Updated: Apr 21, 2022
Author: Robert P Hoffman, MD; Chief Editor: Sasigarn A Bowden, MD 


Practice Essentials

The pituitary gland is called the master endocrine gland of the body because it controls the function of other endocrine organs. The anterior pituitary produces the hormones thyrotropin (thyroid-stimulating hormone [TSH]), corticotropin (adrenocorticotropic hormone [ACTH]), luteinizing hormone (LH), follicle-stimulating hormone (FSH), growth hormone (GH), and prolactin (PRL). The anterior pituitary is controlled by specific hypothalamic-releasing hormones. The posterior pituitary produces vasopressin (antidiuretic hormone [ADH]) and oxytocin.

Panhypopituitarism is a condition of inadequate or absent production of the anterior pituitary hormones. It is frequently the result of other problems that affect the pituitary gland and either reduce or destroy its function or interfere with hypothalamic secretion of the varying pituitary-releasing hormones. Panhypopituitarism can be the end result of various clinical scenarios. The signs and symptoms are diverse. Manifestations that suggest congenital anterior hypopituitarism include micropenis, midline defects, optic atrophy, hypoglycemia, and poor growth.[1, 2, 3]

See the image below.

Pathophysiology of panhypopituitarism. Pathophysiology of panhypopituitarism.

Diagnosis and management

The diagnostic evaluation of a child with hypopituitarism is divided into 2 portions: recognition of the hormonal deficiencies and determination of the cause. Genetic testing is available at various commercial and academic laboratories for mutations associated with hypopituitarism.

Cortisol deficiency requires prompt recognition and treatment. This is particularly true for the child who may be facing surgery or experiencing other significant stresses related to the cause of hypopituitarism.

In TSH deficiency, the dose of L-thyroxine replacement is age dependent. In cases of gonadotropin deficiency, sex steroid replacement should begin at puberty, while in GH deficiency, GH replacement doses should be administered in doses of 0.18-0.3 mg/kg/wk subcutaneously, divided in 6-7 doses. Higher doses of up to 0.7 mg/kg/wk may be beneficial in puberty.

Surgical treatment should be used for operable pituitary and hypothalamic tumors.


The effects of hypopituitarism in children depend on the affected hormones. GH deficiency can result in hypoglycemia and short stature. Gonadotropin deficiency leads to prenatal micropenis and delayed or interrupted puberty in older children. Corticotropin deficiency interferes with normal carbohydrate, protein, and lipid metabolism and may result in weight loss, hypoglycemia, fatigue, hypotension, and death. Thyrotropin deficiency leads to hypothyroidism.


US frequency

Hypopituitarism is caused by various conditions and is associated with various hormonal deficiencies. Thus, data are limited regarding frequency rates of the various etiologies and components. An Italian study reported GH deficiency prevalence to be approximately 9 cases per 1000 individuals in a pediatric population.[4] Data from the Northwest Regional Screening program estimate the frequency of congenital TSH deficiency at 1 case per 29,000 live births.[5]


A study by Kao et al indicated that adults with childhood-onset multiple pituitary hormone deficiencies (COMPHD) have a significantly worse quality of life than do healthy adults. Compared with healthy controls, adults with COMPHD were shorter and more overweight, had less education, were less likely to be married, and had a higher unemployment rate, lower incomes, and fewer children. They also scored lower on the Female Sexual Function Index and Male Sexual Quotient.[6]




Congenital hypopituitarism

Suspect hypopituitarism in children with midline defects or optic atrophy (suggestive of septo-optic dysplasia)[7, 8] and in boys with micropenis (suggestive of gonadotropin deficiency).[9, 10]

Evaluate hypopituitarism prior to the development of overt problems due to hormonal deficiencies.

Infants with hypopituitarism without such abnormalities present in various ways. For example, children with severe growth hormone (GH) deficiency and adrenocorticotropic hormone (ACTH) deficiency may develop hypoglycemia, which leads to the diagnosis.

Another presentation is hypernatremic dehydration due to diabetes insipidus. Accompanying cortisol deficiency may obscure diabetes insipidus because cortisol is necessary to excrete a free water load.[11]

Some infants come to medical attention because of low thyroid hormone concentrations discovered on neonatal thyroid screen. Children with milder defects present with poor growth at varying ages. The symptoms include fatigue, dry skin, and constipation due to thyroid-stimulating hormone (TSH) deficiency and concomitant hypothyroidism and/or nausea, vomiting, and malaise due to ACTH and cortisol deficiency.

Acquired hypopituitarism

Similar to children with congenital hypopituitarism, many children with acquired hypopituitarism are identified before symptoms are observed.

Pituitary function should be routinely evaluated before and after treatment in children with craniopharyngiomas or other hypothalamic or pituitary tumors. The same is true for children who have received cranial irradiation (eg, before bone marrow transplant or for cranial tumors).

Children without a known hypothalamic or pituitary insult with hypopituitarism frequently present with growth failure because of GH deficiency. Some children come to medical attention because of abnormal thyroid function test results suggestive of central hypothyroidism.

Older children may present because of absent or interrupted puberty. Girls may have primary or secondary amenorrhea.

Polyuria and polydipsia due to central diabetes insipidus may also be a presenting symptom.

Rarely, patients with ACTH deficiency may present with hyponatremia. This is not due to mineralocorticoid deficiency because aldosterone secretion is not primarily under pituitary control but is likely due to excess vasopressin release because (as mentioned above) cortisol helps the body excrete a free water load and circulating intravascular volume is depleted in cortisol deficiency.[11]



Evaluate a newborn with midline defects of the nose, lip, teeth, or mouth.

Evaluate the pituitary function in a newborn with nystagmus and optic nerve atrophy on funduscopic examination.

Hypogonadotrophism is suggested in the male with a small, normally shaped penis and small testes.

Hypopituitarism leading to ambiguous genitalia has been reported.

The child with hypoglycemia secondary to hypopituitarism is irritable, jittery, or lethargic. Seizures may be present.

Older children

The most common presenting feature suggestive of hypopituitarism is growth failure with decreased growth rate for age.

Examine optic disks for papilledema and visual fields for bilateral hemianopsia, a sign of optic chiasm compression. These findings quickly suggest the possibility of a craniopharyngioma, other pituitary tumor, or a hypothalamic tumor.

Assessing the child's sexual maturation is also important.


Congenital hypopituitarism

Congenital midline defects, such as septo-optic dysplasia (de Morsier syndrome), midline facial clefts, or single central incisors, may be accompanied by varying anterior pituitary deficiencies.[8] Three fourths of individuals with optic nerve hypoplasia have hormonal abnormalities.[12]

Mutations in various genes (HESX1, LHX3, LHX4, PROP1, POU1F1 [formerly known as PIT1]) have been demonstrated to cause congenital pituitary abnormalities, with varying combinations of one or more hormonal abnormalities occurring with or without anatomic abnormalities. These homeobox genes code various pituitary transcription factors responsible for pituitary development.[13, 14, 15, 16, 17]

Neonatal hypopituitarism, although not truly congenital, may also result from severe asphyxia either at birth or shortly thereafter.

Acquired hypopituitarism

Acquired hypopituitarism frequently occurs as a result of hypothalamic or pituitary tumors and their surgical or radiologic treatment. Craniopharyngiomas, pituitary dysgerminomas, and optic gliomas are particularly common causes of hypopituitarism.[18]  Indeed, a retrospective study by Wijnen et al indicated that compared with adult-onset craniopharyngioma, the childhood-onset form of the disease is more often associated with panhypopituitarism, as well as GH deficiency, diabetes insipidus, morbid obesity, epilepsy, and psychiatric disorders.[19]

Other causes of hypopituitarism include trauma and autoimmune lymphocytic hypophysitis.[20, 21, 22, 23] Hormonal abnormalities are noted in 25% of adults with traumatic brain injury (TBI).[24]

In a study of hypopituitarism in 14 children who had survived moderate to severe inflicted TBI (iTBI), Auble et al determined that 86% had endocrine dysfunction, with 50% having at least two abnormalities. The most common abnormality was elevated prolactin (64%), with patients also showing abnormal thyroid function (33%), short stature (29%), and reduced growth hormone peak (17%).[25]

A retrospective study by You et al indicated that in patients with TBI, longer stay in the intensive care unit (ICU) and intracranial hypertension are independent risk factors for posttraumatic anterior hypopituitarism (odds ratios of 1.253 and 3.206, respectively).[26]

A study by Lin et al found that among other complications and comorbidities, transfrontal surgery for pediatric craniopharyngioma leads to a slightly higher frequency of panhypopituitarism than does the transsphenoidal technique (8% vs 5%, respectively). However, a greater incidence of cerebrospinal fluid leak was associated with the transsphenoidal operation.[27]

A study by van Iersel et al indicated that in patients with craniopharyngioma, panhypopituitarism occurs less frequently with partial resection than with gross total resection.[28]





Laboratory Studies

The diagnostic evaluation of a child with hypopituitarism is divided into 2 portions: recognition of the hormonal deficiencies and determination of the cause. Genetic testing is available at various commercial and academic laboratories for mutations associated with hypopituitarism.

Thyroid-stimulating hormone (TSH) deficiency

Hypothyroidism secondary to TSH deficiency is the easiest of the hormonal abnormalities to diagnose. Children have decreased free thyroxine (T4) levels and TSH levels that are within the reference range or low. Occasionally, a child with hypothalamic hypopituitarism may have a mildly elevated TSH level.

Test any child with TSH deficiency for adrenal function prior to T4 replacement. Correction of hypothyroidism without appropriate cortisol replacement can precipitate an adrenal crisis. This is most likely because of accelerated cortisol metabolism upon thyroid hormone treatment.

Adrenocorticotropic hormone (ACTH) deficiency

Testing for ACTH deficiency is more complex. The key element is not the basal cortisol level present but the response to stress.

In the past, the most frequently used test was the intravenous ACTH stimulation test. In this test, 250 mcg of ACTH 1-24 (Cortrosyn) is administered as an intravenous bolus with measurements of cortisol at 0 minutes, 30 minutes, and 60 minutes. This test has a high specificity. A peak cortisol level below 18 mcg/dL is suggestive of cortisol deficiency either because of ACTH deficiency or because of primary adrenal disease. The test has low sensitivity. Many patients with ACTH deficiency as determined by insulin tolerance test results have responses over 18 mcg/dL. Because of its ease of performance, it may be a reasonable first test but a result within the reference range should never be accepted as an indication of ACTH sufficiency.[29]

A low-dose 1-mcg ACTH stimulation test can be used to increase the specificity of the high-dose test. Results of the 1-mcg test correspond well with results from insulin-induced hypoglycemia. The low dose of ACTH does not stimulate cortisol production in an unprimed adrenal gland. However, care must be taken in diluting the ACTH to obtain the 1-mcg dose.[30]

The insulin tolerance test is much more sensitive and equally specific for ACTH deficiency but entails significant risks. Draw a baseline cortisol level and administer insulin (0.075-0.1 U/kg intravenously). Blood is obtained every 15 minutes for 1 hour to measure cortisol and glucose levels. For the test to be adequate, the plasma glucose level should decrease to less than 45 mg/dL. This usually happens at the 15-minute sample. The plasma cortisol level should increase to more than 18 mcg/dL, or at least double, in response to hypoglycemia.[29]  Obviously, this test involves significant risk to the patient. Therefore, intravenous access must be assured and trained personnel must be present to immediately treat a serious hypoglycemic reaction with intravenous dextrose if needed. Such treatment does not negate the results of the test, and blood sampling should continue until the completion of the study.

The glucagon stimulation test is one last convenient test that may be used. Glucagon, 0.1 mg/kg (maximum 1 mg), is administered intravenously or intramuscularly and blood is obtained every 30 minutes for 3 hours for glucose and cortisol levels. An increase in the plasma cortisol level should occur during the fall in plasma glucose levels over the last 1-2 hours of the test.[31]  This test is useful in neonates, in whom the adequacy of venous access is a concern, if dextrose must be administered during insulin-induced hypoglycemia. As in the insulin tolerance test, the cortisol response that occurs in the glucagon stimulation test depends on an increase in the patient's own ACTH secretion and is therefore useful in assessing the entire hypothalamic-pituitary-adrenal axis.

Single measurement of plasma dehydroepiandrosterone sulfate levels has been shown to be at least a reasonable screening test for ACTH deficiency with good sensitivity and sensitivity when compared with the insulin tolerance test. The disadvantage to this test is that normal levels are age dependent, and, thus, the laboratory must have age-matched control normal levels available.[32]

Gonadotropin deficiency

Gonadotropin deficiency is difficult to assess in girls prior to puberty or in boys after age 3-6 months and before puberty.


Infant males aged 20-60 days have peak testosterone levels of 60-400 ng/dL. At this age, a level below this range with low luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels suggests gonadotropin deficiency.

At puberty, testosterone levels and LH levels in boys should increase, but the reference range testosterone level depends on the pubertal stage. A circadian variation is observed, with higher levels during the night. Suspect hypogonadotropism if a boy has not started puberty by age 16 years, starts puberty but does not progress to completion, or has completed puberty but has a testosterone level less than 300 ng/dL with low LH and FSH levels.


Girls have minimal estradiol secretion during infancy, thus making the diagnosis of gonadotropin deficiency difficult at this age.

Estradiol levels vary throughout the menstrual cycle. Suspect gonadotropin deficiency in girls with no breast development by age 14 years, no periods by age 16 years, or secondary amenorrhea and low LH and FSH levels

Gonadotropin-releasing hormone (GNRH) testing

Testing with any one of numerous short-acting GnRH analogues may also be helpful. For leuprolide acetate, the dose is 20 mcg/kg, and samples are obtained to measure LH and FSH levels at baseline and at 2 hours, 4 hours, 6 hours, and 24 hours after the leuprolide. For males, baseline and 24-hour testosterone levels may also be helpful.

In healthy pubertal children, the LH response exceeds the FSH response. In prepubertal children, the FSH response exceeds the LH response. In patients with complete gonadotropin deficiency, little to no response of either LH or FSH occurs. An intermediate response does not distinguish the prepubertal child with gonadotropin deficiency from the child with simple delayed puberty. Hence, this test is of limited value. An increase in testosterone levels in males after 24 hours suggests an intact hypothalamic-pituitary-gonadal axis.

Inhibin B levels less than 35 pg/mL have recently been shown to have 100% specificity and sensitivity for hypogonadotropism in prepubertal boys aged 14-18 years. For patients with Tanner stage 2 genital development, measurement of inhibin B levels (< 65 pg/mL) also had good sensitivity and specificity for identification of isolated gonadotropin deficiency. For patients with other pituitary deficiencies, low testosterone (< 25 ng/dL) levels were the best diagnostic test.[33]

Growth hormone (GH) deficiency

The best method to diagnose a GH deficiency is controversial.

In the poorly growing child, low baseline measurements of insulinlike growth factor 1, insulinlike growth factor 2, and insulinlike growth factor–binding protein 3 suggest GH deficiency. GH levels less than 5 ng/dL at the time of spontaneous hypoglycemia also suggest GH deficiency. Beyond this, other stimulatory tests are used.

Most physicians perform a combination of 2 tests on children with suspected GH deficiency. Again, the criterion standard is insulin-induced hypoglycemia, as described for cortisol deficiency. Arginine infusion with 0.5 mg/kg over 30 minutes is probably equally efficacious. Beyond these 2 tests, other drugs used include glucagon, clonidine, and propranolol.[34]

The biggest controversy is likely establishing the cutoff point for diagnosis of GH deficiency. Over the past 20 years, a peak level less than 10 ng/dL measured by routine radioimmunoassay was considered diagnostic. Before that, a level of 7 ng/dL was used. Differences in radioimmunoassay techniques may alter reported GH levels. Recent studies question the reliability of any testing. A study of children without deficiencies demonstrated a lower 95% confidence interval of 1.9 ng/mL in prepubertal individuals not primed with sex steroids.[35] Sex steroid priming increased this to 7.2 ng/mL.

Imaging Studies

Head MRI

Perform this test in all children with panhypopituitarism. Look for either underlying structural abnormalities or tumors that may be the cause of the hypopituitarism.[36]

The value of such imaging in children with an isolated pituitary hormonal deficiency is not clear. Perform imaging in such cases based on the clinical judgment of the physician.

Perform imaging in all patients with central diabetes insipidus because diabetes insipidus is frequently associated with an organic mass lesion.

Left hand and wrist radiography for bone age

This radiograph must be read by an experienced individual. The result can provide guidance regarding the patient's growth potential and sex hormone exposure.

Bone ages are frequently delayed in patients with hypopituitarism. The diagnostic sensitivity and specificity are low.



Medical Care

Adrenocorticotropic hormone (ACTH) deficiency

Cortisol deficiency requires prompt recognition and treatment. This is particularly true for the child who may be facing surgery or experiencing other significant stresses related to the cause of hypopituitarism.

Oral replacement is usually with hydrocortisone, usually administered twice daily but can be administered 3 times daily. Prednisone may be considered advantageous because of twice-daily dosing (at about 20-25% of the dose for hydrocortisone). However, growth suppression is a more common problem with prednisone, which should generally be avoided.[37]

Thyroid-stimulating hormone (TSH) deficiency

The dose of L-thyroxine replacement is age dependent. Monitor free T4 levels and adjust the dose of T4 to maintain reference range levels.

Evaluate and treat cortisol deficiency before starting T4 replacement to avoid precipitating an adrenal crisis.

Gonadotropin deficiency

Begin sex steroid replacement at puberty.

Growth hormone (GH) deficiency

Administer GH replacement in doses of 0.18-0.3 mg/kg/wk subcutaneously, divided in 6-7 doses. Higher doses of up to 0.7 mg/kg/wk may be beneficial in puberty.

A literature review by Giagulli et al indicated that neither short- nor long-term GH supplementation significantly reduces cardiovascular risk in adults with a GH deficit resulting from either isolated GH deficiency or compensated panhypopituitarism. However, both groups of patients in the study did show an increase in fat-free mass, a decrease in fat mass, and a reduction in low-density lipoprotein cholesterol.[38]

Surgical Care

Use surgical treatment for operable pituitary and hypothalamic tumors. If the patient has panhypopituitarism prior to surgery, pituitary function is unlikely to recover.


In all incidents of suspected pituitary dysfunction, a pediatric endocrinologist should be involved in the evaluation and treatment of the child. Determine additional consultations based on the cause of the hypopituitarism.



Medication Summary

The goals of pharmacotherapy are to reduce morbidity and prevent complications.


Class Summary

These medications are used for replacement of deficient hormones.

Hydrocortisone (Hydrocortone, Hydrocort, Cortef, Solu-Cortef)

This drug provides cortisol replacement in patients with ACTH deficiency. Possesses both mineralocorticoid activity and glucocorticoid effects.

Levothyroxine (Levothroid, Levoxyl, Synthroid)

This drug is a hormone replacement used in patients with TSH deficiency. Rapidly inhibits the release of thyroid hormones via a direct effect on the thyroid gland and inhibits the synthesis of thyroid hormones. Iodide also appears to attenuate the cAMP-mediated effects of thyrotropin. In active form, influences growth and maturation of tissues. Involved in normal growth, metabolism, and development. The dose of L-thyroxine replacement is age dependent.

Somatropin (Genotropin, Humatrope, Nordotropin, Nutropin, Saizen, TevTropin, Omnitrope)

Primary use of GH is as a hormone replacement in short poorly growing children. Stimulates growth of linear bone, skeletal muscle, and organs. Stimulates erythropoietin, which increases red blood cell mass.

Currently widely available in SC injection form. Adjust dose gradually based on clinical and biochemical responses assessed at monthly intervals, including body weight, waist circumference, serum IGF-1, IGFBP-3, serum glucose, lipids, thyroid function, and whole body dual-energy x-ray absorptiometry. In children, assess response based on height and growth velocity. Continue treatment until final height or epiphysial closure or both have been recorded. Increasing evidence indicates that GH replacement is also beneficial in deficient adults.

Testosterone (Androderm, AndroGel, Andro-LA, Delatest, Depo-Testosterone)

This is used for induction of puberty in hypopituitary males. In the fully developed male, testosterone patches at 5 mg/d provide the advantage of more even control, although some adolescents are uncomfortable wearing them. Administer low-dose testosterone over 1-2 mo to the prepubertal male with gonadotropin deficiency and microphallus who is embarrassed by the small size or the inability to urinate in a standing position.

Conjugated estrogens (Premarin)

This drug is used for initiation of puberty in girls with hypogonadotropism. Continue everyday treatment until breakthrough menstrual bleeding occurs and then initiate cyclical therapy. This can be achieved with any of the various PO contraceptives or the addition of medroxyprogesterone 5 mg to an estradiol regimen during the third wk of every mo with no treatment the last wk. PO contraceptive treatment is easier for patient to follow. Instead of Premarin, ethinyl estradiol (Estrace) can be used.

Estrogen Derivative

Class Summary

These medications are used for replacement of deficient hormones.


Estradiol restores estrogen levels in girls with hypogonadotropism to concentrations that induce negative feedback at gonadotrophic regulatory centers, which, in turn, reduces release of gonadotropins from pituitary.

Multiple studies have shown it will prevent bone loss at the spine and hip when started within 10 years of menopause.

Estradiol is used for the purpose of hormone replacement and induction of puberty. It acts by regulating transcription of a limited number of genes. Estrogens diffuse through cell membranes, distribute themselves throughout the cell, and bind to and activate the nuclear estrogen receptor, a DNA-binding protein found in estrogen-responsive tissues. The activated estrogen receptor binds to specific DNA sequences or hormone-response elements, which enhances transcription of adjacent genes and, in turn, leads to the observed effects.



Further Outpatient Care

Patients with hypopituitarism need close, ongoing, and regular follow-up by a pediatric endocrinologist. Closely monitor growth and measure free T4 levels on a regular basis to assess the adequacy of T4 replacement.

Body size and symptoms and signs of cortisol deficiency (eg, anorexia, recurrent abdominal pain, malaise) or cortisol excess (eg, excess weight gain, Cushingoid features, hypertension) determine the adequacy of cortisol replacement.

Close monitoring of pubertal status is also appropriate.


Adrenal crisis, as mentioned, is the most acute complication that can arise in the treatment of patients with hypopituitarism and occurs when glucocorticoid replacement is not appropriately administered or, more likely, when the child develops a concurrent illness or medical treatment that increases the requirement for glucocorticoid and prevents oral replacement.

Growth hormone (GH) therapy is reported to cause some rare adverse effects. These include benign intracranial hypertension and slipped capital femoral epiphyses. Treatment also increases insulin resistance and, therefore, possibly increases the risk of diabetes. Although questions have been raised about malignancy, most data show little or no risk.

Appropriate monitoring should minimize any risks from thyroid or sex steroid treatment.

Women with panhypopituitarism may become pregnant with the help of reproductive endocrinology, and a study by Feferkorn et al indicated that the outcomes of these pregnancies are comparable to those of the general population. The risk of developing maternal infection and of congenital anomalies were found to be higher in the individuals with panhypopituitarism (odds ratios =  3.14 and 6.97, respectively), but the investigators stated that “due to the small number of cases these results should be interpreted with caution.”[39]

A study by Schönberger et al suggested that children with combined pituitary hormone deficiency (CPHD) may present with drug-resistant epilepsy and catastrophic outcomes from refractory seizures. The investigators found that 12 of 73 pediatric patients (16%) with CPHD had epilepsy, with 11 of these cases being drug resistant. Four of 12 patients with super-refractory status epilepticus (SRSE) were unexpected new-onset cases, with three of these experiencing a devastating clinical course; this included two who suffered major sequelae and one who died.[40]


Morbidity and mortality due to hypopituitarism are caused by the individual hormone deficiencies or the underlying cause of hypopituitarism. Individual hormonal deficiencies are discussed in greater detail in the specific articles, and the underlying causes of death are not discussed here.

Acute mortality due to hormonal deficiencies is rare. When deaths occur due to hormonal deficiencies, they are usually caused by adrenal insufficiency secondary to ACTH deficiency. These deaths are most likely to occur when an accompanying illness prevents appropriate oral glucocorticoid replacement.

Growing, but not completely conclusive, evidence indicates that childhood hypopituitarism may be associated with a shortened adult lifespan, even with adequate hormonal replacement.[41] The increased mortality is due to cardiovascular abnormalities that are related to GH deficiency and past practices of not treating a GH deficiency when growth is complete.[42, 43] GH deficiency is associated with dyslipidemia that is not necessarily improved by GH therapy.[44] Children and adolescents with GH deficiency have been shown to have impaired vascular function.[45] Again, GH treatment may not restore function. Studies of adult growth treatment of GH deficiency have not conclusively demonstrated reductions of cardiovascular morbidity and mortality.[46, 47, 48, 49]

More recently, a French study reported increased adult mortality in childhood GH-treated patients.[50] The increased mortality was primarily in patients who had been small for gestational age at birth and who had received higher GH doses. Other studies have not confirmed the increased mortality.[51, 52]

Patient Education

Educate parents about the dangers of adrenal insufficiency when the child is unable to take oral medication. Instruct parents to rapidly seek medical care. Many families can intramuscularly administer hydrocortisone at home if the child is unable to take oral medications. The home dose is generally 25 mg in children younger than 2 years, 50 mg in children younger than 5 years, and 100 mg in all other children. If children require intramuscular medication, they should be brought to the emergency department. If the family is unable to administer the intramuscular injection, they can take the parenteral hydrocortisone with them to the emergency department to avoid delays in administering appropriate treatment.[53]

Parents also need to be taught home stress coverage with triple the dose of glucocorticoid for less serious illnesses, such as fever greater than 38°C.

For patient education resources, see the Endocrine System Center and Growth Hormone Deficiency Center, as well as Hypopituitarism in Children, Growth Hormone Deficiency in Children, Growth Failure in Children, and Understanding Growth Hormone Deficiency Medications.


Questions & Answers


What is panhypopituitarism?

How is panhypopituitarism diagnosed and treated?

What is the pathophysiology of panhypopituitarism?

What is the prevalence of panhypopituitarism in the US?

What is the prognosis of panhypopituitarism?


Which clinical history findings are characteristic of congenital hypopituitarism in panhypopituitarism?

Which clinical history findings are characteristic of acquired hypopituitarism in panhypopituitarism?

Which physical findings are characteristic of panhypopituitarism in neonates?

Which physical findings are characteristic of panhypopituitarism in older children?

What are the congenital causes of panhypopituitarism?

What are the acquired causes of panhypopituitarism?


What are the differential diagnoses for Panhypopituitarism?


What is included in the workup of panhypopituitarism?

How is thyroid-stimulating hormone (TSH) deficiency assessed in patients with panhypopituitarism?

How is adrenocorticotropic hormone (ACTH) deficiency assessed in patients with panhypopituitarism?

How is gonadotropin deficiency assessed in males with panhypopituitarism?

How is gonadotropin deficiency assessed in females with panhypopituitarism?

What is the role of gonadotropin-releasing hormone (GNRH) testing in the workup of panhypopituitarism?

How is growth hormone (GH) deficiency assessed in patients with panhypopituitarism?

What is the role of MRI in the workup of panhypopituitarism?

How is bone age determined in the workup of panhypopituitarism?


How is adrenocorticotropic hormone (ACTH) deficiency treated in panhypopituitarism?

How is thyroid-stimulating hormone (TSH) deficiency treated in panhypopituitarism?

How is gonadotropin deficiency treated in panhypopituitarism?

How is growth hormone (GH) deficiency treated in panhypopituitarism?

What is the role of surgery in the treatment of panhypopituitarism?

Which specialist consultations are beneficial to patients with panhypopituitarism?


What are the goals of drug treatment for panhypopituitarism?

Which medications in the drug class Estrogen Derivative are used in the treatment of Panhypopituitarism?

Which medications in the drug class Hormones are used in the treatment of Panhypopituitarism?


What is included in long-term monitoring of panhypopituitarism?

What are the possible complications of panhypopituitarism treatment?

What is the prognosis of panhypopituitarism?

What is included in patient education about panhypopituitarism?