Interesting site on Adult Growth Hormone Deficency

[pcgizzmo]

I thought some people might want to read this. It seems like some people with one deficency of the pituitary can also have this.

http://www.medscape.com/viewarticle/531474

[painman]

If you can copy paste that article it would be great. The link won't let me in.

Originally Posted by pcgizzmo

I thought some people might want to read this. It seems like some people with one deficency of the pituitary can also have this.

http://www.medscape.com/viewarticle/531474

[pcgizzmo]

Sorry Guys. Tried to post the copied page last night but the site was down for some reason. Here it is.

May 1, 2006 — The Endocrine Society created guidelines for the evaluation and treatment of adult growth hormone deficiency (GHD), and they are available in the April 24 Rapid Electronic Publications issue of the Journal of Clinical Endocrinology and Metabolism.
Since growth hormone (GH) treatment of adults with GH deficiency was approved by the Food and Drug Administration in 1996, much clinical experience has accumulated regarding the treatment of adults with GHD.
"Although treatment appears to be safe overall, certain areas require long-term surveillance, such as risks of glucose intolerance, pituitary/hypothalamic tumor recurrence, and cancer," write Mark E. Molitch, MD, from the Northwestern University Feinberg School of Medicine in Chicago, Ill, and colleagues for The Endocrine Society's Clinical Guidelines Subcommittee of the Clinical Affairs Committee. "Benefits of GH treatment of GH-deficient adults have been found in body composition, bone health, cardiovascular risk factors, and quality of life indicators. However, reductions in cardiovascular events and mortality have yet to be demonstrated, and treatment costs remain high."
The purpose of these guidelines was to summarize available information regarding adult GHD and to make recommendations concerning several specific questions:
• Who are appropriate candidates for GH therapy?
• What tests should be used in diagnosing GHD, and what diagnostic criteria should be used?
• What are the benefits of GH treatment in GH-deficient adults?
• What are the risks of GH treatment in GH-deficient adults?
• What treatment regimens are recommended, and how should they be monitored?
"The decision to treat adults with GHD requires thoughtful clinical judgment," the authors write. "For each potential patient, a careful evaluation of the benefits and risks is required before a decision to treat can be reached. Furthermore, if there is a decision to treat, then periodic reevaluation of treatment is warranted."
A review of the available literature led the consensus panel to conclude that GHD can persist from childhood or be newly acquired. Unless there is a proven genetic or structural lesion persistent from childhood, stimulation testing is usually required to confirm the diagnosis. Benefits of GH extend to body composition, exercise capacity, skeletal integrity, and quality-of-life measures, especially in those patients with more severe GHD. Although the risks for GH treatment are low, dosing regimens should be individualized. The final decision to treat adults with GHD mandates thoughtful clinical judgment and a careful evaluation of benefits and risks specific to each individual patient.
Specific recommendations made by the panel are as follows:
• Patients with childhood-onset GHD in whom GH therapy is thought to be appropriate should be retested for GHD as adults, unless they have known mutations, embryopathic lesions, or irreversible structural lesions or damage (level of evidence: high).
• In adults with evidence of structural disease, surgery, or irradiation to the hypothalamic/pituitary areas or with other pituitary hormone deficiencies, evaluation for acquired GHD should be considered (level of evidence: high).
• To establish the diagnosis of GHD, the preferred test is the insulin tolerance test or the GH-releasing hormone-arginine test. However, in those with clearly established recent hypothalamic causes of suspected GHD, such as irradiation, testing with GH-releasing hormone-arginine may be misleading (level of evidence: high).
• In children with structural lesions with multiple hormone deficiencies and those with proven genetic causes, the cause of GHD is irreversible. A low insulin-like growth factor I level for at least 1 month off GH therapy is therefore sufficient documentation of persistent GHD without additional provocative testing (level of evidence: moderate).
• In adults with GH deficiency, GH therapy offers significant clinical benefits in body composition, exercise capacity, skeletal integrity, and quality-of-life measures (level of evidence: moderate).
• GH treatment is most likely to benefit patients with more severe clinical and biochemical abnormalities. In such patients, treatment should be encouraged (level of evidence: moderate).
• GH treatment is contraindicated when an active malignancy is present (level of evidence: low).
• GH dosing regimens should be individualized rather than based on weight (level of evidence: high).
• GH treatment should start with low doses and should be titrated on the basis of clinical response, adverse effects, and insulin-like growth factor I levels (level of evidence: high).
• GH dosing should make provision for age, sex, and estrogen status (level of evidence: high).
• During GH treatment, patients should be monitored at 1- to 2-month intervals during dose titration and semiannually thereafter. Monitoring should include a clinical assessment and an evaluation for adverse effects, insulin-like growth factor I levels, and other parameters of GH response (level of evidence: moderate).
Other suggestions made by the guidelines panel are as follows:
• Because a normal insulin-like growth factor I level does not exclude the diagnosis of GHD, provocative testing is mandatory to diagnose GHD in the context of other pituitary disease (level of evidence: high).
• In the absence of catabolic conditions and liver disease, a low insulin-like growth factor I level indicates severe GHD and may help identify patients who will benefit from treatment (level of evidence: moderate).
• Deficiencies in 3 or more pituitary axes strongly suggest the presence of GHD. In this context, provocative testing is optional (level of evidence: moderate).
• In patients with diabetes mellitus, GH treatment may require adjustments in antidiabetic medications (level of evidence: moderate).
"GH therapy has been shown to benefit many adults with GHD," the panel writes. "Confirmation of GHD before beginning therapy is crucial and usually involves biochemical testing. The demonstrated benefits of GH therapy include improvements in body composition, exercise capacity, skeletal integrity, lipids, and quality of life."
The panel notes that GH treatment may reduce the increased vascular mortality associated with hypopituitarism, but this has not yet been proven.
"It should be emphasized that long-term clinical outcome studies on hard endpoints such as fractures, clinical heart disease, cancer, and mortality are still lacking at present," the authors conclude. "Dosing should be individualized with attention to avoidance of side effects. Periodic monitoring will be necessary for adverse effects and physiological benefit."
No corporate funding or individual remuneration was provided for the writing of these guidelines.
J Clinical Endocrinol Metab. Posted online April 24, 2006.
Learning Objectives for This Educational Activity
Upon completion of this activity, participants will be able to:
• Describe possible etiologies of GHD.
• Identify beneficial effects of treatment of GHD with biosynthetic GH.
Clinical Context
GHD is most often idiopathic among children, whereas GHD in adults is usually due to pituitary adenomas and their treatment. Isolated GHD has been linked with autosomal recessive, autosomal dominant, and X-linked genetic disorders, and the authors of the current recommendations note that microadenomas rarely cause GHD. Following pituitary surgery, GH is less likely to recover compared with other pituitary hormones. Finally, radiotherapy can result in GHD, especially in younger patients who received a higher dose of radiotherapy. A longer duration since radiotherapy also increases the risk for GHD.
The current article describes the diagnosis, treatment, and monitoring of GHD.
Study Highlights
• Because idiopathic GHD in childhood may resolve, adults with this history should be retested prior to treatment with GH. However, retesting is not necessary among adults with a history of GHD and known mutations, embryopathic lesions, or irreversible structural changes in the hypothalamus or pituitary gland.
• Adults with structural hypothalamic/pituitary disease, surgery, or irradiation in these anatomic areas, or other pituitary hormone deficiencies should be considered for testing for GHD.
• Testing for serum GH is insufficient to help diagnose GHD, but provocation tests like the insulin tolerance test and GH-releasing hormone-arginine tests are useful. Such provocation testing is usually not necessary among patients with low levels of insulin-like growth factor I and either a history of hypothalamic/pituitary structural lesions and multiple hormone deficiencies or a proven genetic cause of GHD.
• GH therapy can reduce total body fat and may have a preferential effect on visceral fat. This treatment also usually promotes an increase in muscle mass, although this effect is less dramatic than the effect on body fat.
• GH replacement stimulates both bone formation and resorption, and positive effects on bone mineral density, while significant, may not be apparent until after 2 years of treatment. Men benefit more from this therapy in terms of bone health compared with women.
• Although height may return to normal in the adolescent years among children treated with GH replacement, consideration should be given to continuing therapy during the transition to adulthood because bone mass continues to accrue in this period with GH therapy.
• GH may have salutary effects on flow-mediated arterial dilatation, C-reactive protein levels, and lipid levels. The effects of exogenous GH on insulin sensitivity are difficult to predict. Some research has suggested an increase in fasting glucose and insulin levels, although these changes may not be consistent over time as patients improve the percent of lean body mass with GH therapy.
• Quality of life is most likely to improve with GH therapy among patients with quality-of-life scores below normal at baseline.
• The most common adverse effects of GH replacement are related to fluid retention. Carpal tunnel syndrome can occur in approximately 2% of treated patients. Rare complications include retinopathy, benign intracranial hypertension, and gynecomastia. GH therapy is contraindicated in the presence of an active malignancy, but its use has not been demonstrated to increase the recurrence of tumors. Serum glucose and/or diabetes medications, free thyroxine levels, and measures of the hypothalamic-pituitary-adrenal axis should be monitored during therapy.
• Treatment regimens with GH should be individualized rather than based on weight; and age, sex, and estrogen status should be considered when deciding on an initial dose and titration schedule. Patients should be monitored every 1 to 2 months after treatment initiation for clinical response, adverse effects, and insulin-like growth factor I levels, and these factors should all contribute to determining the titration schedule.
Pearls for Practice
• GHD in children is most often idiopathic, whereas GHD in adults is most frequently secondary to pituitary adenomas and their treatment.
• Treatment with GH in GHD can improve bone density, percent body fat, lipid levels, and quality of life among subjects with clinical symptoms of GHD.

[painman]

Excellent, thanks!