Growth Hormone Deficiency in Adults Guidelines

Updated: Jun 26, 2018
  • Author: Mohsen S Eledrisi, MD, FACP, FACE; Chief Editor: George T Griffing, MD  more...
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Guidelines

Guidelines Summary

The Endocrine Society clinical practice guideline on the evaluation and treatment of adult growth hormone (GH) deficiency includes the following recommendations [7] :

  • Patients with childhood-onset GH deficiency who are candidates for GH therapy after adult height achievement should be retested for GH deficiency unless they have known mutations, embryopathic lesions causing multiple hormone deficits, or irreversible structural lesions/damage.
  • Adult patients with structural hypothalamic/pituitary disease, surgery or irradiation in these areas, head trauma, or evidence of other pituitary hormone deficiencies should be considered for evaluation for acquired GH deficiency.
  • Because idiopathic GH deficiency in adults is very rare, stringent criteria are necessary to make this diagnosis, and because in the absence of suggestive clinical circumstances there is a significant false-positive error rate in the response to a single GH stimulation test, it is suggested that two tests be used before making this diagnosis. The presence of a low insulin-like growth factor-1 (IGF-1) also increases the likelihood that this diagnosis is correct.
  • The insulin tolerance test (ITT) and the GH releasing hormone (GHRH)-arginine test have sufficient sensitivity and specificity to establish the diagnosis of GH deficiency, but in those with clearly established, recent (within 10 yr) hypothalamic causes of suspected GH deficiency (eg, irradiation), testing with GHRH-arginine may be misleading.
  • When GHRH is not available and performance of an ITT is either contraindicated or not practical in a given patient, the glucagon stimulation test can be used to diagnose GH deficiency.
  • Because of the irreversible nature of the cause of GH deficiency in children with structural lesions with multiple hormone deficiencies and those with proven genetic causes, a low IGF-1 level at least 1 month off GH therapy is sufficient documentation of persistent GH deficiency without additional provocative testing.
  • A normal IGF-1 level does not exclude the diagnosis of GHD but makes provocative testing mandatory to make the diagnosis of GH deficiency. However, a low IGF-1 level, in the absence of catabolic conditions such as poorly controlled diabetes, liver disease, and oral estrogen therapy, is strong evidence for significant GH deficiency and may be useful in identifying patients who may benefit from treatment and therefore require GH stimulation testing.
  • The presence of deficiencies in three or more pituitary axes strongly suggests the presence of GH deficiency, and in this context provocative testing is optional.
  • GH dosing regimens should be individualized rather than weight-based and started with low doses and be titrated according to clinical response, side effects, and IGF-1 levels.
  • During GH treatment, patients should be monitored at 1- to 2-month intervals during dose titration and semiannually thereafter with a clinical assessment and an evaluation for adverse effects, IGF-1 levels, and other parameters of GH response.