eMedicine Specialties > Endocrinology > Pituitary Gland

Hypopituitarism (Panhypopituitarism)

Author: James R Mulinda, MD, FACP, FACE, Consulting Staff, Department of Endocrinology, Endocrinology Associates, Inc
Contributor Information and Disclosures

Updated: Jul 20, 2009

Introduction

Background

Hypopituitarism is a clinical syndrome of deficiency in pituitary hormone production. This may result from disorders involving the pituitary gland, hypothalamus, or surrounding structures. Panhypopituitarism refers to involvement of all pituitary hormones; however, only one or more pituitary hormones are often involved, resulting in partial hypopituitarism. Pituitary hormones of clinical significance include adrenocorticotropic hormone (ACTH, ie, corticotropin), follicle-stimulating hormone (FSH), luteinizing hormone (LH), growth hormone (GH), prolactin, thyroid-stimulating hormone (TSH, ie, thyrotropin), and antidiuretic hormone (ADH).

Pathophysiology

When pituitary hormone production is impaired, target gland hormone production is reduced because of a lack of trophic stimulus. Normally, subphysiologic target hormone levels stimulate the pituitary gland to increase trophic hormone production; however, in hypopituitarism, the pituitary gland response is absent, suboptimal, or inappropriate with biologically inert hormone production. This results in progressive secondary failure of the target glands. Patients with hypopituitarism typically present with low target hormone levels accompanied by low levels of the corresponding trophic hormone.

The trophic hormone level may appear to be within the reference range with a corresponding subphysiologic target hormone level. Such a trophic hormone level would be inappropriately low for the subphysiologic target hormone level. Sometimes, the assayed trophic hormone level may be biologically inert.

Mortality/Morbidity

Four retrospective studies from the United Kingdom and Sweden show that mortality is increased by 1.3- to 2.2-fold in hypopituitarism compared to age- and sex-matched cohorts.1 Morbidity is variable and may result from hormone deficiency or underlying disease. Underlying disorders, such as tumors, intracranial lesions, or systemic disease, may be asymptomatic or result in morbidity that masks the hormone deficiency.

  • Deficiency of ACTH with adrenal crisis or TSH with myxedema may be life threatening.
  • GH deficiency causes more morbidity in children than in adults.
  • Sudden compromise of ACTH production may result in more profound morbidity than slowly progressive deficiency.
  • Gonadotropin deficiency with hypogonadism may cause morbidity insidiously.
  • Morbidity is more profound in congenital hypopituitarism.

Race

No racial predilection exists.

Sex

Postpartum hypopituitarism causes an overall increase in the prevalence of hypopituitarism in women.

Age

All ages are affected.

Clinical

History

Presentation varies from asymptomatic to acute collapse, depending on the etiology, rapidity of onset, and predominant hormones involved.

  • Initially, a patient with any hormone deficiency may be asymptomatic. Individuals with the following deficiencies present with the indicated condition:
    • ACTH deficiency - Adrenal insufficiency
    • TSH deficiency - Hypothyroidism
    • Gonadotropin deficiency - Hypogonadism
    • GH deficiency - Individuals with GH deficiency present with failure to thrive and short stature in children. Most adults are asymptomatic, but some may experience fatigue and weakness.
    • ADH deficiency - Polyuria and polydipsia
  • Other presenting features may be attributable to the underlying cause.
    • A patient with a space-occupying lesion may present with headaches or visual field deficits.
    • A patient with large lesions involving the hypothalamus may present with polydipsia and syndrome of inappropriate secretion of antidiuretic hormone (SIADH).

Physical

  • Physical examination findings may be normal in subtle presentations.
  • Patients may present with features attributable to deficiency of target hormones, including hypothyroidism, adrenal insufficiency, hypogonadism, and failure to thrive.

Causes

  • Tumors2 - Craniopharyngiomas, pituitary adenomas
  • Infiltrative processes - Sarcoidosis, histiocytosis X, hemochromatosis
  • Infections - Tuberculosis, syphilis, meningitis
  • Ischemia and infarction - Sheehan syndrome, apoplexy
  • Empty sella syndrome
  • Iatrogenic - Radiation,3 surgery, withholding previous chronic glucocorticoid replacement
  • Trauma to the hypophysis
  • Congenital - Kallmann syndrome
  • Autoimmune - Lymphocytic hypophysitis4
  • Transsphenoidal adenomectomy - In a study of 435 patients who underwent endonasal transsphenoidal adenomectomy, Fatemi et al found that hypopituitarism developed in 5.5% of these individuals.5 The results indicated that the likelihood of hypopituitarism development after transsphenoidal adenoma removal is higher when the tumor is larger than 20 mm.

More on Hypopituitarism (Panhypopituitarism)

Overview: Hypopituitarism (Panhypopituitarism)
Differential Diagnoses & Workup: Hypopituitarism (Panhypopituitarism)
Treatment & Medication: Hypopituitarism (Panhypopituitarism)
Follow-up: Hypopituitarism (Panhypopituitarism)
References
Further Reading
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References

  1. Clayton RN. Mortality, cardiovascular events and risk factors in hypopituitarism. Growth Horm IGF Res. Feb 1998;8 Suppl A:69-76. [Medline].

  2. Santos A, Resmini E, Martínez MA, et al. Quality of life in patients with pituitary tumors. Curr Opin Endocrinol Diabetes Obes. Aug 2009;16(4):299-303. [Medline].

  3. Fernandez A, Brada M, Zabuliene L, et al. Radiation-induced hypopituitarism. Endocr Relat Cancer. Jun 4 2009;[Medline].

  4. de Graaff LC, De Bellis A, Bellastella A, et al. Antipituitary antibodies in Dutch patients with idiopathic hypopituitarism. Horm Res. Jan 2009;71(1):22-7. [Medline].

  5. Fatemi N, Dusick JR, Mattozo C, et al. Pituitary hormonal loss and recovery after transsphenoidal adenoma removal. Neurosurgery. Oct 2008;63(4):709-18; discussion 718-9. [Medline].

  6. Nakamoto J. Laboratory diagnosis of multiple pituitary hormone deficiencies: issues with testing of the growth and thyroid axes. Pediatr Endocrinol Rev. Jan 2009;6 Suppl 2:291-7. [Medline].

  7. Walvoord E. Sex steroid replacement for induction of puberty in multiple pituitary hormone deficiency. Pediatr Endocrinol Rev. Jan 2009;6 Suppl 2:298-305. [Medline].

  8. Constine LS, Woolf PD, Cann D, et al. Hypothalamic-pituitary dysfunction after radiation for brain tumors. N Engl J Med. Jan 14 1993;328(2):87-94. [Medline].

  9. Dexter RN. Hypopituitarism. In: Becker KL, ed. Principles and Practice of Endocrinology and Metabolism. 1995. 2nd ed. Baltimore, Md: Williams and Wilkins; 1995:169-80.

  10. Garcia-Heras J, Kilani RA, Martin RA, Lamp S. A deletion of proximal 20p inherited from a normal mosaic carrier mother in a newborn with panhypopituitarism and craniofacial dysmorphism. Clin Dysmorphol. Jul 2005;14(3):137-40. [Medline].

  11. Harzallah L, Migaw H, Harzallah F, Kraiem Ch. Diabetes insipidus and panhypopituitarism revealing pituitary metastasis of small cell lung carcinoma: a case report. Ann Endocrinol (Paris). Apr 2005;66(2 Pt 1):117-20. [Medline].

  12. Koh WJ, Kwon OJ. Mycobacterium avium complex lung disease and panhypopituitarism. Mayo Clin Proc. Jul 2005;80(7):961-2. [Medline].

  13. Lasheen I, Doi SA, Al-Shoumer KA. Glucocorticoid replacement in panhypopituitarism complicated by myelinolysis. Med Princ Pract. Mar-Apr 2005;14(2):115-7. [Medline].

  14. Thorner MO, Vance ML, Horvath E. The anterior pituitary. In: Williams Textbook of Endocrinology. 8th ed. Philadelphia, Pa: WB Saunders and Co; 1992:221-310.

  15. Vance ML. Hypopituitarism. N Engl J Med. Jun 9 1994;330(23):1651-62. [Medline].

  16. Wolfgang KHO. Hypopituitarism. In: Bardin CW, ed. Current Therapy in Endocrinology and Metabolism. 6th ed. St. Louis, Mo: Mosby-Year Book; 1997:27-31.

  17. Yamakita N, Yasuda K. Pulmonary Mycobacterium avium complex infection in patients with panhypopituitarism not receiving hormone replacement therapy. Mayo Clin Proc. Feb 2005;80(2):291. [Medline].

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Keywords

hypopituitarism, panhypopituitarism, pituitary, human hormone, growth hormone, pituitary gland, endocrine system, hormone replacement, pituitary adenoma, hypothalamus, growth hormone deficiency, pituitary hormone, tumor pituitary gland, pituitary tumors, pituitary glands
 
adrenocorticotropic hormone, ACTH, corticotropin, follicle-stimulating hormone, FSH, luteinizing hormone, LH, prolactin, thyroid-stimulating hormone, TSH, thyrotropin, antidiuretic hormone, ADH, pituitary insufficiency, lack of trophic stimulus

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Contributor Information and Disclosures

Author

James R Mulinda, MD, FACP, FACE, Consulting Staff, Department of Endocrinology, Endocrinology Associates, Inc
James R Mulinda, MD, FACP, FACE is a member of the following medical societies: American College of Clinical Endocrinologists and American College of Physicians
Disclosure: Nothing to disclose.

Medical Editor

David S Schade, MD, Chief, Division of Endocrinology and Metabolism, Professor, Department of Internal Medicine, University of New Mexico School of Medicine and Health Sciences Center
David S Schade, MD is a member of the following medical societies: American College of Physicians, American Diabetes Association, American Federation for Medical Research, Endocrine Society, New Mexico Medical Society, New York Academy of Sciences, and Society for Experimental Biology and Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Don S Schalch, MD, Professor Emeritus, Department of Internal Medicine, Division of Endocrinology, University of Wisconsin Hospitals and Clinics
Don S Schalch, MD is a member of the following medical societies: American Diabetes Association, American Federation for Medical Research, Central Society for Clinical Research, and Endocrine Society
Disclosure: Nothing to disclose.

CME Editor

Mark Cooper, MBBS, PhD, FRACP, Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University
Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD, Professor of Medicine, St Louis University School of Medicine
George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

 
 
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