Hypopituitarism

Tarakad S Ramachandran MD (Dr. Ramachandran of SUNY Upstate Medical University has no relevant financial relationships to disclose.)
Arun Ramachandran MD (Dr. Ramachandran of the State University of New York at Syracuse has no relevant financial relationships to disclose.)
Zachary N London MD, editor. (Dr. London of the University of Michigan has no relevant financial relationships to disclose.)
Originally released October 30, 1994; last updated August 25, 2015; expires August 25, 2018

This article includes discussion of hypopituitarism, pituitary insufficiency, and Simmond syndrome. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

Hypopituitarism results from the partial or complete loss of 1 or more of 6 hormones made and released by the anterior pituitary gland. Non-tumoral causes constitute a major group of childhood hypopituitarism. Traumatic brain injury has emerged as an important cause of hypopituitarism. Once fully established and prolonged (greater than 6 months), it is generally permanent, although spontaneous recovery can rarely occur. In congenital hypopituitarism, pituitary stalk interruption is well known.

Key points

 

• Hypopituitarism results from the partial or complete loss of 1 or more of 6 hormones made and released by the anterior pituitary gland.

 

• Non-tumoral causes constitute a major group of childhood hypopituitarism.

 

• Traumatic brain injury has emerged as an important cause of hypopituitarism.

 

• Once fully established and prolonged (greater than 6 months), it is generally permanent, although spontaneous recovery can rarely occur.

 

• Not all sellar enhancing lesions causing hypopituitarism are pituitary adenomas.

 

• Pituitary abscess is a rare disorder; it responds to antibiotic therapy and surgery, and though the abscess resolves eventually, hypopituitarism often remains protracted, needing prolonged hormone replacement therapy.

 

• Hormonal replacement is the key element in the therapy of hypopituitarism.

 

• It is imperative that anterior pituitary hormonal function be assessed to attain maximal improvement in mental and physical functioning as well as in quality of life for victims of traumatic brain injury.

Historical note and terminology

Hypopituitarism results from the partial or complete loss of one or more of 6 hormones made and released by the anterior pituitary gland: growth hormone, adrenocorticotropic hormone, prolactin, thyroid stimulating hormone, luteinizing hormone, and follicle-stimulating hormone. The posterior pituitary is a storage organ for the hypothalamic hormones, antidiuretic hormone and oxytocin. Although complete deficiency of anterior pituitary hormones is often called "panhypopituitarism," this term should be reserved to describe the clinical effects of complete loss of anterior and posterior pituitary hormones, including the neuropeptides vasopressin and oxytocin.

The crucial physiologic roles of the pituitary gland were not suspected until the late 19th century or clearly defined until the first third of the 20th century. Galen (second century AD) believed that the hypophysis acted as a funnel for secreted mucus (pituita) made by the brain to pass into the nasopharynx. This concept was generally accepted with minor modifications, such as Vesalius's hypothesis that phlegm from the cerebral ventricles passed down the infundibulum into the gland and finally out the nose. The first evidence suggesting a more important role for the pituitary gland was published in 1886 when Marie described the disease of acromegaly, which was associated with the replacement of the pituitary body by tumor (Marie 1886). Cushing suspected that a clinical disorder was associated with pituitary destruction (Cushing 1912), but Simmonds provided the first clear description of pituitary insufficiency, which he termed "pituitary cachexia" (Simmonds 1914). Simmonds detailed the necroscopic findings of a 46-year-old woman whose illness began after parturition complicated by severe puerperal fever. The clinical findings were a marked weight loss, premature aging, marked muscular weakness, and anemia. Subsequent reports stressed a common relationship between parturition and the clinical syndrome, which led Reye to speculate in 1926 that pituitary destruction was caused by thrombosis in the setting of pituitary hyperplasia during pregnancy (Reye 1926). This view was fully confirmed by the 1937 report of Sheehan in his classic article on postpartum necrosis of the pituitary (Sheehan 1937).

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