Growth Hormone Deficiency in Adults

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Growth Hormone Deficiency in Adults

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The somatotroph cells of the anterior pituitary gland produce growth hormone (GH), which is stimulated by GH-releasing hormone (GHRH) and inhibited by somatostatin, both of which are produced by the hypothalamus.

GH deficiency in adults usually manifests as reduced physical performance and impaired psychological well-being. It results in alterations in the physiology of different systems of the body, manifesting as altered lipid metabolism, increased subcutaneous and visceral fat, decreased muscle mass, decreased bone density, low exercise performance, and reduced quality of life. [1]

Adult GH deficiency can be a transition from childhood-onset GH deficiency or it can be acquired during adulthood. The majority of cases are caused by pituitary tumors or by their treatment with surgery, radiation therapy, or both. Traumatic brain injury is another important cause. [2, 3, 4]

The goals of GH therapy in adults are to improve conditioning, strength, body composition, and quality of life, as well as reduce the burden of associated medical conditions such as cardiovascular disease and decreased bone mineral density.

Patients should be educated about the technique of subcutaneous injection of GH.

For patient education resources, see Thyroid and Metabolism Center as well as Growth Hormone DeficiencyGrowth Hormone Deficiency Medications, and Growth Hormone Deficiency FAQs.

The main cause of growth hormone (GH) deficiency is a pituitary tumor or the consequences of treatment of the tumor, including surgery and/or radiation therapy. Traumatic brain injury is increasingly recognized as an important cause of GH deficiency, both during the acute stage of the injury and during the rehabilitation stage. [2, 3, 4]

Causes of GH deficiency can be divided into three categories: congenital, acquired, and idiopathic. [5]

Congenital conditions are caused by genetic abnormalities or structural brain defects. Genetic abnormalities include transcription factor defects (PIT-1, PROP-1, LHX3/4, HESX-1, PITX-2), GH-releasing hormone (GHRH) receptor gene defects, GH gene defects, and GH-receptor or post-receptor defects. Structural defects include agenesis of the corpus callosum, septo-optic dysplasia, empty sella syndrome, encephalocele, hydrocephalus, and arachnoid cyst. GH deficiency can occur in association with midline facial defects such as single central incisor, cleft lip, and cleft palate.

Acquired conditions of GH deficiency include tumors of the pituitary gland or the hypothalamus and metastatic disease; surgery or radiation therapy of the pituitary or hypothalamus; infiltrative diseases such as sarcoidosis, tuberculosis, histiocytosis X, hemochromatosis, and lymphocytic hypophysitis; infarction of the pituitary or hypothalamus (which can be spontaneous or result from Sheehan syndrome); and head trauma.

In some cases, no clear etiology can be determined.

 

An estimated 6,000 adults are diagnosed with growth hormone (GH) deficiency every year in the United States. [2] Adult GH deficiency has been estimated to affect 1 in 100,000 people annually, whereas its incidence is approximately 2 cases per 100,000 population when childhood-onset GH deficiency patients are considered. About 15%-20% of the cases represent the transition of childhood GH deficiency into adulthood. [6]

The age of presentation of acquired GH deficiency in adults often coincides with the discovery of pituitary tumors, usually between the fourth and fifth decades of life.

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Mohsen S Eledrisi, MD, FACP, FACE Senior Consultant, Department of Medicine/Endocrinology, Hamad Medical Corporation, Qatar

Mohsen S Eledrisi, MD, FACP, FACE is a member of the following medical societies: American Association of Clinical Endocrinologists, Endocrine Society, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

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 and Translational Research, Endocrine Society

Disclosure: Nothing to disclose.

George T Griffing, MD Professor Emeritus 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, International Society for Clinical Densitometry, Southern Society for Clinical Investigation, American College of Medical Practice Executives, American Association for Physician Leadership, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical and Translational Research, Endocrine Society

Disclosure: Nothing to disclose.

Steven R Gambert, MD Professor of Medicine, Johns Hopkins University School of Medicine; Director of Geriatric Medicine, University of Maryland Medical Center and R Adams Cowley Shock Trauma Center

Steven R Gambert, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for Physician Leadership, American College of Physicians, American Geriatrics Society, Endocrine Society, Gerontological Society of America, Association of Professors of Medicine

Disclosure: Nothing to disclose.

Ali A Al-Qarni, MD, Consulting Endocrinologist, King Abdulaziz National Guard Hospital, Saudi Arabia, contributed to previous versions of this article.

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