What is the pituitary gland?
The thyroid may be known as the “queen of hormones,” but the pituitary gland is the true master controller of the endocrine system. Sitting at the base of the brain, this tiny gland orchestrates the function of key endocrine organs, including the thyroid, adrenal glands, and reproductive system. Its influence extends across growth, puberty, metabolism, and the body’s response to stress, making it essential for normal development and homeostasis. When something goes wrong with the pituitary, the effects can be wide-reaching and significant.
This small but mighty gland, roughly 1 cm in diameter, sits at the base of the brain, just below the hypothalamus. Its name, hypophysis, comes from the Greek for “outgrowth from below,” reflecting its close relationship with the hypothalamus. The two are connected by the infundibulum, a stalk-like structure that serves as a vital communication highway, carrying blood vessels and nerve fibres that transport regulatory hormones. The pituitary itself rests snugly within the sella turcica (Turkish saddle), a protective bony cavity within the butterfly-shaped sphenoid bone. Despite its small size, the pituitary plays a central role in regulating multiple endocrine functions.
The pituitary consists of two lobes, the anterior and posterior, with different structures and development and, therefore, different functions. The posterior pituitary comprises neural tissue, while the anterior hypophysis comprises glandular tissue. This is reflected in their names: neurohypophysis (posterior pituitary) and adenohypophysis (anterior pituitary).
What does the pituitary gland normally do?
Being the “master gland”, the pituitary is a conductor of the metabolic orchestra, but it all comes down to which lobe is responsible for what. Let’s take a closer look, beginning with the anterior pituitary.
Seven hormones are produced by adenohypophysis (anterior pituitary). Their production is controlled by the hormones of the hypothalamus, which can be divided into two groups:
- A releasing hormone that gives the pituitary a green light for secretion.
- An inhibiting hormone that shuts down the production site.
The neurohypophysis (posterior pituitary) produces two hormones. These two are produced in the hypothalamus’s neurons (the supraoptic and paraventricular nuclei) and transported down the pituitary stalk to the posterior pituitary. The neurohypophysis stores and releases them into the bloodstream according to the body’s needs.
What causes hypopituitarism?
Hypopituitarism occurs when the pituitary gland is unable to secrete enough hormones. The pituitary may work partially or not at all.
The causes may be direct when something is wrong with the pituitary gland or indirect when the source is outside the gland. In paediatric cases, we speak of congenital and acquired hypopituitarism.
How might hypopituitarism present?
Hypopituitarism occurs when more than two-thirds of the pituitary gland is damaged or dysfunctional, impairing its ability to regulate essential hormones. The presentation varies depending on the underlying cause, the age at onset, and which hormones are affected. Some children may develop life-threatening symptoms, while others experience more chronic and insidious features that can be mistaken for other conditions. Recognising the varied presentations is key to early diagnosis and effective management.
Presentation in the First 28 Days of Life
Babies presenting with hypopituitarism at birth may have a history of breech presentation, fetal distress, or episodes of reduced oxygen supply to the brain. While these associations aren’t fully understood, some causes of hypopituitarism may originate during fetal development or around the time of birth.
Newborns with pituitary hormone deficiencies may show signs of impaired sexual organ development, as growth hormones and gonadotropins are essential for normal maturation. This can present as undescended testes in boys or a small phallus. In addition, hypothyroidism—caused by low thyroid hormone levels—may lead to coarse facial features, poor feeding, and lethargy. Early recognition of these signs is crucial, as timely hormone replacement can significantly improve outcomes.
Hypoglycaemia is a common and sometimes early red flag in babies with hypopituitarism. It can present with jitteriness, poor feeding, prolonged jaundice, seizures, bluish skin discolouration (cyanosis), lethargy, or even acute collapse.
These symptoms arise because key pituitary hormones—adrenocorticotropic hormone (ACTH), growth hormone (GH), and thyroid-stimulating hormone (TSH)—are crucial for maintaining blood sugar levels and mounting an appropriate stress response. Without these hormones, newborns struggle to regulate glucose, particularly during periods of fasting or illness. Recognising and managing hypoglycaemia promptly is vital, as untreated episodes can lead to serious neurological consequences.
Hyponatraemia is a common feature of hypopituitarism and can occur alongside normal or low potassium levels. This distinguishes it from salt-wasting crises in conditions like congenital adrenal hyperplasia, where adrenal hormone deficiency leads to low sodium and high potassium levels.
Hyponatraemia often results from adrenocorticotropic hormone (ACTH) deficiency in hypopituitarism, leading to secondary adrenal insufficiency and inadequate cortisol production. In some cases, inappropriate antidiuretic hormone (ADH) secretion may also contribute to water retention and dilutional hyponatraemia. Identifying the underlying cause is crucial, as sodium imbalances can be life-threatening if not recognised and managed appropriately.
Infants with hypopituitarism may also present with hypernatraemia due to a deficiency of antidiuretic hormone (ADH), which is produced by the posterior pituitary gland. ADH plays a crucial role in water balance by promoting water reabsorption in the kidneys. When levels are low, the kidneys fail to retain water, leading to excessive urine output (polyuria) and increased thirst (polydipsia). This condition, known as diabetes insipidus (DI), results in dehydration and high sodium concentrations in the blood.
Prolonged jaundice may also occur due to a decreased rate of metabolism, as seen in thyroid-stimulating hormone or adrenocorticotropic hormone deficiency.
Presentation in Infants and Older Children
In infants and older children, growth failure is often one of the earliest signs of hypopituitarism. This is typically characterised by a reduced growth velocity and delayed bone age, which may become evident over time. Subtle early indicators can include delayed tooth eruption, frontal bossing (a disproportionately large forehead relative to the rest of the skull), poor midfacial bone development, and truncal obesity—where excess fat accumulates around the torso while limb growth remains relatively unaffected.
Because these signs can develop gradually, routine growth monitoring is essential for early detection. Without appropriate treatment, children with hypopituitarism may experience severe short stature and delayed puberty, highlighting the importance of timely diagnosis and hormone replacement therapy.
The presentation of hypopituitarism varies depending on which hormones are deficient, the severity of the deficiency, and the underlying cause. Some children show clear signs from birth, while others may gradually develop symptoms as they grow.
- Gonadotropin deficiency – In milder cases, children may appear unaffected at birth but later present with delayed or absent puberty. Some may also have a reduced or absent sense of smell, a hallmark of Kallmann syndrome.
- Congenital thyroid-stimulating hormone (TSH) deficiency – If missed at birth, this can later present with developmental delay, cold intolerance, constipation, hair loss, and weight gain, reflecting the effects of untreated hypothyroidism.
- Adrenocorticotropic hormone (ACTH) deficiency – This can lead to fatigue, recurrent infections, and episodes of hypoglycaemia, as cortisol plays a vital role in immune function and glucose regulation.
- Pituitary tumours (pituitary adenomas) – In some cases, hypopituitarism is caused by a tumour pressing on the gland. Depending on the size and location, children may develop neurological symptoms, such as seizures, developmental delays, or visual disturbances due to compression of the optic pathways. The likelihood of a pituitary adenoma increases with age, accounting for 1% of all intracranial tumours before 15 years but rising to 18% in adolescents aged 15–24.
Recognising these varied presentations is key to ensuring early diagnosis and timely intervention, helping to prevent long-term complications.
Investigating Hypopituitarism in Children
A thorough and systematic approach is essential when evaluating a child with suspected hypopituitarism. The assessment typically includes a detailed history, clinical examination, baseline blood tests, dynamic hormone testing, genetic studies, and neuroimaging to identify the underlying cause.
1. Clinical History and Examination
A comprehensive history should focus on:
- Perinatal events: Breech presentation, birth asphyxia, neonatal hypoglycaemia, or jaundice.
- Growth and developmental milestones: Poor growth velocity, delayed bone age, or signs of hypothyroidism.
- Pubertal status: Delayed or absent puberty, underdeveloped sexual organs.
- Symptoms of hormone deficiencies: Fatigue, cold intolerance, constipation, polyuria/polydipsia, or recurrent infections.
- Family history: Endocrine disorders, genetic syndromes, or consanguinity.
A detailed examination should assess growth parameters, facial features, genital development, and neurological signs that may indicate underlying pathology.
2. Baseline Blood Tests
The first step in laboratory evaluation is to measure the levels of pituitary hormones and the hormones regulated by the pituitary, such as those produced by the thyroid, adrenal glands, and gonads. These measurements are best taken in the early morning, as some hormone levels—particularly growth hormone (GH) and adrenocorticotropic hormone (ACTH)—fluctuate throughout the day.
Initial investigations aim to assess pituitary hormone function and include:
- Growth hormone (GH), insulin-like growth factor-1 (IGF-1)
- Thyroid function tests: Free T4 and TSH
- Adrenocorticotropic hormone (ACTH) and morning cortisol levels
- Luteinising hormone (LH) and follicle-stimulating hormone (FSH)
- Testosterone (males) or oestradiol (females)
- Prolactin (to assess pituitary function and check for prolactinoma)
- Plasma and urine osmolality (to screen for diabetes insipidus)
- Electrolytes (sodium, potassium, glucose) and renin levels
Baseline investigations such as urea, electrolytes, and liver function tests are also crucial, as they can reveal:
- Hypernatraemia due to antidiuretic hormone (ADH) deficiency, which leads to diabetes insipidus.
- Hyponatraemia caused by ACTH or cortisol deficiency, leading to secondary adrenal insufficiency.
In newborns with acute hypoglycaemia and suspected hypopituitarism, measuring serum glucose, cortisol, and GH levels can help confirm adrenal insufficiency or GH deficiency.
3. Dynamic Hormone Testing
Since some hormone deficiencies may not be detected through baseline blood tests, dynamic (provocative) function testing is often required to assess pituitary hormone secretion accurately. These tests account for factors such as time of day, age, season, and the pulsatile nature of hormone release. A stimulating substance is administered to provoke hormone secretion, with levels measured before, during, and after administration at regular intervals.
The most commonly used stimulation tests include:
1. Insulin Tolerance Test (ITT)
The insulin tolerance test is the gold standard for diagnosing growth hormone (GH) and adrenocorticotropic hormone (ACTH) deficiencies.
After an overnight fast, baseline cortisol, GH, and glucose levels are measured. An intravenous dose of insulin (0.05–0.1 units/kg) is then administered to induce hypoglycaemia within 30–45 minutes (defined as a glucose drop of 40 mg/dL or 50% from baseline).
A normal hormonal response involves:
- Cortisol rising above 20 µg/dL
- GH levels reaching 5–10 ng/mL
Since hypoglycaemia carries significant risks, especially in children, this test must be performed under close medical supervision in a controlled setting.
2. ACTH Stimulation Test – Evaluating the HPA Axis
This test assesses the hypothalamic-pituitary-adrenal (HPA) axis and is particularly useful for diagnosing secondary adrenal insufficiency due to ACTH deficiency.
Synthetic ACTH is administered intramuscularly or intravenously, and cortisol levels are measured before and at regular intervals afterwards.
- A normal cortisol response exceeds 18 µg/dL.
- If morning serum cortisol levels exceed 20 µg/dL, adrenal insufficiency can often be excluded.
3. Gonadotropin-Releasing Hormone (GnRH) Stimulation Test – Assessing Puberty-Related Hormones
This test evaluates the function of the hypothalamic-pituitary-gonadal axis by assessing the pituitary’s ability to release luteinising hormone (LH) and follicle-stimulating hormone (FSH) in response to GnRH stimulation.
Random FSH and LH measurements are usually sufficient for diagnosis in infants, as hormone levels remain detectable at this stage. However, spontaneous gonadotropin secretion declines in older children, making stimulation testing necessary.
GnRH is administered, and LH and FSH levels are measured regularly.
- A normal response involves a rise in LH and FSH within 20 minutes, followed by a decline after 60 minutes.
- In hypopituitarism, this response is absent or blunted.
This test is particularly useful in children presenting with delayed or absent puberty and is most effective during the first 18 months of life and around the time of expected puberty.
4. Water Deprivation Test – Diagnosing Diabetes Insipidus (DI)
Children with low ADH levels (often due to posterior pituitary dysfunction) may develop diabetes insipidus (DI), which leads to excessive urine output and dehydration.
Key findings suggesting DI:
- Elevated serum sodium and osmolality
- Low-normal urine osmolality (inability to concentrate urine despite dehydration)
The child fasts for approximately 7 hours under medical supervision, with close monitoring of:
- Body weight
- Plasma sodium levels
- Plasma and urine osmolality
DI is diagnosed if there is weight loss, rising plasma sodium and osmolality, and persistent dilute urine (failure to concentrate urine despite dehydration). As dehydration can rapidly worsen in children, this test must be performed in a hospital setting with strict monitoring.
4. Genetic Testing
If a congenital cause is suspected, genetic studies may identify gene mutations related to pituitary development (e.g., PROP1, POU1F1, LHX3, and LHX4 mutations in congenital hypopituitarism).
5. Neuroimaging – MRI Brain and Pituitary
Magnetic resonance imaging (MRI) is the most reliable imaging modality for evaluating the hypothalamic-pituitary axis (HPA) and should be performed in all children with suspected hypopituitarism. MRI provides a detailed structural assessment of the pituitary gland, stalk, and surrounding brain structures, helping to identify congenital abnormalities, tumours, or other lesions that may contribute to hormone deficiencies.
A study conducted at Helsinki University Hospital in Finland found that brain tumours were the most common cause of childhood-onset hypopituitarism, accounting for 61% of cases. The most frequently identified tumours were craniopharyngiomas and gliomas. Congenital hypopituitarism was diagnosed in 39% of cases, with 15% linked to genetic mutations.
Findings on MRI That Suggest Hypopituitarism
MRI may reveal several key abnormalities associated with pituitary dysfunction, including:
- Pituitary hypoplasia or aplasia – underdevelopment or absence of the gland.
- Ectopic posterior pituitary – the posterior pituitary is displaced along the pituitary stalk, often linked to congenital hypopituitarism.
- Thin or absent pituitary stalk – commonly seen in septo-optic dysplasia and other midline defects.
- Pituitary adenomas – may cause mass-effect symptoms such as headaches and visual disturbances.
- Craniopharyngiomas – benign tumours that can compress the hypothalamus and pituitary, disrupting hormone secretion.
6. Additional Investigations
- Bone age X-ray to assess skeletal maturity.
- ACTH stimulation test to confirm secondary adrenal insufficiency.
- Ophthalmology review if visual symptoms suggest pituitary mass effects.
A multidisciplinary approach involving endocrinologists, geneticists, and neurosurgeons is often required for diagnosis and management. Early identification and treatment can significantly improve long-term outcomes, preventing complications such as severe short stature, metabolic disturbances, and delayed puberty.
Why are we worried about hypopituitarism?
In hypopituitarism, the pituitary gland fails to produce adequate levels of key hormones, including cortisol, growth hormone (GH), and vasopressin (antidiuretic hormone, ADH). These hormones are crucial for maintaining homeostasis, particularly in response to stress, by regulating blood sugar, blood pressure, and fluid balance. Their absence places children at significant risk of hypoglycaemia and hypotension, which can lead to both acute life-threatening episodes and long-term complications if not properly managed.
Cortisol deficiency, caused by a lack of adrenocorticotropic hormone (ACTH), impairs the body’s ability to mount a stress response. Without sufficient cortisol, the body struggles to regulate blood sugar and blood pressure, increasing the risk of hypoglycaemia, weakness, fatigue, and, in severe cases, adrenal crisis. Growth hormone deficiency further exacerbates hypoglycaemia, as GH plays a key role in glucose metabolism and counter-regulation. Meanwhile, a deficiency in vasopressin (ADH) can lead to diabetes insipidus (DI), causing excessive urine output, dehydration, and electrolyte imbalances, which further compromise circulatory stability.
Children with hypopituitarism are particularly vulnerable during periods of illness, fasting, or physiological stress when their bodies are unable to compensate for these hormone deficiencies. Without timely intervention, this can result in severe metabolic instability, circulatory collapse, or adrenal crisis. Long-term complications include growth failure, developmental delays, and impaired stress resilience, underscoring the importance of early recognition, hormone replacement therapy, and stress-dose steroids when necessary. Prompt diagnosis and appropriate management can significantly reduce the risk of serious complications and improve overall outcomes for affected children.
How can we treat complications of hypopituitarism in an emergency?
During illness, vomiting, diarrhoea, or infections, failure of the hypothalamic-pituitary-adrenal (HPA) axis to produce essential hormones can trigger an adrenal crisis. This life-threatening condition leads to low blood sugar, hypotension, increased infection risk, and potential circulatory collapse.
While many families are aware of the need for stress-dose steroids, adrenal insufficiency can sometimes be the first sign of hypopituitarism, presenting as an emergency. Recognising early signs such as lethargy, vomiting, and hypoglycaemia is crucial, as prompt hydrocortisone treatment can be life-saving.
Upon arrival at the emergency unit
The ABC (Airway, Breathing, Circulation) approach to management should be used, including assessing the patient’s level of consciousness.
- Vital signs, particularly blood pressure, are obtained to determine circulatory compromise.
- Consider the early involvement of a senior clinician and endocrinology.
Secure intravenous access using a wide-bore cannula and take blood samples for urgent investigations, including:
- Blood gas (acidosis may indicate mineralocorticoid deficiency)
- Serum glucose
- Urea, electrolytes, and creatinine (low sodium and high potassium may be present)
- Cortisol
- ACTH
- 17-hydroxyprogesterone
- Aldosterone
- Plasma renin activity
- Urine tests for steroid profile and urinary sodium levels
Administer intravenous crystalloids (10 mL/kg) if low blood pressure is present, with reassessments to determine whether additional boluses are required for shock management.
Replace remaining deficits and maintenance fluid requirements evenly over 24 hours using 0.9% sodium chloride with 5% glucose administered intravenously.
Steroid Administration
The emergency care plan of children with a known diagnosis should guide the administration of steroids. However, the following protocol can be used to determine steroid dosages for first-presentation or newly diagnosed cases. Some centres may opt for continuous steroid infusions, which should be carried out under the supervision of an endocrinology team.
These doses will also cover the child’s mineralocorticoid replacement over this dosing period. Once stable, IV medication can be converted to oral replacements.
Repeat blood gas to check acidosis (pH), salt levels (sodium and potassium) and glucose.
Blood gas and blood glucose 1-2 hourly (more frequent if hypoglycaemic), then 2-4 hourly once normoglycaemic and is acidosis correcting
Salt levels (sodium and potassium: 2 hourly initially Interval can then be extended once glucose is stable
Avoid rise in serum sodium >8 mmol/L in 24 hours
Treating Hypoglycaemia
This is a common presentation in infants and small children with an adrenal crisis.
A bolus of 10% glucose 2-5 mL/kg IV and recheck blood glucose level 15 minutes post-treatment, then at 30 minutes, to ensure recovery to greater than 4.0 mmol/L
This can be maintained with 10% glucose in 0.9% sodium chloride IV
Treating high potassium
High potassium often corrects following fluid and steroid administrations, however:
Children with potassium >5.5 mmol/L should have an ECG and be on cardiac monitoring
If potassium is >7.0 mmol/L and ECG changes of hyperkalaemia are present, treat with nebulised salbutamol and insulin and glucose infusions.
What is the long-term treatment of hypopituitarism?
Since hypopituitarism is irreversible, lifelong hormone replacement therapy is required. With good medical care and appropriate treatment, children can lead normal, healthy lives. Treatment aims to replace missing hormones while mimicking the body’s natural rhythms as closely as possible. Timing, dosing, and age-related adjustments are key to optimising therapy.
Hormone Replacement Therapies
- Thyroid hormone replacement – L-thyroxine is given once daily in the morning to maintain stable thyroid function.
- Growth hormone replacement – Given as a subcutaneous injection at night, aligning with the natural peak secretion of growth hormone during sleep.
- ACTH (adrenal hormone) replacement – Hydrocortisone is preferred over prednisolone or dexamethasone in children as it minimises growth suppression. The morning dose is higher than the evening dose, mirroring natural cortisol secretion.
- ADH (antidiuretic hormone) replacement – Desmopressin is used to manage diabetes insipidus, ideally started in a hospital setting for careful monitoring. Fluid intake and daily body weight should be monitored to prevent overhydration.
- Sex hormone replacement – Initiated at 8–13 years, depending on individual needs, to support puberty and secondary sexual development. Testosterone is given to boys, while oestrogen is given to girls, typically over 2–4 years.
Careful dose adjustment and monitoring throughout childhood and adolescence ensure optimal growth, development, and well-being. Regular follow-up with an endocrinologist is essential for long-term management.
Children with hypopituitarism require regular follow-up with a paediatric endocrinologist and specialist nurse to ensure optimal growth, development, and hormone balance. Appointments should ideally be scheduled every 3–6 months, with routine height and weight measurements to track growth progression.
Laboratory tests should be performed if symptoms such as drowsiness, lethargy, or poor growth arise, as these may indicate inadequate hormone replacement. Close monitoring helps prevent delays in growth and puberty, common if treatment is not well-optimised. Regular follow-ups also allow for dose adjustments based on the child’s needs, ensuring they receive the best possible care throughout their development.
What support is available for children and their parents/caregivers?
Empowering families with education on emergency management is essential in hypopituitarism. Parents and children should be instructed on how to recognise and respond to adrenal crises, hypoglycaemia, and dehydration, especially in those with ACTH and GH deficiencies. A medical alert bracelet should be provided, along with an emergency care plan, ensuring that appropriate treatment can be administered quickly if needed.
Medication dose adjustments should be discussed for illness, stress, and physically demanding situations—for example, during infections, exams, or intense exercise. Families should be given clear guidance on when to increase hydrocortisone doses or seek urgent medical care.
Sources of Support
Patient charities and online resources can provide valuable information and peer support. Organisations like The Pituitary Foundation offer guidance on managing school, work, sports, and social life with hypopituitarism. As young people grow, discussions around relationships, fertility, and lifestyle choices (including drugs and alcohol) become increasingly relevant.
A holistic, nonjudgmental approach is essential when supporting adolescents. The HEADSSS screening tool (covering Home, Education, Activities, Drugs, Sexual health, Suicide/self-harm, and Safety) is a useful framework for exploring their emotional well-being, independence, and future aspirations. Providing young people with age-appropriate education and support helps them gain confidence in managing their condition as they transition into adulthood.
Takehome points
The pituitary gland is the conductor of the body’s metabolic orchestra.
Presentation of hypopituitarism varies based on the cause, age at onset, and which hormones are deficient.
In hypopituitarism, the pituitary gland fails to produce adequate levels of key hormones, including cortisol, GH, and vasopressin. Failure to secrete hormones which respond to stressors can result in acute collapse (known as an adrenal crisis).
The primary goals in treating an acute adrenal crisis are correcting low blood pressure, low blood sugar, dehydration and electrolyte deficiency. This is achieved with steroids, fluids, and glucose.
Hypopituitarism needs lifelong treatment with hormone replacement. Growth needs to be monitored, and as the young person grows, they need additional physical and psychological care to support their overall wellbeing.
References
Auron M, Raissouni N; Adrenal Insufficiency. Pediatr Rev March 2015; 36 (3): 92–103. https://doi.org/10.1542/pir.36-3-92
Bornstein SR et al. 2016. Diagnosis and treatment of Primary Adrenal Insufficiency: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab, 101(2), pp. 364-389. https://academic.oup.com/jcem/article/101/2/364/2810222
Bowden SA, Henry R. 2018. Pediatric Adrenal Insufficiency: diagnosis, management and new therapies. International Journal of Pediatrics, DOI: 10.115/2018/1739831.
British Society for Paediatric Endocrinology and Diabetes. BSPED Adrenal insufficiency consensus guidelines. https://www.bsped.org.uk/clinical-resources/bsped-adrenal-insufficiency-consensus-guidelines/ (viewed May 2024)
Cho HY, Kim JH, Kim SW, et al. Different cut-off values of the insulin tolerance test, the high-dose short Synacthen test (250 μg) and the low-dose short Synacthen test (1 μg) in assessing central adrenal insufficiency. Clin Endocrinol (Oxf). 2014;81(1):77-84. doi:10.1111/cen.12397
El-Maouche D et al. 2018. Longitudinal assessment of illnesses, stress dosing and illness sequelae in patients with Congenital Adrenal Hyperplasia. J Clin Endocrinol Metab, 103(6), pp.2336-2345.
Feldt-Rasmussen U, Effraimidis G, Klose M. The hypothalamus-pituitary-thyroid (HPT)-axis and its role in physiology and pathophysiology of other hypothalamus-pituitary functions. Mol Cell Endocrinol. 2021;525:111173. doi:10.1016/j.mce.2021.111173
Fleseriu M, Christ-Crain M, Langlois F, Gadelha M, Melmed S. Hypopituitarism. Lancet. 2024;403(10444):2632-2648. doi:10.1016/S0140-6736(24)00342-8
Güran T. 2017. Latest insights on the etiology and management of Primary Adrenal Insufficiency in children. J Clin Res Pediatr Endocrinol, 9(suppl 2), pp. 9 – 22.
Hietamäki J, Kärkinen J, Iivonen AP, et al. Presentation and diagnosis of childhood-onset combined pituitary hormone deficiency: A single center experience from over 30 years. EClinicalMedicine. 2022;51:101556. Published 2022 Jul 18. doi:10.1016/j.eclinm.2022.101556
Kim SY. Diagnosis and Treatment of Hypopituitarism. Endocrinol Metab (Seoul). 2015;30(4):443-455. doi:10.3803/EnM.2015.30.4.443
Kirkgoz T, Guran T. 2018. Primary adrenal insufficiency in children: diagnosis and management. Best Practice & Research Clinical Endocrinology & Metabolism, 32, pp. 397-424.
Korbonits M, Blair JC, Boguslawska A, et al. Consensus guideline for the diagnosis and management of pituitary adenomas in childhood and adolescence: Part 1, general recommendations. Nat Rev Endocrinol. 2024;20(5):278-289. doi:10.1038/s41574-023-00948-8
Miller B et al. 2019. Emergency management of adrenal insufficiency in children: advocating for treatment options in outpatient and field settings. J Investig Med. Epub doi:10.1136/jim-2019-000999.
Mushtaq T et al. Emergency and perioperative management of adrenal insufficiency in children and young people: British Society for Paediatric Endocrinology and Diabetes consensus guidance. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10646833/ (viewed May 2024)
Nordenström A, Ahmed SF, van den Akker E, et al. Pubertal induction and transition to adult sex hormone replacement in patients with congenital pituitary or gonadal reproductive hormone deficiency: an Endo-ERN clinical practice guideline. Eur J Endocrinol. 2022;186(6):G9-G49. Published 2022 Apr 21. doi:10.1530/EJE-22-0073
Perth Children’s Hospital “Adrenal insufficiency” guideline. https://pch.health.wa.gov.au/For-health-professionals/Emergency-Department-Guidelines/Adrenal-insufficiency (viewed May 2024)
Starship “Stress Steroid Management” guideline. https://starship.org.nz/guidelines/stress-steroid-management/ (viewed May 2024)
Webb EA, Krone N. Current and novel approaches to children and young people with congenital adrenal hyperplasia and adrenal insufficiency. Best Pract Res Clin Endocrinol Metab. 2015;29(3):449-468. doi:10.1016/j.beem.2015.04.002
Yeliosof O, Gangat M. Diagnosis and management of hypopituitarism. Curr Opin Pediatr. 2019;31(4):531-536. doi:10.1097/MOP.0000000000000779
Hypopituitarism can sometimes be tricky to spot in younger patients, as the symptoms might overlap with other conditions. It’s encouraging to see resources like this shedding light on the importance of proper screening and intervention.