surgeon is often suggested because cosmetic surgery cansurgically remove the breast tissue. )ome males choose to live withthe condition.

%menorrheaEhat is amenorrhea

;menorrhea is a menstrual condition characteriBed by absentmenstrual periods for more than three monthly menstrual cycles.

;menorrhea may be classi"ed as primary or secondary.

• primary amenorrhea % from the beginning and usually lifelong?menstruation never begins at puberty.

• secondary amenorrhea % due to some physical cause andusually of later onset? a condition in which menstrual periodswhich were at one time normal and regular become increasingabnormal and irregular or absent.

Ehat causes amenorrhea

There are several possible causes of amenorrhea, including thefollowingD


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• pregnancy % Females no longer ovulate when they arepregnant, thus, menstruation ceases temporarily.

• ovulation abnormality % 4vulation abnormalities are usuallythe 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 bythe age of , a birth defect, anatomical abnormality, or othermedical condition may be suspected.

• eating disorder % Females with anore3ia nervosa #or simplyanore3ia$ andor bulimia nervosa #or simply bulimia$ oftene3perience amenorrhea as a result of maintaining a bodyweight that would be too low to sustain a pregnancy. ;s aresult, as a form of protection for the body, the reproductivesystem Sshuts downS because it is severely malnourished.

• over%e3ercise or strenuous e3ercise % any young femaleathletes in training e3perience absent menstrual cycles due tolow body fat content.

• thyroid disorder % In many cases, an underactive thyroid gland#a condition called hypothyroidism in which the thyroid glandis producing insu&cient amounts of the thyroid hormone$ oran overactive thyroid gland #a condition calledhyperthyroidism in which the thyroid gland secretes too muchthyroid hormone % resulting in too much thyroid hormone inthe bloodstream and overactivity of the bodys metabolism$ is

responsible for the absent menstrual cycles.

• obesity % Females who are obese often e3perience amenorrheaas a result of e3cess fat cells interfering with the process ofovulation.

How is amenorrhea diagnosed

Giagnosis begins with a gynecologist evaluating a females medicalhistory and a complete physical e3amination including a pelvice3amination. ; diagnosis of amenorrhea can only be certain whenthe physician rules out other menstrual disorders, medical

conditions, or medications that may be causing or aggravating thecondition. In addition, a diagnosis of amenorrhea requires that afemale has missed at least three consecutive menstrual cycles,without being pregnant. oung women who have not had their "rstmenstrual period by the age of C should be evaluated promptly, asma+ing an early diagnosis and starting treatment as soon aspossible is very important.

Treatment for amenorrheaD

)peci"c treatment for amenorrhea will be determined by your

physician based onD


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• your age, overall health, and medical history• e3tent of the condition• cause of the condition #primary or secondary$• your tolerance for speci"c medications, procedures, or

therapies• e3pectations for the course of the condition

• your opinion or preference Treatment for amenorrhea may includeD

• progesterone supplements #hormone treatment$• oral contraceptives #ovulation inhibitors$

• dietary modi"cations #to include increased caloric and fatinta+e$

In most cases, physicians will induce menstruation in non%pregnantfemales who have missed two or more consecutive menstrualperiods, because of the danger posed to the uterus if the non%fertiliBed egg and endometrium lining are not e3pelled. Eithout thismonthly e3pulsion, the ris+ of uterine cancer increases.

Causes o2 Secondary amenorrhea in children

. /%hydro3ysteroid dehydrogenase de"ciency

; ver rare form of congenital adrenal hyperplasia involving ade"ciency of /%hydro3ysteroid dehydrogenase which resultsin reduced production of adrenal steroids #mineralocorticoids,se3 steroids and glucocorticoids$. The disorder can occur inclassical...read more X2. ;drenal 9ancer ; malignant cancer that develops in the adrenal gland. Thetumor may be nonfunctioning #does not produce hormones$ orfunctioning in which case e3cessive levels of hormones cancause a variety of symptoms depending on which hormone isinvolved. ;drenal ho...read more X

/. ;nore3ia ervosa ; disorder where a distorted sense of body image leads toself%starvation to the point of death in some cases....readmore X@. 9hiari%Frommel syndrome ; rare condition where galactorrhea and amenorrheacontinues for an abnormal length of time #generally longerthan months$ after giving birth....read more XC. 9ushings syndrome ; rare syndrome where e3cessive secretion of corticosteroids

by the adrenal corte3 leads to a variety of symptoms.Hormone%secreting adrenal or pituitary tumors are often the

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cause of the e3cessive corticosteroid secretion....read more X. 'motional stress ; condition which occurs when a person is under stressa=ecting their emotions...read more X>. Hyperprolactinemia

High levels of prolactin in the blood....read more XL. Hyperthyroidism % Teratogenic ;gent There is strong evidence to indicate that the development ofhyperthyroidism during pregnancy may have a teratogenice=ect on the fetus. ; teratogen is a substance that can causebirth defects. The li+elihood and severity of defects may bea=ected by th...read more X:. 7actotroph adenoma ; benign pituitary tumor that secretes e3cessive prolactinwhich can a=ect the functioning of the reproductive system %testes and ovaries. The tumor may also grow large enough tocompress adacent structures such as the eye nerves....readmore X0. 4besity ;n increase in the body weight greater than that required fornormal function that is characterised by the accumulation ofe3cessive fats

Teen Health Conditions and

/iagnoses

/ysmenorrhea

1hat is dysmenorrhea5

Gysmenorrhea is a menstrual condition characteriBed by severe andfrequent menstrual cramps and pain associated with menstruation.Gysmenorrhea may be classi"ed as primary or secondary.

• !rimary Gysmenorrhea is classi"ed as recurrent, crampy,lower abdominal pain that occurs during menstruation in the

absence of other medical problems. The pain usually occursform days %2 before onset of menses to days 2%/ of

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menstruation. It is the most common gynecologic complaint inadolescent females.

• )econdary Gysmenorrhea is painful menstruation caused by agynecologic abnormality. This is more common in adults intheir fourth and "fth decades of life.

1hat causes dysmenorrhea5

In primary dysmenorrhea, the cause is over production ofprostaglandin < a hormone li+e compound found in the body. Thiscompound increases monthly during the menstrual cycle and causescontraction of the muscles in the uterus resulting in pain. In somepeople this compound a=ects the gastrointestinal tract causingsymptoms such as nausea and vomiting.

1hat are the symptoms5

The most common symptoms of dysmenorrhea areD

• 9ramping in the lower abdomen• !ain in lower abdomen• 7ow bac+ pain• !ain radiating down the legs

4ther symptoms that may be present includeD

• ausea• Aomiting• Giarrhea• Fatigue• Eea+ness• Fainting• Headaches

Ho6 is dysmenorrhea treated5

Treatment is based on many factors and is best if determined withyour health care provider. There are non%pharmacologicaltreatments that perform well in the control of dysmenorrhea.

These treatments includeD

• Heat < via a heating pad or bathing• ;bdominal massage• 6egular e3ercise

!harmacologic treatments that can achieve pain relief includeD

• on%steroidal anti%inJammatory drugs #);IGs$


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• Tylenol• 4ral contraceptive pills• 7ong%acting hormonal contraceptives

Gysmenorrhea is a very common gynecological condition. ; good

treatment plan can help achieve optimal pain relief during monthlymenstrual cycles. 9oordination with a health care provider can helpdetermine if other problems e3ist and to "nd the most e=ectivetreatment options available.

endocrine&metab disorders

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