Norditropin Injection


Overview of Norditropin (Somatropin) Injection

Dosage Strengths of Norditropin Injection

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General Information

Somatropin, or rh-GH, is a pure form of recombinant growth hormone produced by either mammalian or Escherichia coli bacteria. The pituitary produces endogenous human growth hormone (hGH). In 1956, the first growth hormone was extracted, and its structure was discovered in 1972. Growth hormone (GH) was previously generated from human cadavers prior to 1985; however, this practice was discontinued due to Creutzfeldt-Jakob virus contamination of the product. Somatropin is licensed for use in adults with short bowel syndrome, growth hormone deficit (GHD), growth failure, or short stature, as well as cachexia and AIDS wasting. In studies for the treatment of HIV-associated adipose redistribution syndrome (HARS), somatropin has been shown to reduce visceral adipose tissue, according to limited short-term evidence. There are numerous somatropin medications available, each with unique indications and dose guidelines. It is important to choose products carefully because they could not be interchangeable. The FDA initially authorized somatropin in 1987.

Mechanisms of Action

Children and adolescents’ normal skeletal, connective tissue, muscle, and organ growth is stimulated by endogenous growth hormone. Additionally, it’s crucial for adult metabolism. Recombinant goods imitate each of these behaviors. Growth hormone (GH) receptors are occupied by somatropin, which binds to them and causes a variety of direct and indirect physiological consequences. The direct effects include inhibition of insulin’s peripheral action, which in turn stimulates insulin secretion; stimulation of the liver’s and other tissues’ production of somatomedins or insulin-like growth factors (IGFs); stimulation of adipose tissue’s triglyceride hydrolysis; stimulation of the liver’s output of glucose; induction of a favorable calcium balance; and retention of sodium and potassium. These effects, which insulin opposes on the metabolism of fat and carbohydrates, are amplified by glucocorticoids.

The anabolic and growth-promoting actions of somatropin are indirectly mediated by somatomedins or insulin-like growth factors (IGFs). IGFs float around the body and attach to particular IGF receptors. IGF-1 and IGF-2 are the two known IGFs. Growth hormone appears to be primarily mediated by IGF-1, whereas IGF-2 has more insulin-like activity. The main anabolic effects of IGFs include inducing cell proliferation and growth, stimulating amino acid transport, and stimulating DNA, RNA, and protein synthesis. IGF-1 is directly in charge of chondrogenesis, skeletal development, and soft tissue expansion. By altering the cartilaginous growth regions of long bones, linear growth is encouraged. The quantity and size of skeletal muscle cells, the size of organs, and the activation of erythropoietin all contribute to the stimulation of growth. Growth hormones can affect the gut directly or indirectly through the local or systemic synthesis of IGF. Growth hormone has been found to improve the transmucosal transfer of nutrients, electrolytes, and water in in-vivo experiments. Glucocorticoids prevent these collateral effects.


Injected intramuscularly or subcutaneously, somatropin is given. Somatropin reaches its peak plasma concentrations 2 to 6 hours after dosing. Growth hormone-binding protein binds around 20% of the somatropin in circulation. IGF-1 plasma concentration peaks occur roughly 20 hours following somatropin treatment. The liver, kidney, and other tissues all metabolize somatropin. Glomerular filtration of somatropin occurs, and the kidney is where the molecule is broken down. The peptides and amino acids are released back into the bloodstream after being cleaved in the renal cells. Urine excretion is not very common. The half-life of plasma elimination is 20 to 30 minutes. The serum concentrations decrease with a half-life of roughly 3–5 hours as a result of the continuous release of somatropin from the intramuscular or subcutaneous location. The effects of somatropin extend considerably longer than its half-life of elimination due to the sluggish induction and clearance of IGF-1.

Route-Specific Pharmacokinetics:

Subcutaneous Route: Somatropin is first released from the microspheres via diffusion after subcutaneous injection of the depot formulation, and then it is released by both polymer degradation and diffusion. When compared to single dose Nutropin AQ and when compared to chronically dosed Protropin, the estimated bioavailability after a single dose of Nutropin Depot varies from 33 to 38% and 48 to 55%, respectively. Somatropin is thought to be distributed and removed in a similar way to somatropin designed for everyday use once it has been released and absorbed. The dose has an impact on both the Cmax and AUC. After a single dose of 0.75 or 1.5 mg/kg, serum growth hormone levels remain over 1 mcg/l for 11–14 days.

Special Populations:

Pediatrics: Although no pharmacokinetic studies have been carried out in children with short bowel syndrome, it appears that the clearance of somatropin in children and adults is comparable.

Gender Differences: Males may eliminate somatropin more quickly than females, according to biomedical literature, while there is no gender-based analysis available.


For the treatment of growth hormone deficiency, growth failure, or short stature:

NOTE: In pediatric patients, the response to somatropin therapy typically deteriorates over time. However, the inability to increase growth rate, particularly in the first year of therapy, calls for a close examination of compliance and a search for underlying factors that may be contributing to growth failure, such as hypothyroidism, undernutrition, advanced bone aging, and antibodies to recombinant human growth hormone.

Adults with growth hormone deficiency (GHD) with onset in childhood (due to congenital, genetic, acquired, or idiopathic reasons) or adult onset may consider replacement therapy (endogenous or associated with multiple hormone deficiencies, i.e., hypopituitarism, as a result of pituitary disease, hypothalamic disease, surgery, radiation therapy, or trauma):

NOTE: In general, a suitable growth hormone stimulation test should be used to confirm the diagnosis of both adult and juvenile onset growth hormone deficit. Patients with numerous pituitary hormone shortages resulting from organic disease or congenital/genetic growth hormone insufficiency may not require stimulation tests.

NOTE: To help with dose titration, clinical response, adverse effects, and age- and gender-adjusted serum IGF-I levels may be considered. This strategy will typically lead to higher dosages for women than for males, lower doses for patients with adult-onset GHD than for those with childhood-onset GHD, and lower doses for elderly and obese patients.

NOTE: Before continuing somatropin medication, patients with childhood-onset growth hormone insufficiency and closed epiphyses should be reevaluated.

Geriatric: See adult dosage. Consider giving a lower starting dose and smaller dose increments to minimize adverse events.

Subcutaneous dosage: Adults: Not more than 0.004 mg/kg SC every day at first. The dose may be increased after six weeks, in accordance with tolerance, up to a daily maximum of 0.016 mg/kg. Alternative methods include the following non-weight-based ones: Initial dose: 0.15–0.30 mg SC/day (0.15–0.2 mg SC/day); gradually increase dose by 0.1–0.2 mg/day every 1–2 months dependent on clinical response and serum insulin-like growth factor I (IGF-I) concentrations. If there are any negative side effects or serum IGF-I concentrations that are higher than the usual range for the patient’s age and gender, reduce the dose as appropriate. Male and female patients receive very different maintenance dosages from one another. NOTE: When given a dose based on weight, obese patients are more prone to experience negative effects.

Geriatric: See adult dosage. To reduce adverse effects, consider administering a lower initial dose and smaller dose increments.

To treat children with growth failure over the long term who lack growth hormone due to insufficient growth hormone secretion:

Subcutaneous dosageChildren: 0.024—0.034 mg/kg/dose SC given 6 to 7 times a week. Dosage should be individualized for each patient.

For growth failure due to Prader-Willi syndrome:

Subcutaneous dosage: NOTE: Genotropin and Omnitrope are contraindicated in Prader-Willi syndrome patients who are excessively obese or who have severe respiratory impairment. Genotropin and Omnitrope should only be used in Prader-Willi syndrome patients who have been diagnosed with a growth hormone shortage.

Children: Usually, 0.24 mg/kg SC is given over the course of a week in 6 or 7 equal daily injections.

For the long-term treatment of growth failure in children born small for gestational age (SGA) who fail to manifest catch-up growth by age 2-4:

Subcutaneous dosage: Children: 0.067 mg/kg/day SC (or 0.47 mg/kg/week) is indicated for children. According to recent studies, the initial dose for smaller children with a baseline HSDS between -2 and -3 is 0.033 mg/kg/day SC with upward titration as necessary. If significant catch-up growth is observed during the first few years of treatment, the initial dose should be reduced to 0.033 mg/kg/day SC for children with a baseline HSDS -3 or older/prepubertal children.

For short stature associated with Turner’s syndrome:

Subcutaneous dosage: Children: Up to 0.067 mg/kg/day SC is recommended.

For short stature in children with Noonan Syndrome:

Subcutaneous dosage: Children: SC up to 0.066 mg/kg/day is advised. Make sure the patient is low in stature before starting somatropin. Not all Noonan syndrome patients are short-statured. 24 kids between the ages of 3 and 14 were given doses of 0.033 mg/kg/day SC or 0.066 mg/kg/day SC for two years. After that, the dose was modified based on the kids’ growth responses and continued until the kids reached their final height. The height gain from baseline increased by 1.5 SDS using the national reference (mean height gain of 9.9 cm in males and 9.1 cm in females at 18 years of age). According to the Noonan reference, there was an increase in height from baseline of 1.6 SDS, or a mean height gain of 11.5 cm for men and 11 cm for women at the age of 18.

Maximum Dosage Limits: The dosage of somatropin, rh-GH must be customized for each patient and varies greatly based on the kind and severity of the disease, the formulation being utilized, and the patient’s response.

Route-Specific Administration:

Injectable AdministrationInject somatropin intramuscularly or subcutaneously to administer. Give nothing intravenously. If the epiphyseal fusion or final height are reached, stop the therapy. When the solution and container allow, visually examine parenteral items for debris and discolouration prior to administration.

Subcutaneous AdministrationIt is not advised to inject somatropin subcutaneously in amounts more than 1 ml of reconstituted solution. Be careful not to inject intradermally when injecting SC. Prior to injection, let chilled solutions thaw to room temperature. Injections under the skin can be administered to the abdomen, buttocks, or thighs. daily site rotation for injections.

Intramuscular AdministrationDeeply inject somatropin into a sizable muscle. To prevent injecting into a blood vessel, aspirate before administering. daily site rotation for injections.

Contraindications / Precautions

The FDA informed medical experts that it had evaluated SAGhE (Sante Adulte GH Enfant) trial data in August 2011. (a long-term epidemiological study conducted in France). Compared to the general population, individuals treated with somatropin as children with idiopathic growth hormone insufficiency and idiopathic or gestational low stature had a 30% higher risk of death, according to the SAGhe Study. Recombinant human growth hormone with an elevated risk of death: The FDA found this evidence to be inconclusive.  An enhanced mortality model was developed in 2016 utilizing the Swedish Medical Birth Registry to calculate the standard mortality rates for growth hormone-treated patients in comparison to the general population. The authors came to the conclusion that, rather than being caused by the administration of growth hormone therapy itself, the rise in mortality observed in the SAGhE study was likely related to fundamental traits of the population affected by growth hormone deficiency (such as birth weight, birth length, and congenital malformations).

Some laboratory results may vary as a result of somatropin medication. With somatropin medication, serum levels of inorganic phosphorus, alkaline phosphatase, and parathyroid hormone may rise.

Patients with a known hypersensitivity to somatropin or any of the product excipients should not take somatropin products. With the usage of somatropin drugs beyond their first release, severe systemic hypersensitivity responses, including anaphylactic reactions and angioedema, have been documented. Patients and caregivers should be made aware that major hypersensitivity responses or anaphylaxis are possible, and that if this happens, quick medical help should be sought. Any hormonal product has the potential to cause a local or systemic allergic reaction. M-cresol is a preservative that is present in a number of the items. In patients with m-cresol hypersensitivity, some formulations advise using sterile water for injection as a diluent; other brands advise using different formulations. When taking somatropin in patients with m-cresol hypersensitivity, the package insert of the individual drug should be consulted for more details. In a similar vein, glycerin is also present in several of the formulas. Glycerin-containing somatropin formulations shouldn’t be used in people who have glycerin hypersensitivity.

Somatropin is contraindicated for promoting growth in children who have epiphyseal closure. These patients are no longer capable of linear growth. In addition, people with endocrine abnormalities or those going through rapid growth may experience slipping capital femoral epiphysis more frequently.

Children’s response to somatropin medication tends to deteriorate over time. However, compliance as well as other causes of growth failure such as thyroid problems, malnutrition, advanced bone age, and antibodies to somatropin should be evaluated in children whose growth rate is not enhanced, particularly during the first year of treatment. A clinician should examine any youngster using somatropin who complains of hip or knee pain or who develops a limp. Patients with endocrine issues or growing youngsters may experience slipped capital femoral epiphysis more commonly. Children who experience growth failure due to renal impairment should also be examined for the development of renal osteodystrophy. Children with advanced renal osteodystrophy may develop slipped capital femoral epiphysis or avascular necrosis of the femoral head; x-rays of the hip should be taken prior to starting somatropin medication. Idiopathic growth hormone deficiency and idiopathic or gestational short stature patients treated with somatropin during childhood had a 30% increased risk of death compared to the general population, according to data from the SAGhE (Sante Adulte GH Enfant) study, which the FDA reviewed in August 2011. Recombinant human growth hormone and an elevated risk of death have been linked, but the data isn’t definitive, according to the FDA; a number of flaws in the study’s design have been identified that restrict how well the findings can be understood. The FDA also examined information from the Agency’s Adverse Event Reporting System and the medical literature (AERS). The FDA will continue to investigate this safety concern and anticipates more information from the SAGhE study in the spring of 2012. When fresh information becomes available, the FDA will tell the public. Recombinant human growth hormone should continue to be prescribed and used by medical professionals and patients in accordance with labeling instructions.

In neonates and individuals who have benzyl alcohol hypersensitivity, several multi-dose somatropin preparations that contain benzyl alcohol should be used with caution. In newborns, benzyl alcohol has been linked to poisoning. Sterile water for injection, USP should be used for reconstitution and only one dose should be administered per vial if somatropin is to be administered to newborns or patients who have benzoyl alcohol hypersensitivity.

Somatropin is contraindicated in patients with active neoplastic disease. Any pre-existing neoplastic disease, specifically intracranial lesions (including pituitary tumors) must be inactive, and chemotherapy and radiation therapy complete, prior to beginning somatropin therapy. In childhood cancer survivors who were treated with radiation to the brain/head for their first neoplasm and who developed subsequent growth hormone deficiency and were treated with somatropin, an increased risk of a secondary malignancy has been reported. Intracranial tumors, in particular meningiomas, were the most common of these second neoplasms. It is unknown whether there is any relationship between somatropin replacement therapy and CNS tumor recurrence in adults. Monitor all patients with a history of growth hormone deficiency secondary to an intracranial neoplasm routinely while on somatropin therapy for progression or recurrence of the tumor. Because children with certain rare genetic causes of short stature have an increased risk of developing malignancies, consider the risks and benefits of starting somatropin in these patients. If treatment with somatropin is initiated, these patients should be carefully monitored for development of neoplasms. Monitor patients on somatropin therapy carefully for increased growth, or potential malignant changes, of preexisting nevi. Somatropin therapy should be discontinued if evidence of neoplasia develops.

Somatropin should not be used in individuals with severe critical illnesses brought on by complications from open heart surgery or abdominal surgery, multiple accidental injuries, or acute respiratory failure. Two placebo-controlled clinical trials in adult patients (n=522) with these conditions found that somatropin treatment (5.3–8 mg/day) resulted in a statistically significant increase in mortality (41.9% vs. 19.3%). It has not been determined if it is safe to continue somatropin therapy in individuals getting replacement dosages for medical conditions for which the drug has been licensed. Therefore, the possible benefit of continuing somatropin medication should be balanced against the potential risk in patients with acute critical diseases (see Prader-Willi discussion).

Genotropin and Norditropin’s manufacturers warn that adult patients with obesity taking somatropin for growth hormone insufficiency may be more susceptible to side effects when dosed based on weight (see Dosage). It could be better to use a daily dosage that is not depending on weight. Additionally, there have been cases of mortality associated with somatropin usage in pediatric patients with obesity and Prader-Willi syndrome (see Prader-Willi discussion).

Patients with Prader-Willi syndrome who are extremely obese or have severe respiratory impairment should not take somatropin. Somatotropin is not recommended for the long-term therapy of pediatric patients with genetically proven Prader-Willi syndrome who have growth failure unless they also have a diagnosis of growth hormone insufficiency. Growth hormone use has been linked to mortality in pediatric Prader-Willi syndrome children who had one or more of the risk factors listed below: severe obesity, a history of respiratory failure or sleep apnea, or an unexplained respiratory infection. Patients who are male and have one or more of these risk factors may be at higher risk. Before starting growth hormone therapy, patients with Prader-Willi syndrome should have their upper airways inspected for obstruction. Treatment with growth hormone should be stopped if patients exhibit symptoms of upper airway blockage (including the beginning or worsening of snoring). If sleep apnea is suspected in any Prader-Willi syndrome patient, that patient should also be watched. All Prader-Willi syndrome patients should also maintain healthy weights and be closely watched for any indications of respiratory infections, which should be identified as soon as possible and quickly treated. Additionally, cerebral hypertension may be more common in Prader-Willi syndrome patients.

Patients with diabetes should utilize somatropin with caution. During somatropin therapy, patients with diabetes or glucose intolerance, as well as those who have risk factors for developing these conditions, should be continuously watched. Obesity (including obesity in Prader-Willi syndrome individuals), Turner syndrome, or a family history of type II diabetes are risk factors for glucose intolerance. Patients should be watched for signs of glucose intolerance since somatropin may decrease insulin sensitivity, especially at larger dosages. Chronic somatropin overdose may result in glucose intolerance or acromegaly. When somatropin is started, it may be required to modify the dosage of antidiabetic drugs. Somatropin is not recommended for use in people with diabetic retinopathy because of how it affects blood glucose levels and insulin sensitivity.

Somatropin administration should be cautious for patients with a history of scoliosis. Growth hormone accelerates growth, which might cause scoliosis sufferers to undergo scoliosis progression. Scoliosis progression should be tracked in patients. In addition, people with untreated Turner’s syndrome, Noonan’s syndrome, and Prader-Willi syndrome may exhibit skeletal deformities, such as scoliosis. These anomalies, which could appear with growth hormone therapy, should be known to clinicians.

Patients using somatropin may experience decreased blood cortisol levels and/or the masking of central (secondary) adrenal insufficiency if they have or are at risk for pituitary hormone shortages. Following the start of somatropin therapy, patients receiving glucocorticoid replacement therapy for previously identified adrenal insufficiency might need to increase their maintenance or stress dosages. Patients who have untreated hypothyroidism will also not respond well to somatropin medication. Due to the increased risk of autoimmune thyroid disease in Turner’s syndrome patients, changes in thyroid hormone plasma levels may occur with somatropin therapy. Periodic thyroid function testing should be carried out, and when necessary, thyroid hormone treatment should be started.

It has been shown that somatropin medication can result in elevated intracranial pressure, papilledema, visual abnormalities, headaches, nausea, and/or vomiting. Within the first eight weeks of somatropin medication, symptoms often started to appear. The symptoms of intracranial hypertension went away either when somatropin medication was stopped or after the hormone’s dosage was decreased. When starting somatropin therapy and at intervals thereafter, funduscopic examination is advised. Patients with Prader-Willi syndrome, Turner’s syndrome, and chronic renal insufficiency may be more likely to develop intracranial hypertension.

Somatropin has not been the subject of adequate and controlled research in pregnant women, and it is unclear whether it could have harmful effects on the developing fetus or the reproductive system. Different levels above the typical human dose used in animal research have not been associated with any fetal damage or reduced fertility. Remind women of reproductive age that somatropin usage during pregnancy has not been investigated in humans, therefore it is uncertain how the medicine may affect the fetus.

There is no information available on somatropin’s presence in human milk, its effects on breastfed infants, or its impact on milk production. There are no known negative effects on nursing infants when somatropin is administered to the mother, and there is no evidence that somatropin treatment results in decreased milk production or altered milk composition. Think about the advantages of breastfeeding, the chance that your baby may be exposed to drugs, and the possibility that your condition won’t be treated at all or only partially. Healthcare professionals are urged to notify the FDA if a breast-fed baby develops an adverse reaction to a medication taken by the mother.

Turner’s syndrome patients should have rigorous otitis media and other ear diseases evaluations while receiving somatropin because these patients have a higher risk of ear or hearing abnormalities. Turner’s syndrome patients should also be constantly watched for cardiovascular diseases such stroke, aortic aneurysms, and hypertension because they are also at risk for developing these ailments.

Although significant numbers of elderly individuals were not included in somatropin clinical investigations, published clinical experience has not revealed any variations in reactions between geriatric and younger adult patients. An older adult should generally be given care when choosing a dose, usually beginning at the low end of the dosing range. Patients who are elderly are more susceptible to the side effects of therapy than patients who are children or younger adults. Practice recommendations state that only patients with clinical signs of adult growth hormone deficit (GHD) and biochemical proof of adult GHD should be given growth hormone/somatropin.

Patients with HIV-associated adipose redistribution syndrome (HARS) have been treated with somatropin (Serostim); somatropin therapy may be less successful in female patients with HARS than in male patients. In clinical trials, visceral adipose tissue reduction in 47 women receiving somatropin was comparable to placebo (VAT). The concurrent use of estrogen (6 patients) or a lower baseline VAT level compared to men may be the causes of the lack of effectiveness. Numerous clinical research have shown that lower VAT levels are related to a diminished response to somatropin.

Patients, especially children, who experience severe, ongoing stomach pain while using somatropin should be checked for pancreatitis. Patients who have a history of pancreatitis or who have risk factors for it should use this medication with caution. Rare reports of pancreatitis in both adults and children receiving somatropin have been made, with pediatric patients appearing to be at higher risk than adults. When receiving somatropin medication, girls with Turner syndrome may have an even higher chance of getting pancreatitis than other patients.


Somatropin has not been the subject of adequate and controlled research in pregnant women, and it is unclear whether it could have harmful effects on the developing fetus or the reproductive system. Different levels above the typical human dose used in animal research have not been associated with any fetal damage or reduced fertility. Remind women of reproductive age that because somatropin usage during pregnancy has not been researched in humans, it is uncertain how the medicine may affect the fetus.


There is no information available on somatropin’s presence in human milk, its effects on breastfed infants, or its impact on milk production. According to the few published research, somatropin medication has no negative effects on nursing infants, and neither does it cause a drop in milk production or alter the composition of the mother’s milk. Think about the advantages of nursing, the chance that your baby will be exposed to drugs, and the possibility that they won’t get the treatment they need. Healthcare professionals are urged to notify the FDA if a medicine delivered to the mother causes an adverse effect in a breastfeeding infant.

Adverse Reactions / Side Effects

Patients with adult-onset growth hormone deficit and adults with childhood-onset GH deficiency still needing somatropin medication have had their impact on bone mineral density (BMD) and bone mineral content (BMC) assessed (transition patients). In the adult-onset research, men experienced a 4% increase in lumbar spine BMD compared to placebo, but not women. Neither males nor women’s hip BMD significantly changed. Patients in the transition group who were randomly assigned to receive 12.5 mcg/kg/day of somatropin as opposed to 25 mcg/kg/day or a placebo saw a rise of 2.9% in total BMC; patients in the other two groups saw no changes. The 12.5 mcg/kg/day treatment group likewise experienced statistically significant increases in lumbar spine BMD and BMC. The occurrence of osteoporotic fracture was not studied.

Adult patients with both childhood-onset and adult-onset GH insufficiency were included in an open-label trial to assess the impact of somatropin (Nutropin AQ) on visceral adipose tissue. For 32 weeks, somatropin doses of up to 0.006 mg/kg per day were given to men over the age of 35 and up to 0.012 mg/kg per day to women (all of whom were receiving estrogen replacement therapy). After 32 weeks, somatropin-treated patients’ visceral adipose tissue (VAT) decreased by 14.2% (p = 0.012) as compared to untreated patients (p 0.0001). Somatropin administration to adult GHD patients to lower VAT has not been shown to affect long-term cardiovascular morbidity and mortality.

Somatropin has been linked to an increased chance of developing a secondary cancer. In a limited percentage of patients with growth hormone deficiency who received somatropin, leukemia has been observed. It is unclear if the pathology of growth hormone shortage itself, growth hormone therapy, or other related treatments like radiation therapy for brain tumors are to blame for this elevated risk. A secondary malignancy is also more likely to occur in pediatric cancer survivors who received radiation to the brain or head for their initial tumor and who later experienced growth hormone insufficiency and were treated with somatropin. Meningiomas, in particular, were the most prevalent of these second neoplasms, which included intracranial tumors. It is unclear if adult CNS tumor recurrence and somatropin replacement therapy are related in any way. While receiving somatropin therapy, all patients who have a history of growth hormone shortage as a result of an intracranial neoplasm should be routinely checked for tumor development or recurrence. Consider the hazards and advantages of initiating somatropin in patients who have certain rare genetic reasons of low stature since they have an elevated chance of developing cancer. These patients should be closely watched for the emergence of neoplasms if somatropin medication is started. Patients receiving somatropin medication should be closely watched for any signs of accelerated nevi growth or potential malignant alterations. If signs of neoplasia appear, somatropin medication should be stopped.​​​​​​​

According to the brand of somatropin used, incidences of edema or peripheral edema have varied and ranged from about 5% to 45% in studies of individuals with growth hormone deficiency (GHD). The rates have been around 3% in kids with GHD. The edema seems to start off early in the course of treatment, and it can go away or respond to a dose reduction. Patients using somatropin have frequently reported both fluid retention and peripheral edema. Adults get peripheral edema more frequently than children do.​​​​​​​

In a rare percentage of patients using growth hormone products, increased intracranial pressure (intracranial hypertension), together with papilledema, visual abnormalities, excruciating headache pain, nausea, and vomiting, has been documented. Within the first 8 weeks of starting treatment, symptoms typically start to appear. In every case that was recorded, symptoms went away after the therapy was stopped or the dosage was lowered. It is advised to have patients undergo periodic fundoscopic examinations after starting therapy and as needed after that. When receiving treatment, somatropin should be discontinued if papilledema is seen. A reduced dose of medication can be restarted if intracranial hypertension is found. Additionally, cerebral hypertension may be more likely to occur in Turner syndrome patients.​​​​​​​

Somatropin therapy has frequently been linked to joint edema (5–6%), myalgia (3–30%), musculoskeletal discomfort (5–14%), pain and stiffness in the limbs (2–19%), and back pain (3–11%). In example, arthralgia (11–37%) appears to occur more commonly in adults than in children when it comes to certain events connected to fluid retention. Muscle and joint discomfort typically appeared early in somatropin therapy in adults and tended to be temporary or react to dosage reduction. With the use of analgesics or a decrease in the frequency of somatropin dose, pain, edema, and/or stiffness may go away. In addition, reports of arthrosis (8–11%) and carpal tunnel syndrome (1–5% nerve entrapment syndrome) have been made. Pediatric patients have experienced more severe adverse effects, such as slipping capital femoral epiphysis and scoliosis development (4–19%).

Somatropin medication has frequently been associated with metabolic side effects. There have been instances of newly developed glucose intolerance, hyperglycemia, diabetes mellitus, and worsening of pre-existing diabetes mellitus during post-marketing surveillance of various medicines.​​​​​​​ Some patients experienced diabetic coma and diabetic ketoacidosis.​​​​​​​ Some patients improved after medication was stopped, whereas glucose intolerance continued in others. During therapy, closely monitor glucose levels; start or modify antidiabetic medicine as necessary. A brief overdose may cause hypoglycemia.​​​​​​​ A greater incidence of impaired glucose tolerance has been observed with higher doses. In patients with Turner syndrome treated with Norditropin, impaired fasting glucose after 4 years of treatment occurred in 22% of patients receiving 0.045 mg/kg/day for 1 year followed by 0.067 mg/kg/day thereafter compared with 5% of patients receiving 0.045 mg/kg/day. About 5–16% of people on somatropin therapy have been shown to have hypothyroidism.​​​​​​​ In a 6-month placebo-controlled experiment utilizing the Saizen brand on people with growth hormone deficiency (GHD), 10% needed minor changes to thyroid hormone replacement treatment for underlying hypothyroidism, and 1 patient received a new diagnosis of hypothyroidism. Additionally, during the course of the experiment, 2 individuals needed upward modifications to their hydrocortisone maintenance therapy for preexisting hypoadrenalism (unrelated to concurrent stress, surgery, or disease), and 1 patient received a new diagnosis of adrenal insufficiency. Follow up on periodic thyroid tests and start or modify thyroid replacement therapy as needed.​​​​​​​ Hyperlipidemia (8%) has also been reported, most often as hypertriglyceridemia (1—5%).

The most frequent adverse responses to the central nervous system (CNS) in somatropin clinical trials were headache (6–18%), paresthesias (2–17%), and hypoesthesia (2–15%) in adults. In trials, participants also reported experiencing asthenia or weakness (3–6%), fatigue (4–9%), insomnia (5%), sadness (5%) and dizziness. Seizures have been reported rarely.

In clinical trials, between 4 and 23% of somatropin-treated individuals reported experiencing flu-like symptoms. Similar numbers of cases of upper respiratory tract infections have been documented, including nasopharyngitis (3–14%), bronchitis (9%), and rhinitis (6–14%).​​​​​​​ Children with Turner syndrome reported otitis media (16—43%) and ear disorders (18%). Patients in group 1 (0.045 mg/kg/day for the first year, 0.067 mg/kg/day for the second year, and 0.089 mg/kg/day thereafter) in a study with Norditropin had a higher rate of otitis media (86.4%) compared to patients in group 2 (0.045 mg/kg/day for the first year, followed by 0.067 mg/kg/day thereafter) and patients in group 3 (0.045 mg/kg/day), who experienced Given that 40–50% of the cases were deemed to be serious, these data imply that greater doses may raise the risk of otitis media. Increased cough (6%) has also been reported.

Administration of somatropin is accompanied by injection site reactions (pain or burning at the injection site), lipoatrophy, or nodule formation; lipoatrophy can be prevented by rotating the injection site often. Hematoma (9%), fibrosis, erythema, pruritus, rash, swelling, hemorrhage, and skin darkening are a few other injection site responses.​​​​​​​

Approximately 2% of patients receiving somatropin develop antibodies. Growth attenuation has not been linked to growth hormone antibody binding capabilities below 2 mg/L, however it has occasionally been noted when binding capacities higher than 2 mg/L are present. Any patient who does not react to somatropin therapy should be tested for antibodies to growth hormone.​​​​​​​

Dermatologic and severe systemic hypersensitivity responses, such as anaphylactoid reactions and angioedema, have been observed throughout somatropin’s post-marketing experience. Acne vulgaris (6%), diaphoresis (8%), alopecia, and eczema have been reported in patients taking somatropin therapy. Rash (unspecified) and worsening of pre-existing psoriasis have both been mentioned as possible allergic responses.​​​​​​​

Rare reports of pancreatitis in both adults and children on somatropin suggest that children, particularly Turner syndrome-affected girls, may be at higher risk than adults. Any patient who experiences abdominal pain should be checked for pancreatitis. Other gastrointestinal side effects mentioned in clinical trials include gastritis (6%), gastroenteritis (8%), and increased liver enzymes (6–13%).​​​​​​​

In clinical trials, gynecomastia was noted in both adults (3–6%) and children (5–8%) using somatropin.​​​​​​​

Patients using somatropin in clinical trials have reported chest pain (unspecified) and hypertension (3–8%) respectively.​​​​​​​  Eosinophilia was reported in approximately 12% of pediatric patients receiving somatropin in clinical trials.1 Hematuria has been rarely observed.


Store this medication at 68°F to 77°F (20°C to 25°C) and away from heat, moisture and light. Keep all medicine out of the reach of children. Throw away any unused medicine after the beyond use date. Do not flush unused medications or pour down a sink or drain.


1.Omnitrope (somatropin) package insert. Princeton, NJ: Sandoz, Inc.; 2016 Dec.
2.Genotropin (somatropin) package insert. New York, NY: Pharmacia & Upjohn Company; 2016 Dec.
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5.Humatrope (somatropin) package insert. Indianapolis, IN: Eli Lilly and Company; 2016 Dec.
6.Serostim (somatropin) package insert. Rockland, MA: EMD Serono, Inc.; 2017 May.
7.Nutropin (somatropin) package insert. San Francisco, CA: Genentech; 2016 Dec.
8.Accretropin (somatropin) package insert. Winnipeg, Canada: Cangene Corporation; 2016 Dec.
9.Nutropin AQ (somatropin) package insert. San Francisco, CA: Genentech; 2016 Dec.
10.Saizen (somatropin) package insert. Rockland, MA: EMD Serono Inc; 2017 May.
11.Norditropin (somatropin) package insert. Plainsboro, NJ: Novo Nordisk; 2016 Dec.
12.Zomacton (somatropin) package insert. Parsippany, NJ: Ferring Pharmaceuticals, Inc; 2016 Dec.
13.Zorbtive (somatropin) injection package insert. Rockland, MA: EMD Serono, Inc.; 2017 May.
14.The American Geriatrics Society 2015 Beers Criteria Update Expert Panel. American Geriatrics Society updated Beers Criteria for potentially inappropriate medication use in older adults. J Am Geriatr Soc 2015;63:2227-46.
15.Zomig (zolmitriptan) nasal spray package insert. Hayward, CA: Impax Specialty Pharma; 2015 Jun.


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