SAIZEN® (somatropin [rDNA origin] injection)
Saizen® somatropin is a bio-identical human growth hormone (HGH) treatment for adults diagnosed with hormone deficiency or imbalance. It is identical to the natural growth hormone made by your body.
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SAIZEN® GROWTH HORMONE USAGE INSTRUCTIONS
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Replacement Therapy and HGH Injections – HGH Therapy
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DESCRIPTION OF SAIZEN (HGH)
Saizen is a human growth hormone made using recombinant DNA (rDNA) technology. Saizen has 191 amino acid residues with an identical sequence to that of hGH of pituitary origin. Saizen protein is synthesized using a lab strain of E. coli as a precursor.
Saizen hGH is a highly purified preparation with biological potency determined using cell proliferation bioassay. Saizen may contain up to 15% deamidated growth hormone (with an amide functional group removed from the compound) at expiration. Deamidated growth hormone has been studied and found to be fully active and safe for use.
Saizen hGH is a sterile liquid preparation designed for subcutaneous injection. Saizen is almost isotonic at a concentration of 5mg of growth hormone per mL with a pH of about 6.0.
Each 2 mL vial of growth hormone contains 10 mg (approximately 30 IU) somatropin, formulated in 17.4 mg sodium chloride, 5 mg phenol, 4 mg polysorbate 20, and 10 mM sodium citrate.
CLINICAL PHARMACOLOGY- Serono Saizen HGH Somatropin Human Growth Hormone
General – Actions and Finding HGH Somatropin
Preclinical and clinical in vivo and in vitro tests have found that Saizen is equivalent to human growth hormone derived from the pituitary gland. Children who have insufficient endogenous GH secretion as well as Turner syndrome patients and those with chronic renal insufficiency treated with Saizen or Nutropin had an increased growth rate and an improvement in insulin-like growth factor-I (IGF-I) levels similar to those demonstrated with hGH derived from the pituitary gland.
Actions demonstrated for Saizen, somatropin, somatrem and/or hGH of pituitary origin:
1. Tissue Growth
Organ Growth: Growth hormone affects the size of internal organs while improving red cell mass. Genetic dwarf rats and rats with pituitary glands removed experienced increased organ growth that correlated with body growth after treatment with GH.
Skeletal Growth: Growth hormone prompts skeletal growth in children with growth failure caused by insufficient secretion of endogenous growth hormone as well as Turner syndrome patients and those with chronic renal insufficiency. Growth hormone affects epiphyseal plates at the end of long bones for increased linear growth until plates fuse after puberty.
IGF-I serum levels in pediatric patients with GHD are increased during growth hormone treatment.
Cell Growth: Growth hormone treatment increases the size and quantity of skeletal muscle cells.
2. Protein Metabolism
Growth hormone increases linear growth by assisting with protein synthesis, which is reflected through increased nitrogen retention and a decrease in blood urea nitrogen and urinary nitrogen excretion during growth hormone treatment.
3. Carbohydrate Metabolism
Growth hormone modulates the metabolism of carbohydrates. Some patients with GHD experience fasting low blood sugar, which is alleviated through growth hormone treatment. GH treatment may also reduce insulin sensitivity, and increase serum fasting and postprandial insulin levels, particularly in patients who are overweight or obese.
4. Lipid Metabolism
In patients with GHD, growth hormone treatment improve lipid mobilization and plasma fatty acids while decreasing plasma cholesterol levels and body fat stores.
5. Mineral Metabolism
Growth hormone improves retention of potassium due to cellular growth. Inorganic phosphorus serum levels may raise slightly in patients with GHD, chronic renal insufficiency or Turner syndrome during growth hormone treatment due to associated bone growth and phosphate reabsorption in the kidneys.
6. Connective Tissue Metabolism
Growth hormone has been shown to boost synthesis of collagen and chondroitin sulfate and the urinary excretion of hydroxyproline, a non-proteinogenic amino acid.
Pharmacokinetics – HGH Saizen Somatropin Injection
Subcutaneous absorption: Absolute bioavailability of rhGH following subcutaneous injection in healthy adult males is 81±20%. The mean terminal half-life following subcutaneous injection is much longer than that following intravenous injection, which indicates subcutaneous absorption is rate-limiting.
Distribution: Animal rhGH studies find that growth hormone localizes in very perfused organs like the kidney and liver, with a distribution volume at steady state in healthy adult males of about 50mL/kg.
Metabolism: The kidneys and liver have been found to be the main metabolizing organs for growth hormone, with studies suggesting the kidney is the dominate organ.
Elimination: The mean terminal half-life after intravenous injection of rhGH in healthy adult males is estimated at 19.5±3.1 minutes. Clearance following intravenous injection is reported to be 116-174mL/hr/kg.
Growth Hormone Deficiency (GHD): Reported clearance values of rhGH in children and adults with GHG is 138-245 mL/hr/kg, similar to that seen in healthy children and adults. Mean terminal half-lifes following intravenous and subcutaneous injection in GHD patients is similar to that observed in healthy adult males.
Race: Reported half-life values for endogenous growth hormone is no different among normal black and white adult males. There is currently no data available for other races.
Gender: There is no data available for exogenously injected recombinant growth hormone, although data for GH of pituitary origin, endogenous growth hormone and methionyl recombinant growth hormone suggests no gender-based different in clearance.
Pediatric: Available data suggests human growth hormone clearances are similar in children and adults.
Geriatric: Limited data suggests plasma clearance and average steady state plasma concentration is no different among young and geriatric patients.
Renal Insufficiency: Adults and children with chronic renal failure and end-stage renal disease usually have reduced clearance compared to normal clearance ranges. Endogenous growth hormone production may also be raised in some patients with ESRD. No rhGH accumulation is reported in pediatric patients with ESRD or CRF.
Tuner Syndrome: There is no data available for exogenously injected recombinant growth hormone, although reported absorption, half-lifes and elimination rates of endogenous growth hormone in Turner Syndrome patients are similar to ranges in normal patients.
Hepatic Insufficiency: a reduced rhGH clearance has been observed in patients with severe lver dysfunction, although the clinical significance is not known.
Summary of Saizen HGH Pharmacokinetic Parameters
in Healthy Adult Males 0.1 mg
(approximately 0.3 IU a )/kg SC C max
(µg/L) T max
(hr) t ½
(hr) AUC 0-(infinity)
(µg·hr/L) CL/F sc
MEAN b 71.1 3.9 2.3 677 150
CV% 17 56 18 13 13
Abbreviations: C max =maximum concentration; t 1/2 =half-life; AUC 0-(infinity) =area under the curve; CL/F sc =systemic clearance; F sc =subcutaneous bioavailability (not determined); CV%=coefficient of variation in %; SC=subcutaneous
a Based on current International Standard of 3 IU=1 mg
Efficacy Studies of Saizen HGH Somatropin Injection
Effects of SAIZEN / Nutropin® [somatropin (rDNA origin) for injection] on Growth Failure Due to Chronic Renal Insufficiency (CRI)
Two multicenter, randomized, controlled clinical trials were conducted to determine whether treatment with Nutropin prior to renal transplantation in patients with chronic renal insufficiency could improve their growth rates and height deficits. One study was a double-blind, placebo-controlled trial and the other was an open-label, randomized trial.
The dose of SAIZEN / Nutropin in both controlled studies was 0.05 mg/kg/day (0.35 mg/kg/wk) administered daily by subcutaneous injection. Combining the data from those patients completing two years in the two controlled studies results in 62 patients treated with Nutropin and 28 patients in the control groups (either placebo-treated or untreated). The mean first year growth rate was 10.8 cm/yr for Nutropin-treated patients, compared with a mean growth rate of 6.5 cm/yr for placebo/untreated controls (p<0.00005). The mean second year growth rate was 7.8 cm/yr for the Nutropin-treated group, compared with 5.5 cm/yr for controls (p<0.00005). There was a significant increase in mean height standard deviation (SD) score in the Nutropin group (-2.9 at baseline to -1.5 at Month 24, n=62) but no significant change in the controls (-2.8 at baseline to -2.9 at Month 24, n=28). The mean third year growth rate of 7.6 cm/yr in the Nutropin-treated patients (n=27) suggests that Nutropin stimulates growth beyond two years.
However, there are no control data for the third year because control patients crossed over to Nutropin treatment after two years of participation. The gains in height were accompanied by appropriate advancement of skeletal age. These data demonstrate that Nutropin therapy improves growth rate and corrects the acquired height deficit associated with chronic renal insufficiency. Currently there are insufficient data regarding the benefit of treatment beyond three years. Although predicted final height was improved during Nutropin therapy, the effect of Nutropin on final adult height remains to be determined.
Post-Transplant Growth: GH Treatment
The North American Pediatric Renal Transplant Cooperative Study (NAPRTCS) has reported data for growth post-transplant in children who did not receive GH. The average change in height SD score during the initial two years post-transplant was 0.18 (n=300, J Pediatr. 1993;122:397-402).
Controlled studies of GH treatment for the short stature associated with CRI were not designed to compare the growth of treated or untreated patients after they received renal transplants. However, growth data are available from a small number of patients who have been followed for at least 11 months. Of the 7 control patients, 4 increased their height SD score and 3 had either no significant change or a decrease in height SD score. The 13 patients treated with Nutropin® [somatropin (rDNA origin) for injection] prior to transplant had either no significant change or an increase in height SD score after transplantation, indicating that the individual gains achieved with GH therapy prior to transplant were maintained after transplantation. The differences in the height deficit narrowed between the treated and untreated groups in the post-transplant period.
One long-term, randomized, open-label, multicenter, concurrently controlled study, two long-term, open-label, multicenter, historically controlled studies and one long-term, randomized, dose-response study were conducted to evaluate the efficacy of GH for the treatment of girls with short stature due to Turner syndrome.
In the randomized study GDCT, comparing GH-treated patients to a concurrent control group who received no GH, the GH-treated patients who received a dose of 0.3 mg/kg/week given 6 times per week from a mean age of 11.7 years for a mean duration of 4.7 years attained a mean near final height of 146.0 cm (n=27) as compared to the control group who attained a near final height of 142.1 cm (n=19). By analysis of covariance, the effect of GH therapy was a mean height increase of 5.4 cm (p=0.001).
In two of the studies (85-023 and 85-044), the effect of long-term GH treatment (0.375 mg/kg/week given either 3 times per week or daily) on adult height was determined by comparing adult heights in the treated patients with those of age-matched historical controls with Turner syndrome who never received any growth-promoting therapy. In Study 85-023, estrogen treatment was delayed until patients were at least age 14. GH therapy resulted in a mean adult height gain of 7.4 cm (mean duration of GH therapy of 7.6 years) vs. matched historical controls by analysis of covariance.
In Study 85-044, patients treated with early GH therapy were randomized to receive estrogen-replacement therapy (conjugated estrogens, 0.3 mg escalating to 0.625 mg daily) at either age 12 or 15 years. Compared with matched historical controls, early GH therapy (mean duration of GH therapy 5.6 years) combined with estrogen replacement at age 12 years resulted in an adult height gain of 5.9 cm (n=26), whereas girls who initiated estrogen at age 15 years (mean duration of GH therapy 6.1 years) had a mean adult height gain of 8.3 cm (n=29). Patients who initiated GH therapy after age 11 (mean age 12.7 years; mean duration of GH therapy 3.8 years) had a mean adult height gain of 5.0 cm (n=51).
Thus, in both studies, 85-023 and 85-044, the greatest improvement in adult height was observed in patients who received early GH treatment and estrogen after age 14 years.
In a randomized, blinded, dose-response study, GDCI, patients were treated from a mean age of 11.1 years for a mean duration of 5.3 years with a weekly dose of either 0.27 mg/kg or 0.36 mg/kg administered 3 or 6 times weekly. The mean near final height of patients receiving growth hormone was 148.7 cm (n=31). This represents a mean gain in adult height of approximately 5 cm compared with previous observations of untreated Turner syndrome girls.
In these studies, Turner syndrome patients (n=181) treated to final adult height achieved statistically significant average estimated adult height gains ranging 5.0-8.3 cm.
Design a N at Adult
Height GH Age
(yr) Estrogen Age
(yr) GH Duration
(yr) Adult Height
Gain (cm) b
GDCT RCT 27 11.7 13 4.7 5.4
85-023 MHT 17 9.1 15.2 7.6 7.4
85-044: A * MHT 29 9.4 15.0 6.1 8.3
B * 26 9.6 12.3 5.6 5.9
C * 51 12.7 13.7 3.8 5.0
GDCI RDT 31 11.1 8-13.5 5.3 ~5 c
a RCT: randomized controlled trial; MHT: matched historical controlled trial;
RDT: randomized dose-response trial.
b Analysis of convariance vs. controls
c Compared with historical data
* A: GH age <11 yr, estrogen age 15 yr
B: GH age <11 yr, estrogen age 12 yr
C: GH age >11 yr, estrogen at Month 12
Adult Growth Hormone Deficiency (AGHD) – Saizen HGH Soamtropin Injection Clinical Studies
Two multicenter, double-blind, placebo-controlled clinical trials were conducted using Nutropin® [somatropin (rDNA origin) for injection] in GH-deficient adults. One study was conducted in subjects with adult-onset GHD, mean age 48.3 years, n=166, at doses of 0.0125 or 0.00625 mg/kg/day; doses of 0.025 mg/kg/day were not tolerated in these subjects. A second study was conducted in previously treated subjects with childhood-onset GHD, mean age 23.8 years, n=64, at randomly assigned doses of 0.025 or 0.0125 mg/kg/day. The studies were designed to assess the effects of replacement therapy with GH on body composition.
Significant changes from baseline to Month 12 of treatment in body composition (i.e., total body % fat mass, trunk % fat mass, and total body % lean mass by DEXA scan) were seen in all Nutropin groups in both studies (p<0.0001 for change from baseline and vs. placebo), whereas no statistically significant changes were seen in either of the placebo groups. In the adult-onset study, the Nutropin group improved mean total body fat from 35.0% to 31.5%, mean trunk fat from 33.9% to 29.5%, and mean lean body mass from 62.2% to 65.7%, whereas the placebo group had mean changes of 0.2% or less (p=not significant). Due to the possible effect of GH-induced fluid retention on DEXA measurements of lean body mass, DEXA scans were repeated approximately 3 weeks after completion of therapy; mean % lean body mass in the Nutropin group was 65.0%, a change of 2.8% from baseline, compared with a change of 0.4% in the placebo group (p<0.0001 between groups).
In the childhood-onset study, the high-dose Nutropin group improved mean total body fat from 38.4% to 32.1%, mean trunk fat from 36.7% to 29.0%, and mean lean body mass from 59.1% to 65.5%; the low-dose Nutropin group improved mean total body fat from 37.1% to 31.3%, mean trunk fat from 37.9% to 30.6%, and mean lean body mass from 60.0% to 66.0%; the placebo group had mean changes of 0.6% or less (p=not significant).
Mean Changes from Baseline to Month 12 in Proportion of Fat and
Lean by DEXA for Studies M0431g and M0381g
(Adult-onset and Childhood-onset GHD, Respectively) M0431g M0381g
(n=15) Placebo vs.
Total body percent fat
Baseline 36.8 35.0 0.38 35.0 37.1 38.4 0.45
Month 12 36.8 31.5 35.2 31.3 32.1
Baseline to Month 12 change -0.1 -3.6 <0.0001 +0.2 -5.8 -6.3 <0.0001
Post-washout 36.4 32.2 N/A N/A N/A
Baseline to post-washout change -0.4 -2.8 <0.0001 N/A N/A N/A
Trunk percent fat
Baseline 35.3 33.9 0.50 32.5 37.9 36.7 0.23
Month 12 35.4 29.5 33.1 30.6 29.0
Baseline to Month 12 change 0.0 -4.3 <0.0001 +0.6 -7.3 -7.6 <0.0001
Post-washout 34.9 30.5 N/A N/A N/A
Baseline to post-washout change -0.3 -3.4 N/A N/A N/A
Total body percent lean
Baseline 60.4 62.2 0.37 62.0 60.0 59.1 0.48
Month 12 60.5 65.7 61.8 66.0 65.5
Baseline to Month 12 change +0.2 +3.6 <0.0001 -0.2 +6.0 +6.4 <0.0001
Post-washout 60.9 65.0 N/A N/A N/A
Baseline to post-washout change +0.4 +2.8 <0.0001 N/A N/A N/A
In the adult-onset human growth hormone deficiency study, significant decreases from baseline to Month 12 in LDL cholesterol and LDL:HDL ratio were seen in the Nutropin group compared to the placebo group, p<0.02; there were no statistically significant between-group differences in change from baseline to Month 12 in total cholesterol, HDL cholesterol, or triglycerides. In the childhood-onset study, significant decreases from baseline to Month 12 in total cholesterol, LDL cholesterol, and LDL:HDL ratio were seen in the high-dose Nutropin group only, compared to the placebo group, p<0.05. There were no statistically significant between-group differences in HDL cholesterol or triglycerides from baseline to Month 12.
Muscle strength, physical endurance, and quality of life measurements were not markedly abnormal at baseline, and no statistically significant effects of Nutropin therapy were observed in the two studies.
INDICATIONS AND USAGE
Saizen® [somatropin (rDNA origin) injection] is indicated for the long-term treatment of growth failure due to a lack of adequate endogenous GH secretion.
Saizen® [somatropin (rDNA origin) injection] is also indicated for the treatment of growth failure associated with chronic renal insufficiency up to the time of renal transplantation.
Saizen growth homone therapy should be used in conjunction with optimal management of chronic renal insufficiency.
Saizen® [somatropin (rDNA origin) injection] is also indicated for the long-term treatment of short stature associated with Turner syndrome.
Saizen is indicated to replace endogenous growth hormone in patients diagnosed with adult growth hormone deficiency (GHD) who meet both criteria:
Biochemical diagnosis of adult GHD with a subnormal response to a standard GH stimulation test.
- Adult onset:Patients who have adult GHD that is alone or in conjunction with multiple hormone deficiencies due to pituitary disease, trauma, radiation therapy, surgery or hypothalamic disease, or
- Childhood-onset:Patients who were growth hormone deficient during childhood that is confirmed as an adult before beginning Saizen replacement therapy.
Growth hormone should not be started to treat patients with acute critical illness following abdominal or open heart surgery, multiple accidental trauma or those with acute respiratory failure. Clinical studies in non-GHD adults with the above conditions found a significantly higher mortality rate (41.9% versus 19.3%) among patients treated with somatropin compared to patients who received a placebo.
Saizen injections are not appropriate for growth promotion in pediatric patients who have fused epiphyses.
Saizen treatment should not be used in patients with active neoplasia, and discontinued if neoplasia develops.
See CONTRAINDICATIONS for data on a significantly increased mortality rate for patients with certain acute critical illnesses when treated with growth hormone. The safety of continuing GH therapy in patients with acute respiratory failure, multiple accident trauma or acute critical illness following open heart surgery or abdominal surgery is not known.
General: Saizen should be prescribed by physicians familiar with the diagnosis and management of GHD patients and patients with chronic renal insufficiency or Turner syndrome.
Experience with prolonged growth hormone therapy is adults is limited.
Geriatric Usage: Clinical studies of Saizen did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. Other reported clinical experience has not identified differences in responses between the elderly and younger patients. In general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy.
Patients with epiphyseal closure who were treated with GH-replacement therapy in childhood should be re-evaluated according to the criteria in the INDICATIONS AND USAGE SECTION before continuation of GH therapy at the reduced dose level recommended for GH-deficient adults.
Because Saizen may reduce insulin sensitivity, patients should be monitored for evidence of glucose intolerance.
For patients with diabetes mellitus, the insulin dose may require adjustment when GH therapy is instituted. Because GH may reduce insulin sensitivity, particularly in obese individuals, patients should be observed for evidence of glucose intolerance. Patients with diabetes or glucose intolerance should be monitored closely during GH therapy.
Saizen Growth Hormone / Nutropin therapy in adults with GH deficiency of adult onset was associated with an increase of median fasting insulin in the Nutropin 0.0125 mg/kg/day group from 9.0 µU/mL at baseline to 13.0 µU/mL at Month 12 with a return to the baseline median after a 3-week post-washout period off GH therapy. In the placebo group there was no change from 8.0 µU/mL at baseline to Month 12, and after the post-washout the median was 9.0 µU/mL. The between-treatment-groups difference in change from baseline to Month 12 was significant, p<0.0001. In childhood-onset subjects there was a change of median fasting insulin in the Nutropin 0.025 mg/kg/day group from 11.0 µU/mL at baseline to 20.0 µU/mL at Month 12, in the Nutropin 0.0125 mg/kg/day group from 8.5 µU/mL to 11.0 µU/mL, and in the placebo group from 7.0 µU/mL to 8.0 µU/mL. The between-treatment-groups difference for these changes was significant, p=0.0007.
In subjects with adult-onset GH deficiency, there was no between-treatment-group difference in changes from baseline to Month 12 in mean HbA1c, p=0.08. In childhood-onset mean HbA1c increased in the Nutropin 0.025 mg/kg/day group from 5.2% at baseline to 5.5% at Month 12, and did not change in the Nutropin 0.0125 mg/kg/day group from 5.1% at baseline or in the placebo group from 5.3% at baseline. The between-treatment-groups difference was significant, p=0.009.
Patients with a history of an intracranial lesion should be examined frequently for progression or recurrence of the lesion. In pediatric patients, clinical literature has demonstrated no relationship between GH-replacement therapy and CNS tumor recurrence or new extracranial tumors. In adults, it is unknown whether there is any relationship between GH-replacement therapy and CNS tumor recurrence.
Patients with growth failure secondary to chronic renal insufficiency should be examined periodically for evidence of progression of renal osteodystrophy. Slipped capital femoral epiphysis or avascular necrosis of the femoral head may be seen in children with advanced renal osteodystrophy, and it is uncertain whether these problems are affected by GH therapy. X-rays of the hip should be obtained prior to initiating GH therapy for CRI patients. Physicians and parents should be alert to the development of a limp or complaints of hip or knee pain in patients treated with Saizen.
Slipped capital femoral epiphysis may occur more frequently in patients with endocrine disorders or in patients undergoing rapid growth.
Progression of scoliosis can occur in patients who experience rapid growth. Because GH increases growth rate, patients with a history of scoliosis who are treated with GH should be monitored for progression of scoliosis. GH has not been shown to increase the incidence of scoliosis. Skeletal abnormalities including scoliosis are commonly seen in untreated Turner syndrome patients. Physicians should be alert to these abnormalities, which may manifest during GH therapy.
Patients with Turner syndrome should be evaluated carefully for otitis media and other ear disorders since these patients have an increased risk of ear or hearing disorders. In a randomized, controlled trial, there was a statistically significant increase, as compared to untreated controls, in otitis media (43% vs. 26%) and ear disorders (18% vs. 5%) in patients receiving GH. In addition, patients with Turner syndrome should be monitored closely for cardiovascular disorders (e.g., stroke, aortic aneurysm, hypertension) as these patients are also at risk for these conditions.
Intracranial hypertension (IH) with papilledema, visual changes, headache, nausea, and/or vomiting has been reported in a small number of patients treated with GH products. Symptoms usually occurred within the first eight (8) weeks of the initiation of GH therapy. In all reported cases, IH-associated signs and symptoms resolved after termination of therapy or a reduction of the GH dose. Funduscopic examination of patients is recommended at the initiation and periodically during the course of GH therapy. Patients with CRI and Turner syndrome may be at increased risk for development of IH.
As with any protein, local or systemic allergic reactions may occur. Parents/Patient should be informed that such reactions are possible and that prompt medical attention should be sought if allergic reactions occur.
Laboratory Tests: Serum levels of inorganic phosphorus, alkaline phosphatase, and parathyroid hormone (PTH) may increase with Saizen therapy.
Untreated hypothyroidism prevents optimal response to Saizen. Patients with Turner syndrome have an inherently increased risk of developing autoimmune thyroid disease.
Changes in thyroid hormone laboratory measurements may develop during Saizen treatment. Therefore, patients should have periodic thyroid function tests and should be treated with thyroid hormone when indicated.
Drug Interaction: Excessive glucocorticoid therapy will inhibit the growth-promoting effect of human GH. Patients with ACTH deficiency should have their glucocorticoid-replacement dose carefully adjusted to avoid an inhibitory effect on growth.
The use of Saizen growth hormone in patients with chronic renal insufficiency receiving glucocorticoid therapy has not been evaluated. Concomitant glucocorticoid therapy may inhibit the growth-promoting effect of Saizen. If glucocorticoid replacement is required, the glucocorticoid dose should be carefully adjusted.
There was no evidence in the controlled studies of GH’s interaction with drugs commonly used in chronic renal insufficiency patients. Limited published data indicate that GH treatment increases cytochrome P450 (CP450) mediated antipyrine clearance in man.
These data suggest that GH administration may alter the clearance of compounds known to be metabolized by CP450 liver enzymes (e.g., corticosteroids, sex steroids, anticonvulsants, cyclosporin). Careful monitoring is advisable when GH is administered in combination with other drugs known to be metabolized by CP450 liver enzymes.
Carcinogenesis, Mutagenesis, Impairment of Fertility: Carcinogenicity, mutagenicity, and reproduction studies have not been conducted with Saizen.
Pregnancy Pregnancy (Category C): Animal reproduction studies have not been conducted with Saizen. It is also not known whether Saizen can cause fetal harm when administered to a pregnant woman or can affect reproduction capacity. Saizen should be given to a pregnant woman only if clearly needed.
Nursing Mothers: It is not known whether Saizen is excreted in human milk. Because many drugs are excreted in human milk, caution should be exercised when Saizen is administered to a nursing mother.
HGH Information for Patients: Patients being treated with GH and/or their parents should be informed of the potential benefits and risks associated with treatment. If home use is determined to be desirable by the physician, instructions on appropriate use should be given, including a review of the contents of the Patient Information Insert. This information is intended to aid in the safe and effective administration of the medication. It is not a disclosure of all possible adverse or intended effects.
If home use is prescribed, a puncture-resistant container for the disposal of used syringes and needles should be recommended to the patient. Patients and/or parents should be thoroughly instructed in the importance of proper disposal and cautioned against any reuse of needles and syringes (see Patient Information Insert).
As with all protein pharmaceuticals, a small percentage of patients may develop antibodies to the protein. GH antibody binding capacities below 2 mg/L have not been associated with growth attenuation. In some cases when binding capacity exceeds 2 mg/L, growth attenuation has been observed. In clinical studies of pediatric patients that were treated with Nutropin® [somatropin (rDNA origin) for injection] for the first time, 0/107 growth hormone-deficient (GHD) patients, 0/125 CRI patients, and 0/112 Turner syndrome patients screened for antibody production developed antibodies with binding capacities >/=2 mg/L at six months. In a clinical study of patients that were treated with
Saizen® [somatropin (rDNA origin) injection] for the first time, 0/38 GHD patients screened for antibody production, for up to 15 months, developed antibodies with binding capacities >/=2 mg/L.
Additional short-term immunologic and renal function studies were carried out in a group of patients with chronic renal insufficiency after approximately one year of treatment to detect other potential adverse effects of antibodies to GH. Testing included measurements of C1q, C3, C4, rheumatoid factor, creatinine, creatinine clearance, and BUN. No adverse effects of GH antibodies were noted.
In addition to an evaluation of compliance with the prescribed treatment program and thyroid status, testing for antibodies to GH should be carried out in any patient who fails to respond to human growth hormone therapy.
Growth Hormone Injection site discomfort has been reported. This is more commonly observed in children switched from another GH product to Saizen. Experience with Saizen in adults is limited.
Leukemia has been reported in a small number of GHD patients treated with GH. It is uncertain whether this increased risk is related to the pathology of GH deficiency itself, GH therapy, or other associated treatments such as radiation therapy for intracranial tumors. On the basis of current evidence, experts cannot conclude that GH therapy is responsible for these occurrences. The risk to GHD, CRI, or Turner syndrome patients, if any, remains to be established.
Other adverse drug reactions that have been reported in GH-treated patients include the following: 1) Metabolic: Mild, transient peripheral edema. In GHD adults, edema or peripheral edema was reported in 41% of GH-treated patients and 25% of placebo-treated patients. 2) Musculoskeletal: Arthralgias; carpal tunnel syndrome. In GHD adults, arthralgias and other joint disorders were reported in 27% of GH-treated patients and 15% of placebo-treated patients. 3) Skin: Rare increased growth of pre-existing nevi; patients should be monitored for malignant transformation. 4) Endocrine: Gynecomastia. Rare pancreatitis.
GH – Growth Hormone OVERDOSAGE
Acute overdosage could lead to hyperglycemia. Long-term overdosage could result in signs and symptoms of gigantism and/or acromegaly consistent with the known effects of excess GH. (See recommended and maximal dosage instructions given below.)
DOSAGE AND ADMINISTRATION
The Saizen growth hormone dosage and administration schedule should be individualized for each patient. Response to GH therapy in pediatric patients tends to decrease with time. However, in pediatric patients failure to increase growth rate, particularly during the first year of therapy, suggests the need for close assessment of compliance and evaluation of other causes of growth failure, such as hypothyroidism, under-nutrition, and advanced bone age.
GH Growth Hormone Dosage
Pediatric Growth Hormone Deficiency (GHD)
A weekly dosage of up to 0.30 mg/kg of body weight divided into daily subcutaneous injection is recommended.
Adult Growth Hormone Deficiency (GHD)
The recommended dosage at the start of therapy is not more than 0.006 mg/kg given as a daily subcutaneous injection. The dose may be increased according to individual patient requirements to a maximum of 0.025 mg/kg daily in patients under 35 years and to a maximum of 0.0125 mg/kg daily in patients over 35 years.
To minimize the occurrence of adverse events in older or overweight patients, lower doses may be necessary. During therapy, dosage should be decreased if required by the occurrence of side effects or excessive IGF-I levels.
Chronic Renal Insufficiency (CRI)
A weekly dosage of up to 0.35 mg/kg of body weight divided into daily subcutaneous injection is recommended.
Saizen growth hormone therapy may be continued up to the time of renal transplantation.
In order to optimize therapy for patients who require dialysis, the following guidelines for injection schedule are recommended:
Hemodialysis patients should receive their injection at night just prior to going to sleep or at least 3-4 hours after their hemodialysis to prevent hematoma formation due to the heparin.
Chronic Cycling Peritoneal Dialysis (CCPD) patients should receive their injection in the morning after they have completed dialysis.
Chronic Ambulatory Peritoneal Dialysis (CAPD) patients should receive their injection in the evening at the time of the overnight exchange.
Turner Syndrome. A weekly dosage of up to 0.375 mg/kg of body weight divided into equal doses 3 to 7 times per week by subcutaneous injection is recommended.
Growth Hormone Administration
The growth hormone solution should be clear immediately after removal from the refrigerator. Occasionally, after refrigeration, you may notice that small colorless particles of protein are present in the solution. This is not unusual for solutions containing proteins. Allow the vial to come to room temperature and gently swirl. If the solution is cloudy, the contents MUST NOT be injected.
Before needle insertion, wipe the septum of the Saizen vial with rubbing alcohol or an antiseptic solution to prevent contamination of the contents by microorganisms that may be introduced by repeated needle insertions. It is recommended that Saizen be administered using sterile, disposable syringes and needles. The syringes should be of small enough volume that the prescribed dose can be drawn from the vial with reasonable accuracy.
HGH STABILITY AND STORAGE
Vial contents are stable for 28 days after initial use when stored at 2-8°C/36-46°F (under refrigeration). Avoid freezing the vial of Saizen.
HOW HGH INJECTION IS SUPPLIED
Saizen HGH growth hormone is supplied as 8.8 mg and 5mg of sterile liquid somatropin per vial.
Saizen® [somatropin (rDNA origin) injection]
Learn more about HGH Therapy at HGH Therapy Info or contact an HGH doctor specializing in bio-identical HRT for growth hormone replacement therapy today – Contact an HGH Physician
(Above information has been provided by PDR.)
Consult a human growth hormone doctor HGH Doctor from a reputable human growth hormone clinic HGH Clinic before administration of injectable HGH (Somatropin Injection for Hormone Replacement of GH – Hormone Replacement Therapy).
HGH Hormone Medications – FDA Approved