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Hyperpituitarism Clinical Presentation

  • Author: Alicia Diaz-Thomas, MD, MPH; Chief Editor: Stephen Kemp, MD, PhD  more...
Updated: May 28, 2014


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

Excess prolactin

The presentation of prolactinomas may vary, depending on the age and sex of the child.

Prepubertal children typically present with a combination of headache, visual disturbance, and growth failure.

Pubertal females frequently present with symptoms of pubertal arrest or hypogonadism (with or without galactorrhea) due to suppression of gonadotropin secretion or local compression of the pituitary.

Pubertal males may present with headaches, visual impairment, and pubertal arrest or growth failure.

Excess adrenocorticotropic hormone

The most sensitive indicator of excess glucocorticoid secretion in children is weight gain with concurrent growth failure, which generally precedes other manifestations.

Patients commonly present with weight gain that tends to be generalized rather than centripetal.

Hirsutism and premature adrenarche may occur in prepubertal children.

Hypertension may be present.

Pubertal arrest, acne, fatigue, and depression are also common.

Snoring, poor sleep quality, deteriorating academic performance (compared with prior school terms), or other signs of obstructive sleep apnea (OSA) should prompt a formal sleep study and consultation with a pulmonologist.

Excess growth hormone

The presentation of gigantism in a child is usually dramatic, unlike the insidious onset of acromegaly in adults.

The cardinal clinical feature of gigantism is longitudinal growth acceleration secondary to GH excess.

Presentation depends on whether the epiphyseal growth plate is open. Before epiphyseal fusion, accelerated growth velocity is prominent. As epiphyseal fusion approaches, the spectrum of symptoms resembles the presentation in adults (eg, coarsening of facial features, change in ring and shoe size).



Prolactinoma may include the following:

  • Hypogonadism, leading to pubertal arrest, pubertal failure, or pubertal delay
  • Menstrual abnormalities, including primary or secondary amenorrhea
  • Galactorrhea
  • Gynecomastia

Cushing disease may include the following (see images below):

A 16-year-old boy with Cushing disease. A 16-year-old boy with Cushing disease.
On the left is an unaffected patient aged 12 years On the left is an unaffected patient aged 12 years. On the right is the same patient aged 13 years after developing Cushing disease.

See the list below:

  • Cushingoid appearance includes a dorsal cervical fat pad, moon facies, bruising, and striae. These features are only observed in patients with advanced long-standing disease.
  • Growth failure and short stature may be observed.
  • Weight gain and obesity in children with Cushing disease tends to be generalized rather than centripetal.
  • Pubertal arrest, failure, or delay may occur.
  • Amenorrhea may be noted.
  • Hypertension may be present.

In patients with gigantism, all growth parameters are affected, although not necessarily symmetrically. GH excess over time is characterized by progressive cosmetic disfigurement and systemic organ manifestations. The following may be noted:

  • Tall stature
  • Mild-to-moderate obesity (common)
  • Macrocephaly, which may precede linear growth
  • Exaggerated growth of the hands and feet with thick fingers and toes
  • Coarse facial features, including frontal bossing and prognathism
  • Hyperhidrosis
  • Menstrual irregularities
  • Peripheral neuropathies (eg, carpal tunnel syndrome)
  • Cardiovascular disease: Prolonged GH excess can result in cardiac hypertrophy, hypertension, and left ventricular hypertrophy.
  • Tumors: Although benign tumors, including uterine myomas, prostatic hypertrophy, colon polyps, and skin tags, may be frequently encountered in acromegaly, the documentation of the overall prevalence of malignancies in patients with acromegaly remains controversial.
  • Endocrinopathies: Frequently associated endocrinopathies include hypogonadism, diabetes, decreased glucose tolerance, and hyperprolactinemia. OSA has been reported in up to half of patients with acromegaly, particularly those who are obese or older than 50 years.


Hypothalamic dysfunction can promote tumor growth, but overwhelming evidence points to intrinsic pituicyte genetic disruption as the main underlying cause of pituitary tumorigenesis. The monoclonal nature of most pituitary adenomas, confirmed with X-inactivation studies, implies their origin from a clonal event in a single cell. Most pituitary adenomas are functional, and clinical presentation typically depends on the particular pituitary hormone that is hypersecreted. Nonfunctioning pituitary adenomas are rare in children, accounting for only 3-6% of all adenomas in 2 large series; they comprise 30% of adenomas in adults.

Contributor Information and Disclosures

Alicia Diaz-Thomas, MD, MPH Assistant Professor of Pediatrics, University of Tennessee Health Science Center

Alicia Diaz-Thomas, MD, MPH is a member of the following medical societies: American Association of Clinical Endocrinologists, Endocrine Society, Pediatric Endocrine Society, Tennessee Medical Association

Disclosure: Nothing to disclose.


Melanie Shim, MD 

Melanie Shim, MD is a member of the following medical societies: American Diabetes Association, Endocrine Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London) Professor and Chair, First Department of Pediatrics, Athens University Medical School, Aghia Sophia Children's Hospital, Greece; UNESCO Chair on Adolescent Health Care, University of Athens, Greece

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London) is a member of the following medical societies: American Academy of Pediatrics, American College of Physicians, American Pediatric Society, American Society for Clinical Investigation, Association of American Physicians, Endocrine Society, Pediatric Endocrine Society, Society for Pediatric Research, American College of Endocrinology

Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD Former Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas for Medical Sciences College of Medicine, Arkansas Children's Hospital

Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Additional Contributors

Thomas A Wilson, MD Professor of Clinical Pediatrics, Chief and Program Director, Division of Pediatric Endocrinology, Department of Pediatrics, The School of Medicine at Stony Brook University Medical Center

Thomas A Wilson, MD is a member of the following medical societies: Endocrine Society, Pediatric Endocrine Society, Phi Beta Kappa

Disclosure: Nothing to disclose.


Robert J Ferry Jr, MD Le Bonheur Chair of Excellence in Endocrinology, Professor and Chief, Division of Pediatric Endocrinology and Metabolism, Department of Pediatrics, University of Tennessee Health Science Center

Robert J Ferry Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Diabetes Association, American Medical Association, Endocrine Society, Pediatric Endocrine Society, Society for Pediatric Research, and Texas Pediatric Society

Disclosure: Eli Lilly & Co Grant/research funds Investigator; MacroGenics, Inc Grant/research funds Investigator; Ipsen, SA (formerly Tercica, Inc) Grant/research funds Investigator; NovoNordisk SA Grant/research funds Investigator; Diamyd Grant/research funds Investigator; Bristol-Myers-Squibb Grant/research funds Other; Amylin Other; Pfizer Grant/research funds Other; Takeda Grant/research funds Other

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Pituitary macroadenoma.
A 16-year-old boy with Cushing disease.
On the left is an unaffected patient aged 12 years. On the right is the same patient aged 13 years after developing Cushing disease.
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