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 (IGF1) and its binding protein concentrations, results of the peak GH concentrations after two provocation tests, and the child/family preferences.

Rapid short-term growth is followed by normalisation of long-term growth. Treatment should be continued until final height or epiphyseal closure is achieved.[61]

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 GHD, pre-pubertal growth on receiving treatment.[23][62]

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 physiological hyperinsulinaemia at puberty.[42][69]

The recommended starting dose of rhGH is 0.16 to 0.24 mg/kg/week subcutaneously (preferably in the evenings, 22-35 micrograms/kg per day), titrated against IGF1 concentrations which should be kept within the normal range.[36][42]​ Lower doses (10-20 micrograms/kg/day) can also lead to excellent responses. GH treatment can contribute to hypoglycaemia recovery and may improve cholestasis during the neonatal period.[37] Doses may vary depending on the brand of rhGH used. Alternative dosing may need to be considered in a child who is obese at the start of treatment.[78]​ Somatrogon is approved in the UK and Europe for the treatment of GHD in children ≥3 years of age and adolescents; however, it has been rejected for approval by the US Food and Drug Administration (FDA). Currently, somatrogon is the only long-acting GH formulation which has been recommended by NICE.[79]

​Subsequent dosing should be individualised 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.[36] Neonates with isolated GHD (IGHD) or combined pituitary hormone deficiencies (CPHD) will require long-term follow-up to detect early evolving endocrinopathies and optimise 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 tumour 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 oncological 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

Additional treatment recommended for SOME patients in selected patient group

If a central nervous system tumour is present, urgent neurosurgical and neuro-oncological referral should be sought. GH should not be given with an active malignant condition. Tumour marker tests (prolactin, alpha-fetoprotein, beta-human chorionic gonadotrophin) should be performed prior to definitive treatment in all patients with sellar/suprasellar lesions to exclude the diagnosis of a prolactinoma and germinoma, 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.

Optimisation of blood transfusion/chelation therapy may be required in patients who develop 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

Additional treatment recommended for SOME patients in selected patient group

Confirmation of the diagnosis of GHD 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.

Adrenocorticotrophic 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 diabetes insipidus.

Central precocious puberty can be treated with gonadotrophin-releasing hormone analogues.

Gonadotrophin deficiency should be treated with oestrogen in girls (eventually with progesterone) and with testosterone in boys.

Diabetes insipidus is treated with desmopressin (DDAVP) 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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