Indications for Growth Hormones

Overview of Recombinant Human Growth Hormone (rhGH)

Recombinant human GH (rhGH) indicated for promotion of linear growth.
Utilized to replace endogenous deficiency or augment growth in specific non-GH-deficient conditions.
Administered primarily via daily subcutaneous injections.

There are 8 FDA approved indications for GH in pediatric pracice

Indication	Year of FDA Approval	Clinical Context
Growth Hormone Deficiency (GHD)	1985	Pituitary or hypothalamic failure to secrete adequate GH.
Chronic Renal Insufficiency (CRI)	1993	Pre-transplant growth failure.
Turner Syndrome	1996	Haploinsufficiency of SHOX gene on X chromosome.
Prader-Willi Syndrome (PWS)	2000	Growth failure, indicated to improve body composition.
Small for Gestational Age (SGA)	2001	Failure to manifest catch-up growth by 2-3 years of age.
Idiopathic Short Stature (ISS)	2003	Height below -2.25 SD (1.2 percentile) without identified pathology.
SHOX Gene Haploinsufficiency	2007	Short stature associated with Leri-Weill dyschondrosteosis.
Noonan Syndrome	2008	Syndromic short stature lacking organic GH deficiency.

Arises from congenital malformations, genetic defects, or acquired central nervous system (CNS) insults.
Replaces absolute lack of GH to restore physiological growth velocity.
Highly effective; accelerates linear growth rapidly within first year of treatment.

Affects 45,X females (or mosaic variants) presenting with universal short stature.
Short stature driven by SHOX haploinsufficiency impairing growth plate chondrogenesis.
GH therapy normalizes adult stature if initiated early in mid-to-early childhood.

Characterized by short stature, morbid obesity, and hypotonia.
GH indicated to increase linear growth, increase lean muscle mass, and decrease fat mass.
High risk of obstructive sleep apnea (OSA); mandates pre-treatment polysomnography.

Defined by birth weight/length below -2 SD.
Approximately 10% fail to demonstrate spontaneous catch-up growth by age 2 years.
GH therapy increases linear growth to prevent permanent adult short stature.

Pre-transplant growth failure driven by anorexia, glucocorticoid use, GH insensitivity, and IGF-binding protein excess.
GH therapy accelerates height velocity prior to renal transplantation.

Indicated for severe short stature (←2.25 SD) lacking alternative treatable pathology.
Shared decision-making mandated due to highly variable individual response.
Mean adult height gain approximately 6 cm after 6 years of therapy.

Standard GHD dose: 0.16–0.24 mg/kg/week (22–35 $μ$ g/kg/day).
Higher doses often required during puberty or for non-GHD indications (e.g., Turner syndrome requires ~50 $μ$ g/kg/day).
Administered via daily subcutaneous injection; long-acting weekly formulations recently FDA approved.

Auxological measurements and Tanner staging every 6 months.
Monitor Insulin-like Growth Factor-1 (IGF-1) to assess adherence and dose responsiveness.
Obtain bone age radiograph when growth velocity drops to 2–2.5 cm/year to confirm epiphyseal fusion.
Evaluate thyroid and adrenal function; GH physiologically alters glucocorticoid metabolism and increases peripheral T4-to-T3 conversion, potentially unmasking central hypothyroidism or adrenal insufficiency.

Intracranial Hypertension (Pseudotumor Cerebri): Incidence of 28 per 100,000 treatment-years; manifests as headache and papilledema during dose initiation/escalation. Resolves with dose suspension.
Slipped Capital Femoral Epiphysis (SCFE): Incidence of 73 per 100,000 treatment-years; presents as hip pain/gait disturbance. Requires surgical pinning.
Scoliosis Progression: Rapid growth velocity may exacerbate pre-existing spinal curvatures, particularly in Turner syndrome and PWS.
Carbohydrate Metabolism: GH physiologically decreases insulin sensitivity. Induces transient glucose intolerance or unmasks type 2 diabetes. Resolves upon treatment discontinuation.