Treatment algorithm

Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer

ACUTE

confirmed GH deficiency

1st line – recombinant human growth hormone (rhGH)

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ACUTE
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confirmed GH deficiency
1st line – 

recombinant human growth hormone (rhGH)

The decision to treat a patient with rhGH should be undertaken after taking into consideration the growth pattern, insulin-like growth factor 1 and its binding protein concentrations, results of the peak GH concentrations after two provocation tests, and the child/family preferences.

A rapid short-term growth is followed by a normalization of long-term growth. Treatment should be continued until final height or epiphyseal closure is achieved.[59]

A good predictor of response to treatment is the first year height-gain. Other factors include age and height at the start of treatment, duration of treatment, and, in patients with isolated growth hormone deficiency (GHD), the prepubertal growth on receiving treatment.[23][60]

rhGH is safe and well tolerated. There is no risk of Creutzfeldt-Jakob disease. Adverse effects include benign intracranial hypertension, progression of scoliosis, salt and water retention, acute pancreatitis, and slipped capital femoral epiphysis. Thyroid function tests should be carried out regularly because hypothyroidism may be unmasked by treatment.[68] GH treatment also results in an increase in conversion of cortisol to cortisone. Therefore, patients with combined pituitary hormone deficiencies on multiple hormone replacements may need an adjustment in the dose. A routine increase in the dose of GH at puberty is not recommended unless the predicted adult height is low, because a high dose can exacerbate physiologic hyperinsulinemia at puberty.[42][69]

The recommended starting dose of rhGH varies and depends on the brand and formulation used. The dose is titrated against IGF1 concentrations which should be kept within the normal range.[42][67]​​​​​ Lower doses can lead to excellent responses. GH treatment can contribute to hypoglycemia recovery and may improve cholestasis during the neonatal period.[66] A dose adjustment may need to be considered in children with obesity at the start of treatment.[77]

Somatrogon, a long-acting rhGH analog, is approved in the US and Europe for the treatment of GHD in children ages ≥3 years and adolescents. Somatrogon is administered once weekly rather than daily.

​Subsequent dosing should be individualized via monitoring of IGF1 concentrations (at least every 3 months initially after treatment has been commenced). Patients also should be monitored for hypothyroidism and adrenal insufficiency as GH treatment increases metabolism of thyroid hormone and cortisol and may unmask these conditions.[67] Neonates with isolated GHD (IGHD) or combined pituitary hormone deficiencies (CPHD) will require long-term follow-up to detect early evolving endocrinopathies and optimize treatment.

There is no evidence to suggest an increased risk of malignancies above that of the general population in patients without other risk factors, or tumor progression/recurrence in patients successfully treated for their primary lesion using the current dosage recommendations for rhGH.[42][44] In general, GH should not be given with an active malignant condition. Current recommendations, based on widespread clinical practice, are that treatment should only be commenced after waiting 12 months from the end of oncologic treatment, with the exception of craniopharyngiomas and optic pathway gliomas.[42][44]

Primary options

somatropin (recombinant): consult specialist for guidance on dose

OR

somatrogon: consult specialist for guidance on dose

Consider – treatment of underlying cause

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ACUTE
|
confirmed GH deficiency
Consider – 

treatment of underlying cause

Treatment recommended for SOME patients in selected patient group

If a central nervous system tumor is present, urgent neurosurgical and neuro-oncologic referral should be sought. GH should not be given with an active malignant condition. Tumor marker tests (prolactin, alpha-fetoprotein, beta-human chorionic gonadotropin) should be performed prior to definitive treatment in all patients with sellar/suprasellar lesions to exclude the diagnosis of a prolactinoma and germ cell tumor, respectively, which may not require immediate neurosurgical intervention. Apart from craniopharyngiomas and optic pathway gliomas, current recommendations are to wait for 1 year from the end of treatment before replacing GH.

Optimization of blood transfusion/chelation therapy may be required in patients who develop growth hormone deficiency (GHD) due to iron overload, although this complication is not typically reversible.

Patients with eye abnormalities should be referred to an ophthalmologist to detect optic nerve hypoplasia or a suprasellar space-occupying lesion pressing on the optic chiasm/nerves.

Psychosocial causes of GHD need to be treated as appropriate, because the GHD is entirely reversible and would not respond as well to recombinant human GH.

Consider – treatment of associated pituitary hormone deficiencies

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ACUTE
|
confirmed GH deficiency
Consider – 

treatment of associated pituitary hormone deficiencies

Treatment recommended for SOME patients in selected patient group

Confirmation of the diagnosis of growth hormone deficiency requires a full pituitary evaluation to rule out other anterior and/or posterior pituitary hormone dysfunction.

Thyroid-stimulating hormone deficiency should be treated with levothyroxine.

Adrenocorticotropic hormone deficiency should be treated with glucocorticoid treatment. These patients do not require treatment with mineralocorticoids as this axis is intact. Glucocorticoid replacement may unmask arginine vasopressin deficiency (AVP-D; central diabetes insipidus).

Central precocious puberty can be treated with gonadotropin-releasing hormone analogs.

Gonadotropin deficiency should be treated with estrogen in girls (eventually with progesterone) and with testosterone in boys. Common practice is to delay pubertal induction for at least 6 months after commencing GH replacement to optimize adult height.

AVP-D is treated with desmopressin therapy.

There are no known deleterious effects of prolactin or oxytocin deficiency in children.

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Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups. See disclaimer

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