What it's for (Indications)
- Growth hormone deficiency (in pediatric patients with endogenous deficiency and adults requiring replacement therapy), Turner syndrome, growth retardation in children with chronic renal insufficiency, Prader-Willi syndrome in children, Idiopathic Short Stature (ISS), SHOX deficiency, and Small for Gestational Age (SGA) without catch-up growth.
Dosage Information
| Type | Guideline |
|---|---|
| Standard | Administer by subcutaneous injection to the back of the upper arm, abdomen, buttock, or thigh with regular rotation of injection sites. **Pediatric Dosage:** The calculated weekly dosage should be divided into equal doses given either 3, 6, or 7 days per week. - GH deficiency: 0.18 mg/kg/week to 0.3 mg/kg/week. - Turner syndrome: Up to 0.375 mg/kg/week. - Idiopathic Short Stature (ISS): Up to 0.37 mg/kg/week. - SHOX deficiency: 0.35 mg/kg/week. - Small for Gestational Age (SGA): Up to 0.47 mg/kg/week. **Adult Dosage:** Either of the following two dosing regimens may be used: - **Non-weight based dosing:** Initiate with approximately 0.2 mg/day (range, 0.15 mg/day to 0.3 mg/day). Increase the dose every 1 to 2 months by increments of approximately 0.1 mg/day to 0.2 mg/day, according to individual patient requirements. - **Weight-based dosing (not recommended for obese patients):** Initiate at 0.006 mg/kg daily and increase the dose according to individual patient requirements. |
Safety & Warnings
Common Side Effects
- Commonly reported side effects include hypothyroidism, transient edema/fluid retention, headache, glucosuria, hyperglycemia/glucose intolerance, muscle pain, weakness, and pain at the injection site.
- More severe adverse reactions include increased mortality (particularly in acute critical illness), fatalities in pediatric patients with Prader-Willi syndrome, neoplasms, intracranial hypertension, severe hypersensitivity reactions (including anaphylaxis and angioedema), hypoadrenalism, slipped capital femoral epiphysis in pediatric patients, progression of pre-existing scoliosis, and pancreatitis.
Serious Warnings
- Black Box Warning: Increased mortality in patients with acute critical illness. Fatalities in pediatric patients with Prader-Willi syndrome who are severely obese, have a history of upper airway obstruction or sleep apnea, or have severe respiratory impairment.
- Increased mortality has been observed in patients with acute critical illness (e.
- g.
- , after open heart surgery, abdominal surgery, multiple accidental trauma, or acute respiratory failure).
- Fatalities have occurred in pediatric patients with Prader-Willi syndrome who are severely obese, have a history of upper airway obstruction or sleep apnea, or have severe respiratory impairment.
- The risk of neoplasms may be increased.
- Somatropin use can lead to glucose intolerance and diabetes mellitus; glucose levels should be monitored.
- Benign intracranial hypertension (pseudotumor cerebri) can occur, requiring caution in patients with intracranial lesions.
- Severe hypersensitivity reactions have been reported.
- Fluid retention may occur.
- Hypoadrenalism may occur or worsen existing conditions.
- Hypothyroidism can be caused or worsened; thyroid function should be monitored regularly.
- Pediatric patients should be monitored for slipped capital femoral epiphysis and progression of pre-existing scoliosis.
- Pancreatitis can occur.
- The effects of this medication are undetermined in pregnant and nursing females; caution is advised, and healthcare provider consultation is recommended.
- Patients should avoid driving and consuming alcohol due to potential effects on their ability.
- Precautions are also necessary for patients with ACTH deficiency.
How it Works (Mechanism of Action)
Somatropin binds to dimeric growth hormone (GH) receptors located within the cell membranes of target tissue cells. This interaction initiates intracellular signal transduction and subsequent induction of transcription and translation of GH-dependent proteins, including IGF-1, IGF BP-3, and acid-labile subunit. Somatropin exerts direct tissue and metabolic effects or effects mediated indirectly by IGF-1, including stimulation of chondrocyte differentiation and proliferation, hepatic glucose output, protein synthesis, and lipolysis. In pediatric patients with GHD, it stimulates skeletal growth through effects on the growth plates (epiphyses) of long bones, increasing linear growth rate (height velocity) and facilitating growth in part by increased cellular protein synthesis.