Nutropin AQ (Injection, Solution)

Source:http://www4.wiwiss.fu-berlin.de/dailymed/resource/drugs/273

Statements in which the resource exists.
SubjectPredicateObjectContext
dailymed-drugs:273rdf:typehttp://www4.wiwiss.fu-berli...lld:dailymed
dailymed-drugs:273rdf:typedailymed-instance:drugslld:dailymed
dailymed-drugs:273rdfs:labelNutropin AQ (Injection, Solution)lld:dailymed
dailymed-drugs:273dailymed-instance:dosageThe Nutropin AQ [somatropin (rDNA origin) injection] 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.<br/>Dosage:<br/>Pediatric Growth Hormone Deficiency (GHD): A weekly dosage of up to 0.3 mg/kg of body weight divided into daily subcutaneous injection is recommended. In pubertal patients, a weekly dosage of up to 0.7 mg/kg divided daily may be used.<br/>Adult Growth Hormone Deficiency (GHD): Based on the weight-based dosing utilized in the original pivotal studies described herein, 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 old and to a maximum of 0.0125 mg/kg daily in patients over 35 years old. Clinical response, side effects, and determination of age- and gender-adjusted serum IGF-I levels may be used as guidance in dose titration. Alternatively, taking into account more recent literature, a starting dose of approximately 0.2 mg/day (range, 0.15-0.30 mg/day) may be used without consideration of body weight. This dose can be increased gradually every 1-2 months by increments of approximately 0.1-0.2 mg/day, according to individual patient requirements based on the clinical response and serum IGF-I concentrations. During therapy, the dose should be decreased if required by the occurrence of adverse events and/or serum IGF-I levels above the age- and gender-specific normal range. Maintenance dosages vary considerably from person to person. A lower starting dose and smaller dose increments should be considered for older patients, who are more prone to the adverse effects of somatropin than younger individuals. In addition, obese individuals are more likely to manifest adverse effects when treated with a weight-based regimen. In order to reach the defined treatment goal, estrogen-replete women may need higher doses than men. Oral estrogen administration may increase the dose requirements in women.<br/>Chronic Renal Insufficiency (CRI): A weekly dosage of up to 0.35 mg/kg of body weight divided into daily subcutaneous injection is recommended. Nutropin AQ 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:<br/>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.<br/>Idiopathic Short Stature (ISS): A weekly dosage of up to 0.3 mg/kg of body weight divided into daily subcutaneous injection has been shown to be safe and efficacious, and is recommended.<br/>Administration: The 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 or pen cartridge to come to room temperature and gently swirl. If the solution is cloudy, the contents MUST NOT be injected.<br/>For Nutropin AQ Vial: Before needle insertion, wipe the septum of the Nutropin AQ 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 Nutropin AQ 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.<br/>For Nutropin AQ Pen Cartridge: The Nutropin AQ pen cartridge is intended for use only with the Nutropin AQ Pen. Wipe the septum of the Nutropin AQ pen cartridge 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 Nutropin AQ be administered using sterile, disposable needles. Follow the directions provided in the Nutropin AQ Pen Instructions for Use. The Nutropin AQ pen allows for administration of a minimum dose of 0.1 mg to a maximum dose of 4.0 mg, in 0.1 mg increments.lld:dailymed
dailymed-drugs:273dailymed-instance:descripti...Nutropin AQ [somatropin (rDNA origin) injection] is a human growth hormone (hGH) produced by recombinant DNA technology. Nutropin AQ has 191 amino acid residues and a molecular weight of 22,125 daltons. The amino acid sequence of the product is identical to that of pituitary���derived human growth hormone. The protein is synthesized by a specific laboratory strain of E. coli as a precursor consisting of the rhGH molecule preceded by the secretion signal from an E. coli protein. This precursor is directed to the plasma membrane of the cell. The signal sequence is removed and the native protein is secreted into the periplasm so that the protein is folded appropriately as it is synthesized. Nutropin AQ is a highly purified preparation. Biological potency is determined using a cell proliferation bioassay. Nutropin AQ may contain not more than fifteen percent deamidated growth hormone (GH) at expiration. The deamidated form of GH has been extensively characterized and has been shown to be safe and fully active. Nutropin AQ is a sterile liquid intended for subcutaneous administration. The product is nearly isotonic at a concentration of 5 mg of GH per mL and has a pH of approximately 6.0. The Nutropin AQ 2 mL vial contains 10 mg (approximately 30 International Units [IU]) somatropin, formulated in 17.4 mg sodium chloride, 5 mg phenol, 4 mg polysorbate 20, and 10 mM sodium citrate. The Nutropin AQ 2 mL pen cartridge contains 10 mg (approximately 30 International Units) somatropin, formulated in 17.4 mg sodium chloride, 5 mg phenol, 4 mg polysorbate 20, and 10 mM sodium citrate.lld:dailymed
dailymed-drugs:273dailymed-instance:clinicalP...General: In vitro and in vivo preclinical and clinical testing have demonstrated that Nutropin AQ is therapeutically equivalent to pituitary-derived human GH (hGH). Pediatric patients who lack adequate endogenous GH secretion, patients with chronic renal insufficiency, and patients with Turner syndrome that were treated with Nutropin AQ or Nutropin [somatropin (rDNA origin) for injection] resulted in an increase in growth rate and anincrease in insulin���like growth factor-I (IGF-I) levels similar to that seen with pituitary���derived hGH. Actions that have been demonstrated for Nutropin AQ, somatropin, somatrem, and/or pituitary-derived hGH include:<br/>Tissue Growth:<br/>Protein Metabolism: Linear growth is facilitated in part by GH���stimulated protein synthesis. This is reflected by nitrogen retention as demonstrated by a decline in urinary nitrogen excretion and blood urea nitrogen during GH therapy.<br/>Carbohydrate Metabolism: GH is a modulator of carbohydrate metabolism. For example, patients with inadequate secretion of GH sometimes experience fasting hypoglycemia that is improved by treatment with GH. GH therapy may decrease insulin sensitivity. Untreated patients with chronic renal insufficiency and Turner syndrome have an increased incidence of glucose intolerance. Administration of hGH to adults or children resulted in increases in serum fasting and postprandial insulin levels, more commonly in overweight or obese individuals. In addition, mean fasting and postprandial glucose and hemoglobin Alevels remained in the normal range.<br/>Lipid Metabolism: In GH���deficient patients, administration of GH resulted in lipid mobilization, reduction in body fat stores, increased plasma fatty acids, and decreased plasma cholesterol levels.<br/>Mineral Metabolism: The retention of total body potassium in response to GH administration apparently results from cellular growth. Serum levels of inorganic phosphorus may increase slightly in patients with inadequate secretion of endogenous GH, chronic renal insufficiency, or patients with Turner syndrome during GH therapy due to metabolic activity associated with bone growth as well as increased tubular reabsorption of phosphate by the kidney. Serum calcium is not significantly altered in these patients. Sodium retention also occurs. Adults with childhood���onset GH deficiency show low bone mineral density (BMD). GH therapy results in increases in serum alkaline phosphatase.<br/>Connective Tissue Metabolism: GH stimulates the synthesis of chondroitin sulfate and collagen as well as the urinary excretion of hydroxyproline.<br/>Pharmacokinetics:<br/>Subcutaneous Absorption: The absolute bioavailability of recombinant human growth hormone (rhGH) after subcutaneous administration in healthy adult males has been determined to be 81��20%. The mean terminal tafter subcutaneous administration is significantly longer than that seen after intravenous administration (2.1��0.43 hours vs. 19.5��3.1 minutes) indicating that the subcutaneous absorption of the compound is slow and rate���limiting.<br/>Distribution: Animal studies with rhGH showed that GH localizes to highly perfused organs, particularly the liver and kidney. The volume of distribution at steady state for rhGH in healthy adult males is about 50 mL/kg body weight, approximating the serum volume.<br/>Metabolism: Both the liver and kidney have been shown to be important metabolizing organs for GH. Animal studies suggest that the kidney is the dominant organ of clearance. GH is filtered at the glomerulus and reabsorbed in the proximal tubules. It is then cleaved within renal cells into its constituent amino acids, which return to the systemic circulation.<br/>Elimination: The mean terminal tafter intravenous administration of rhGH in healthy adult males is estimated to be 19.5��3.1 minutes. Clearance of rhGH after intravenous administration in healthy adults and children is reported to be in the range of 116���174 mL/hr/kg.<br/>Bioequivalence of Formulations: Nutropin AQ has been determined to be bioequivalent to Nutropin based on the statistical evaluation of AUC and C.<br/>SPECIAL POPULATIONS:lld:dailymed
dailymed-drugs:273dailymed-instance:activeIng...dailymed-ingredient:Somatro...lld:dailymed
dailymed-drugs:273dailymed-instance:supplyNutropin AQ [somatropin (rDNA origin) injection] is supplied as either 10 mg (approximately 30 International Units) of sterile liquid somatropin per vial, a 10 mg (approximately 30 International Units) of sterile liquid somatropin per pen cartridge. Each vial carton contains one single vial containing 2 mL of Nutropin AQ [somatropin (rDNA origin) injection] 10 mg/2 mL (5 mg/mL). DC 50242���022���20. Each pen cartridge carton contains one single pen cartridge containing 2 mL of Nutropin AQ [somatropin (rDNA origin) injection] 10 mg/2 mL (5 mg/mL). DC 50242���043���14.lld:dailymed
dailymed-drugs:273dailymed-instance:activeMoi...dailymed-ingredient:Somatro...lld:dailymed
dailymed-drugs:273dailymed-instance:inactiveI...dailymed-ingredient:Sodium_...lld:dailymed
dailymed-drugs:273dailymed-instance:inactiveI...dailymed-ingredient:Phenollld:dailymed
dailymed-drugs:273dailymed-instance:inactiveI...dailymed-ingredient:Polysor...lld:dailymed
dailymed-drugs:273dailymed-instance:inactiveI...dailymed-ingredient:Sodium_...lld:dailymed
dailymed-drugs:273dailymed-instance:precautio...General: 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. 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 Alevels rose slightly from baseline as expected during adolescence; sporadic values outside normal limits occurred transiently. Nutropin therapy in adults with GH deficiency 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��U/mL at baseline to 13.0��U/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��U/mL at baseline to Month 12, and after the post���washout period, the median was 9.0��U/mL. The between���treatment groups difference on the change from baseline to Month 12 in the 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��U/mL at baseline to 20.0��U/mL at Month 12, in the Nutropin 0.0125 mg/kg/day group from 8.5��U/mL to 11.0��U/mL, and in the placebo group from 7.0��U/mL to 8.0��U/mL. The between���treatment groups difference for these changes were significant, p = 0.0007. In subjects with adult onset GH deficiency, there were no between���treatment group difference on change from baseline to Month 12 in mean HbA, p = 0.08. In childhood���onset mean HbAincreased 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 differences were significant, p = 0.009. Patients with preexisting 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. 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 eight (8) weeks after 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. In patients with hypopituitarism (multiple hormone deficiencies), standard hormonal replacement therapy should be monitored closely when somatropin therapy is administered. 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. Patients should be monitored carefully for any malignant transformation of skin lesions. When somatropin is administered subcutaneously at the same site over a long period of time, tissue atrophy may result. This can be avoided by rotating the injection site. As with any protein, local or systemic allergic reactions may occur. Parents/Patients should be informed that such reactions are possible and that prompt medical attention should be sought if allergic reactions occur.<br/>Pediatric 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. 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. 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 occurence 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. Patients with Turner syndrome should be evaluated carefully for otitis media and other ear disorders since these patients have an increased risk of ear and 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 somatropin. In addition, patients with Turner syndrome should be monitored closely for cardiovascular disorders (e.g., stroke, aortic aneurysm/dissection, hypertension) as these patients are also at risk for these conditions.<br/>Adult Patients: Patients with epiphyseal closure who were treated with somatropin replacement therapy in childhood should be reevaluated according to the criteria in INDICATIONS AND USAGE before continuation of somatropin therapy at the reduced dose level recommended for GH deficient adults. Fluid retention during somatropin replacement therapy in adults may occur. Clinical manifestations of fluid retention are usually transient and dose dependent . Experience with prolonged somatropin treatment in adults is limited.<br/>Information for Patients: Patients being treated with Nutropin AQ (and/or their parents) should be informed about the potential benefits and risks associated with Nutropin AQ treatment, including a review of the contents of the Patient Information Insert. This information is intended to better educate patients (and caregivers); it is not a disclosure of all possible adverse or intended effects. Patients and caregivers who will administer Nutropin AQ should receive appropriate training and instruction on the proper use of Nutropin AQ from the physician or other suitably qualified health care professional. A puncture���resistant container for the disposal of used syringes and needles should be strongly recommended. Patients and/or parents should be thoroughly instructed in the importance of proper disposal, and cautioned against any reuse of needles and syringes. This information is intended to aid in the safe and effective administration of the medication (see Patient Information Insert).<br/>Laboratory Tests: Serum levels of inorganic phosphorus, alkaline phosphatase, and parathyroid hormone (PTH) may increase during somatropin therapy.<br/>Drug Interactions: Somatropin inhibits 11�����hydroxysteroid dehydrogenase type 1 (11��HSD���1) in adipose/hepatic tissue and may significantly impact the metabolism of cortisol and cortisone. As a consequence, in patients treated with somatropin, previously undiagnosed central (secondary) hypoadrenalism may be unmasked requiring glucocorticoid replacement therapy. In addition, patients treated with glucocorticoid replacement therapy for previously diagnosed hypoadrenalism may require an increase in their maintenance or stress doses; this may be especially true for patients treated with cortisone acetate and prednisone since conversion of these drugs to their biologically active metabolites is dependent on the activity of the 11��HSD���1 enzyme. Excessive glucocorticoid therapy may attenuate the growth-promoting effects of somatropin in children. Therefore, glucocorticoid replacement therapy should be carefully adjusted in children with concomitant GH and glucocorticoid deficiency to avoid both hypoadrenalism and an inhibitory effect on growth. The use of Nutropin AQ in patients with CRI requiring glucocorticoid therapy has not been evaluated. Concomitant glucocorticoid therapy may inhibit the growth promoting effect of Nutropin AQ. Therefore, if glucocorticoid replacement is required for CRI, the glucocorticoid dose should be carefully adjusted to avoid an inhibitory effect on growth. There was no evidence in the controlled studies of Nutropin's interaction with drugs commonly used in chronic renal insufficiency patients. Limited published data indicate that somatropin treatment increases cytochrome P450 (CP450) mediated antipyrine clearance in man. These data suggest that somatropin 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 somatropin is administered in combination with other drugs known to be metabolized by CP450 liver enzymes. However, formal drug interaction studies have not been conducted. In adult women on oral estrogen replacement, a larger dose of somatropin may be required to achieve the defined treatment goal . In patients with diabetes mellitus requiring drug therapy, the dose of insulin and/or oral agent may require adjustment when somatropin therapy is initiated .<br/>Carcinogenesis, Mutagenesis, Impairment of Fertility: Carcinogenicity, mutagenicity, and reproduction studies have not been conducted with Nutropin AQ.<br/>Pregnancy:<br/>Pregnancy: Pregnancy (Category C). Animal reproduction studies have not been conducted with Nutropin AQ. It is also not known whether Nutropin AQ can cause fetal harm when administered to a pregnant woman or can affect reproduction capacity. Nutropin AQ should be given to a pregnant woman only if clearly needed.<br/>Nursing Mothers: 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.<br/>Geriatric Usage: Clinical studies of Nutropin AQ did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. Elderly patients may be more sensitive to the action of somatropin, and therefore may be more prone to develop adverse reactions. A lower starting dose and smaller dose increments should be considered for older patients .lld:dailymed
dailymed-drugs:273dailymed-instance:overdosag...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.)lld:dailymed
dailymed-drugs:273dailymed-instance:genericMe...Somatropinlld:dailymed
dailymed-drugs:273dailymed-instance:fullNameNutropin AQ (Injection, Solution)lld:dailymed
dailymed-drugs:273dailymed-instance:adverseRe...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, and 0/117 ISS 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 Nutropin AQ 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 CRI 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 therapy. In a post marketing surveillance study, the National Cooperative Growth Study, the pattern of adverse events in over 8000 patients with idiopathic short stature was consistent with the known safety profile of GH, and no new safety signals attributable to GH were identified. The frequency of protocol-defined targeted adverse eventsis described in the table, below. Injection site discomfort has been reported. This is more commonly observed in children switched from another GH product to Nutropin AQ. Experience with Nutropin AQ 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:lld:dailymed
dailymed-drugs:273dailymed-instance:indicatio...Pediatric Patients: Nutropin AQ [somatropin (rDNA origin) injection] is indicated for the long-term treatment of growth failure due to a lack of adequate endogenous GH secretion. Nutropin AQ [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. Nutropin AQ therapy should be used in conjunction with optimal management of chronic renal insufficiency. Nutropin AQ [somatropin (rDNA origin) injection] is also indicated for the long���term treatment of short stature associated with Turner syndrome. Nutropin AQ [somatropin (rDNA origin) injection] is also 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<br/>Adult Patients: Nutropin AQ [somatropin (rDNA origin) injection] is indicated for replacement of endogenous growth hormone in adults with growth hormone deficiency who meet either of the following two criteria: Adult Onset: Patients who have growth hormone 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 growth hormone deficient during childhood as a result of congenital, genetic, acquired, or idiopathic causes. In general, confirmation of the diagnosis of adult growth hormone deficiency in both groups usually requires an appropriate growth hormone stimulation test. However, confirmatory growth hormone stimulation testing may not be required in patients with congenital/genetic growth hormone deficiency or multiple pituitary hormone deficiencies due to organic disease.lld:dailymed
dailymed-drugs:273dailymed-instance:represent...http://www4.wiwiss.fu-berli...lld:dailymed
dailymed-drugs:273dailymed-instance:routeOfAd...http://www4.wiwiss.fu-berli...lld:dailymed
dailymed-drugs:273dailymed-instance:nameNutropin AQlld:dailymed
http://www4.wiwiss.fu-berli...dailymed-instance:producesD...dailymed-drugs:273lld:dailymed