Hypopituitarism

Mousa K Hamad MD (

Dr. Hamad of Albert Einstein College of Medicine has no relevant financial relationships to disclose.

)
Ryan M Holland MD (

Dr. Holland of Albert Einstein College of Medicine has no relevant financial relationships to disclose.

)
Aisha S Obeidallah BA (

Ms. Obeidallah of Albert Einstein College of Medicine has no relevant financial relationships to disclose.

)
Reza Yassari MD MS (Dr. Yassari of Albert Einstein College of Medicine has no relevant financial relationships to disclose.)
Douglas J Lanska MD FAAN MS MSPH, editor. (

Dr. Lanska of the University of Wisconsin School of Medicine and Public Health, the Medical College of Wisconsin, and IM Sechenov First Moscow State Medical University has no relevant financial relationships to disclose.

)
Originally released October 30, 1994; last updated July 17, 2020; expires July 17, 2023

Overview

The pituitary gland sits in the sella and is divided into 2 parts, the anterior and posterior. 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. There are many causes of hypopituitarism, including tumors in or around the pituitary gland, whole brain radiation therapy or focused radiation therapy that includes the sella in the treatment field, chemotherapy, damage intraoperatively, major head trauma, subarachnoid hemorrhage, infections, and peri and prenatal causes, which will all be discussed in this update.

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.

 

• 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.

 

• A pituitary abscess is an intrasellar infection; it responds to antibiotic therapy and surgery, and although the abscess resolves eventually, hypopituitarism often remains protracted, requiring prolonged hormone replacement therapy.

 

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

Historical note and terminology

Hypopituitarism results from the partial or complete loss of 1 or more of the 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 the storage gland 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 and were not 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. 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 childbirth 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 childbirth 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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