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Indications

Pediatric patients

Nutropin AQ is indicated for the long-term treatment of growth failure due to a lack of adequate endogenous GH secretion.

Nutropin AQ is indicated for the treatment of growth failure associated with chronic renal insufficiency up to the time of renal transplantation. Nutropin AQ and Nutropin therapy should be used in conjunction with optimal management of chronic renal insufficiency.

Nutropin AQ is indicated for the long-term treatment of short stature associated with Turner syndrome.

Nutropin AQ is indicated for the long-term treatment of idiopathic short stature, also called non-growth hormone deficient short stature, defined by height SDS ≤-2.25, and associated with growth rates unlikely to permit attainment of adult height in the normal range, in pediatric patients whose epiphyses are not closed and for whom diagnostic evaluation excludes other causes associated with short stature that should be observed or treated by other means.

Adult patients

Nutropin AQ is indicated for the replacement of endogenous GH in adults with GH deficiency who meet either of the following two criteria:

• Adult-Onset: Patients who have GH deficiency, either alone or associated with multiple hormone deficiencies (hypopituitarism), as a result of pituitary disease, hypothalamic disease, surgery, radiation therapy, or trauma; or
• Childhood-Onset: Patients who were GH deficient during childhood as a result of congenital, genetic, acquired, or idiopathic causes

In general, confirmation of the diagnosis of adult GH deficiency in both groups usually requires an appropriate GH stimulation test. However, confirmatory GH stimulation testing may not be required in patients with congenital/genetic GH deficiency or multiple pituitary hormone deficiencies due to organic disease.

Nutropin AQ is available in both a vial and prefilled pen cartridge and may be administered using the Nutropin AQ NuSpin 5, 10, or 20, the Nutropin AQ Pen 20, the Nutropin AQ Pen 10, or by vial and syringe.

Pediatric clinical studies and safety

Nutropin AQ has been determined to be bioequivalent to Nutropin.¹

Growth Hormone Deficiency (GHD) in pubertal patients^1,3

One open-label, multicenter, randomized clinical trial of 2 dosages of Nutropin was performed in pubertal patients with GHD. Ninety-seven patients (mean age 13.9 years, 83 male, 14 female) currently being treated with approximately 0.3 mg/kg/wk of GH were randomized to 0.3 mg/kg/wk or 0.7 mg/kg/wk Nutropin doses. All patients were already in puberty (Tanner stage ≥2) and had bone ages ≤14 years in males or ≤12 years in females. Mean baseline height standard deviation (SD) score was -1.3.

The mean last measured height in all 97 patients after a mean duration of 2.7±1.2 years, by analysis of covariance (ANCOVA) adjusting for baseline height, is shown below.

Last Measured Height by Sex and Nutropin Dose

• The mean height SD score at last measured height (n=97) was -0.7 ± 1.0 in the 0.3 mg/kg/wk group and -0.1 ± 1.2 in the 0.7 mg/kg/wk group
• For patients completing 3.5 or more years (mean 4.1 years) of Nutropin treatment (15/49 patients in the 0.3 mg/kg/wk group and 16/48 patients in the 0.7 mg/kg/wk group), the mean last measured height was 166.1 ± 8.0 cm in the 0.3 mg/kg/wk group and 171.8 ± 7.1 cm in the 0.7 mg/kg/wk group, adjusting for baseline height and sex
• The mean change in bone age was approximately one year for each year in the study in both dose groups. Patients with baseline height SD scores above -1.0 were able to attain normal adult heights with the 0.3 mg/kg/wk dose of Nutropin (mean height SD score at near-adult height = -0.1, n = 15)
• Thirty-one patients had bone mineral density (BMD) determined by dual energy x-ray absorptiometry (DEXA) scans at study conclusion. The 2 dose groups did not differ significantly in mean SD score for total body BMD (-0.9 ± 1.9 in the 0.3 mg/kg/wk group vs -0.8 ± 1.2 in the 0.7 mg/kg/wk group, n = 20) or lumbar spine BMD (-1.0 ± 1.0 in the 0.3 mg/kg/wk group vs -0.2 ± 1.7 in the 0.7 mg/kg/wk group, n = 21)
• Over a mean duration of 2.7 years, patients in the 0.7 mg/kg/wk group were more likely to have IGF-I values above the normal range than patients in the 0.3 mg/kg/wk group (27.7% vs 9.0% of IGF-I measurements for individual patients). The clinical significance of elevated IGF-I values is unknown

Precautions

Nutropin AQ should be prescribed by physicians experienced in the diagnosis and management of patients with GH deficiency, idiopathic short stature, Turner syndrome, or chronic renal insufficiency (CRI). No studies have been completed evaluating Nutropin AQ therapy in patients who have received renal transplants. Currently, treatment of patients with functioning renal allografts is not indicated.

Treatment with somatropin may decrease insulin sensitivity, particularly at higher doses in susceptible patients. As a result, previously undiagnosed impaired glucose tolerance and overt diabetes mellitus may be unmasked during somatropin treatment. Therefore, glucose levels should be monitored periodically in all patients treated with somatropin, especially in those with risk factors for diabetes mellitus, such as obesity (including obese patients with Prader-Willi syndrome), Turner syndrome, or a family history of diabetes mellitus. Patients with preexisting type 1 or type 2 diabetes mellitus or impaired glucose tolerance should be monitored closely during somatropin therapy. The doses of antihyperglycemic drugs (i.e., insulin or oral agents) may require adjustment when somatropin therapy is instituted in these patients.

Slipped capital femoral epiphysis may occur more frequently in patients with endocrine disorders (including GH deficiency and Turner syndrome) or in patients undergoing rapid growth. Any pediatric patient with the onset of a limp or complaints of hip or knee pain during somatropin therapy should be carefully evaluated.

Progression of scoliosis can occur in patients who experience rapid growth. Because somatropin increases growth rate, patients with a history of scoliosis who are treated with somatropin should be monitored for progression of scoliosis. However, somatropin has not been shown to increase the occurrence of scoliosis. Skeletal abnormalities including scoliosis are commonly seen in untreated Turner syndrome patients. Scoliosis is also commonly seen in untreated patients with Prader-Willi syndrome. Physicians should be alert to these abnormalities, which may manifest during somatropin therapy.

Chronic renal insufficiency^1,3

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 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 the 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 patients treated with Nutropin (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.

Post-Transplant Growth^1,3

The North American Pediatric Renal Transplant Cooperative Study (NAPRTCS) has reported data for growth post-transplant in children who did not receive GH prior to transplantation as well as children who did receive Nutropin during the clinical trails prior to transplantation. The average change in height SD score during the initial two years post-transplant was 0.15 for the 2391 patients who did not receive GH pre-transplant and 0.28 for the 57 patients who did. For patients who were followed for 5 years post-transplant, the corresponding changes in height SD score were also similar between groups.

Precautions

Children with growth failure secondary to CRI 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 somatropin therapy. X-rays of the hip should be obtained prior to initiating somatropin therapy in CRI patients. Physicians and parents should be alert to the development of a limp or complaints of hip or knee pain in CRI patients treated with Nutropin AQ.

Intracranial hypertension (IH) with papilledema, visual changes, headache, nausea, and/or vomiting has been reported in a small number of patients treated with somatropin products. Symptoms usually occurred within the first 8 weeks of the initiation of somatropin therapy. In all reported cases, IH-associated signs and symptoms rapidly resolved after cessation of therapy or a reduction of the somatropin dose. Funduscopic examination should be performed routinely before initiating treatment with somatropin to exclude preexisting papilledema, and periodically during the course of somatropin therapy. If papilledema is observed by funduscopy during somatropin treatment, treatment should be stopped. If somatropin-induced IH is diagnosed, treatment with somatropin can be restarted at a lower dose after IH-associated signs and symptoms have resolved. Patients with Turner syndrome, CRI, and Prader-Willi syndrome may be at increased risk for the development of IH.

Undiagnosed/untreated hypothyroidism may prevent an optimal response to somatropin, in particular, the growth response in children. Patients with Turner syndrome have an inherently increased risk of developing autoimmune thyroid disease and primary hypothyroidism. In patients with growth hormone deficiency, central (secondary) hypothyroidism may first become evident or worsen during somatropin treatment. Therefore, patients treated with somatropin should have periodic thyroid function tests and thyroid hormone replacement therapy should be initiated or appropriately adjusted when indicated.

Turner Syndrome^1,3

To evaluate the efficacy of GH for the treatment of girls with short stature due to Turner syndrome, the following studies were conducted:

• One long-term, randomized, open-label, multicenter, concurrently controlled study
• Two long-term, open-label, multicenter, historically controlled studies
• One long-term, randomized dose-response study

In the randomized study GDCT, which compared 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/wk 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), while the control group 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/wk 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 GH 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 from 5.0-8.3 cm.

Precautions

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 with untreated controls, in otitis media (43% vs 26%) and ear disorders (18% vs 5%) in patients receiving somatropin. In addition, patients with Turner syndrome should be monitored closely for cardiovascular disorders (eg, stroke, aortic aneurysm/dissection, hypertension), as these patients are also at risk for these conditions.

Progression of scoliosis can occur in patients who experience rapid growth. Because somatropin increases growth rate, patients with a history of scoliosis who are treated with somatropin should be monitored for progression of scoliosis. However, somatropin has not been shown to increase the occurrence 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 somatropin therapy.

Intracranial hypertension (IH) with papilledema, visual changes, headache, nausea, and/or vomiting has been reported in a small number of patients treated with somatropin products. Symptoms usually occurred within the first 8 weeks of the initiation of somatropin therapy. In all reported cases, IH-associated signs and symptoms rapidly resolved after cessation of therapy or a reduction of the somatropin dose. Funduscopic examination should be performed routinely before initiating treatment with somatropin to exclude preexisting papilledema, and periodically during the course of somatropin therapy. If papilledema is observed by funduscopy during somatropin treatment, treatment should be stopped. If somatropin-induced IH is diagnosed, treatment with somatropin can be restarted at a lower dose after IH-associated signs and symptoms have resolved. Patients with Turner syndrome, CRI, and Prader-Willi syndrome may be at increased risk for the development of IH.

Undiagnosed/untreated hypothyroidism may prevent an optimal response to somatropin, in particular, the growth response in children. Patients with Turner syndrome have an inherently increased risk of developing autoimmune thyroid disease and primary hypothyroidism. In patients with growth hormone deficiency, central (secondary) hypothyroidism may first become evident or worsen during somatropin treatment. Therefore, patients treated with somatropin should have periodic thyroid function tests and thyroid hormone replacement therapy should be initiated or appropriately adjusted when indicated.

Idiopathic short stature (ISS)^1,3

A long-term, open-label, multicenter study (86-053) was conducted to examine the safety and efficacy of Nutropin in pediatric patients with idiopathic short stature, also called non-GH deficient short stature.

• For the first year, 122 pre-pubertal subjects over the age of 5 years with stimulated serum GH ≥10 ng/mL were randomized into two treatment groups of approximately equal size; one group was treated with Nutropin 0.3 mg/kg weekly divided into three doses per week (TIW) and the other group served as untreated controls
• For the second and subsequent years of the study, all subjects were re-randomized to receive the same total weekly dose of Nutropin (0.3 mg/kg weekly) administered either daily or TIW. Treatment with Nutropin was continued until a subject's bone age was <15.0 years (boys) or <14.0 years (girls) and the growth rate was >2 cm/yr, after which subjects were followed until adult height was achieved. The mean baseline values were: height SD score -2.8, IGF-I SD score -0.9, age 9.4 years, bone age 7.8 years, growth rate 4.4 cm/yr, mid-parental target height SD score -0.7, and Bayley Pinneau predicted adult height SD score -2.3. Nearly all subjects had predicted adult height that was less than mid-parental target height
• During the one-year controlled phase of the study, the mean height velocity increased by 0.5 ± 1.8 cm (mean ± SD) in the no-treatment control group and by 3.1 ± 1.7 cm in the Nutropin group (p>0.0001). For the same period of treatment the mean height SD score increased by 0.4 ± 0.2 and remained unchanged (0.0 ± 0.2) in the control group (p>0.001)
• Of the 118 subjects who were treated with Nutropin in Study 86-053, 83 (70%) reached near-adult height after 2-10 years of Nutropin therapy. Their last measured height, including post-treatment follow-up, was obtained at a mean age of 18.3 years in males and 17.3 years in females. The mean duration of therapy was 6.2 and 5.5 years, respectively. Adult height was greater than pretreatment predicted adult height in 49 of 60 males (82%) and 19 of 23 females (83%). The mean difference between adult height and pretreatment predicted adult height was 5.2 cm (2.0 inches) in males and 6.0 cm (2.4 inches) in females (p>0.0001 for both)
• Nutropin therapy resulted in an increase in mean IGF-I SD score from -0.9±1.0 to -0.2±0.9 in Treatment Year 1. During continued treatment, mean IGF-I levels remained close to the normal mean. IGF-I scores above +2 occurred sporadically in 14 subjects
• In subjects treated in a long-term study of Nutropin for idiopathic short stature, mean fasting and postprandial insulin levels increased, while mean fasting and postprandial glucose levels remained unchanged. Mean hemoglobin A1c levels rose slightly from baseline as expected during adolescence; sporadic values outside normal limits occurred transiently.

Precautions

In subjects treated in a long-term study of Nutropin for idiopathic short stature, mean fasting and postprandial insulin levels increased, while mean fasting and postprandial glucose levels remained unchanged. Mean hemoglobin A1c levels rose slightly from baseline as expected during adolescence; sporadic values outside normal limits occurred transiently.

Slipped capital femoral epiphysis may occur more frequently in patients with endocrine disorders (including GH deficiency and Turner syndrome) or in patients undergoing rapid growth. Any pediatric patient with the onset of a limp or complaints of hip or knee pain during somatropin therapy should be carefully evaluated.

Progression of scoliosis can occur in patients who experience rapid growth. Because somatropin increases growth rate, patients with a history of scoliosis who are treated with somatropin should be monitored for progression of scoliosis. However, somatropin has not been shown to increase the occurrence of scoliosis. Skeletal abnormalities including scoliosis are commonly seen in untreated Turner syndrome patients. Scoliosis is also commonly seen in untreated patients with Prader-Willi syndrome. Physicians should be alert to these abnormalities, which may manifest during somatropin therapy.

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Adult clinical studies and safety

Adult Growth Hormone Deficiency (AGHD)^1,3

Body composition and lipid profile data

Two multicenter, double-blind, placebo-controlled trials were conducted to assess the effects of replacement therapy with GH on body composition.

• One study was conducted in patients 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

Body composition results

Significant reduction in mean total body fat and trunk fat and a significant increase in lean body mass were observed in both childhood- and adult-onset AGHD patients.

Body Composition

• Significant changes from baseline to Month 12 of treatment in body composition (ie, 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)
• In the adult-onset 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

Bone mineral density (BMD) data

An additional objective of the AGHD studies was to determine the effects of prolonged Nutropin treatment on BMD in childhood-onset AGHD and adult-onset AGHD.

• In the childhood-onset study, 55% of the patients had decreased spine bone mineral density (BMD) (z-score >-1) at baseline. The administration of Nutropin (n = 16) (0.025 mg/kg/day) for two years resulted in increased spine BMD from baseline when compared to placebo (n = 13) (4.6% vs 1.0%, respectively, p>0.03); a transient decrease in spine BMD was seen at six months in the Nutropin-treated patients. Thirty-five percent of subjects treated with this dose had supraphysiological levels of IGF-I at some point during the study, which may carry unknown risks. No significant improvement in total body BMD was found when compared to placebo. A lower GH dose (0.0125 mg/kg/day) did not show significant increments in either of these bone parameters when compared to placebo
• No statistically significant effects on BMD were seen in the adult-onset study where patients received GH (0.0125 mg/kg/day) for one year

Precautions/adverse events

Nutropin therapy in adults with GHD of adult onset was associated with an increase of median fasting insulin level 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 level after a 3-week post-washout period of 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 period, the median level was 9.0 μU/mL.

The between-treatment groups difference on change from baseline to Month 12 in median fasting insulin level was significant, p<0.0001. In childhood-onset subjects, there was an increase of median fasting insulin level 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 differences for these changes were significant, p=0.0007.

In subjects with adult-onset GHD, there were no between-treatment-group differences on change from baseline to Month 12 in mean HbAIc, p=0.08. In childhood-onset, mean HbAIc level 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-group differences were significant, p=0.009.

Patients with pre-existing tumors or growth hormone deficiency secondary to an intracranial lesion should be examined routinely for progression or recurrence of the underlying disease process. In pediatric patients, clinical literature has revealed no relationship between somatropin replacement therapy and central nervous system (CNS) tumor recurrence or new extracranial tumors. However, in childhood cancer survivors, an increased risk of a second neoplasm has been reported in patients treated with somatropin after their first neoplasm. Intracranial tumors, in particular meningiomas, in patients treated with radiation to the head for their first neoplasm, were the most common of these second neoplasms. In adults, it is unknown whether there is any relationship between somatropin replacement therapy and CNS tumor recurrence.

Experience with prolonged somatropin treatment in adults is limited.

Nutropin AQ should be given to a pregnant woman only if clearly needed. It is not known whether Nutropin AQ is excreted in human milk. Because many drugs are excreted in human milk, caution should be exercised when Nutropin AQ is administered to a nursing mother.

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

Dosage and administration

Click here for more information about Dosing and Administration for Nutropin products.

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