Growth Hormone Deficiency in Adults Guidelines

Updated: Jun 17, 2022
  • Author: Mohsen S Eledrisi, MD, FACP, FACE; Chief Editor: George T Griffing, MD  more...
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2019 American Association of Clinical Endocrinologists and American College of Endocrinology Guidelines

Guidelines for the management of growth hormone (GH) deficiency in adults and patients transitioning from pediatric to adult care were published in 2019 by the American Association of Clinical Endocrinologists (AACE) and American College of Endocrinology (ACE). [18] Select recommendations are summarized below.

In the setting of clinical suspicion of adult GH deficiency, it is crucial to establish the diagnosis before considering replacement therapy with recombinant human GH (rhGH).

Consider the possibility of adult GH deficiency in patients with a history of hypothalamic-pituitary disease.

It is important to recognize the differences in the etiology of childhood-onset GH deficiency (CO-GHD) versus adult-onset GH deficiency (AO-GHD). Because CO-GHD occurs during the developmental years, adults with this condition may have been GH-deficient for a longer period than patients with AO-GHD.

GH–stimulation testing should be performed to confirm the diagnosis, as random serum GH and insulin-like growth factor-1 (IGF-1) levels cannot be used alone to diagnosis adult GH deficiency.

Use the insulin tolerance test (ITT) to establish a diagnosis of GH deficiency. If this test is contraindicated, then use the glucagon stimulation test or macimorelin stimulation test instead.

Perform one GH-stimulation test to confirm the diagnosis in patients with two or fewer pituitary hormone deficiencies (PHD), as low-serum IGF-1 levels alone are not sufficient to make a diagnosis of adult GH deficiency.

Use body mass index (BMI)–appropriate GH cut-points to diagnose adult GH deficiency. Use the GH cut-point of 3 μg/L for normal-weight (BMI < 25 kg/m2) and overweight (BMI 25 to 30 kg/m2) patients with a high pretest probability, and a lower GH cut-point of 1 μg/L for obese (BMI >30 kg/m2) and overweight (BMI 25 to 30 kg/m2) patients with a low pretest probability.

Closely monitor adults with CO-GHD caused by structural pituitary or brain tumors during their transition to adult-care services. These patients tend to have lower bone mineral density, impaired bone microarchitecture, and more adverse body composition abnormalities and cardiovascular risk markers than patients with AO-GHD.

Individualize rhGH replacement therapy and initiate at low dosages. Suggested starting doses are as follows:

  • Age < 30 years: 0.4-0.5 mg/day (doses may be higher for those transitioning from pediatric care. For transitioning patients, resume rhGH at half the dose used in childhood.)
  • Age 30-60 years: 0.2-0.3 mg/day
  • Age >60 years: 0.1-0.2 mg/day

Lower starting rhGH doses (eg, 0.1-0.2 mg/day) are recommended for those with concurrent diabetes mellitus or previous gestational diabetes, obesity, and older age.

Reduce rhGH dosing in the elderly, patients with elevated serum IGF-1, persons discontinuing use of oral estrogen or changing from oral to transdermal estrogen, individuals with worsening glucose tolerance, or those who have fluid retention-related side effects.

After starting rhGH therapy, follow patients at 1- to 2-month intervals, increasing the rhGH dose in increments of 0.1 to 0.2 mg/day.

Never use rhGH replacement therapy for age-related conditions or to enhance athletic performance.


2011 Endocrine Society Guidelines

The Endocrine Society clinical practice guideline on the evaluation and treatment of adult growth hormone (GH) deficiency includes the following recommendations [15] :

  • 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 y) 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.