Saizen 5 mg

Withdrawals for this study during both the double-blind, placebo controlled phase and the open-label phase were due to patient decision (7%), protocol violation (0.9%), adverse events (12.2%), lost to follow-up (0.9%) and other (2.6%).

Edema, muscle pain, joint pain, and joint disorders were reported to occur in up to 10% of adult patients receiving growth hormone replacement therapy. These side effects occurred primarily early in therapy and tended to be transient.

Adult patients with growth hormone deficiency, following diagnosis of growth hormone deficiency in childhood, reported side effects less frequently than those with adult onset growth hormone deficiency.

Common: Injection site reactions: Some patients may experience redness and itching at the site of injection, particularly when the subcutaneous route is used.

Localized lipoatrophy, which can be avoided by varying the site of injection.

Uncommon: idiopathic intracranial hypertension.

Uncommon (in children): Fluid retention: peripheral oedema, stiffness, arthralgia, myalgia, paresthesia.

SAIZEN is indicated for the replacement therapy in adult patients with acquired or idiopathic growth hormone deficiency (GHD) as diagnosed by a single dynamic test for growth hormone deficiency (peak GH ≤5 µg/L). Patients with a growth hormone deficiency with onset in childhood should be retested before treatment starts.

SAIZEN is indicated for growth disturbance (current height Standard Deviation Score (SDS) <−2) in short children born small for gestational age (SGA) with a birth weight and/or length below −2 standard deviations (SD), who failed to show catch-up growth (Height Velocity SDS <0 during the last year) by 2 years of age or later.

SAIZEN is indicated for the long-term treatment of children with growth failure due to inadequate secretion of normal endogenous growth hormone. Other causes for growth failure should be ruled out.

SAIZEN is indicated for the treatment of growth failure in children due to Chronic Renal Failure.

SAIZEN is indicated for the treatment of short stature in girls with gonadal dysgenesis (Turner’s Syndrome) when epiphyses are not closed.

Each vial of sterile, nonpyrogenic, lyophilized powder contains: somatropin 5 mg. Nonmedicinal ingredients: phosphoric acid, sodium hydroxide and sucrose. Cartons of 1 and 2 vials with diluent (10 mL Bacteriostatic Water for Injection, USP).

Each vial of sterile, nonpyrogenic, lyophilized powder contains: somatropin 3.33 mg. Nonmedicinal ingredients: disodium phosphate dihydrate, mannitol and sodium dihydrogen phosphate monohydrate. Cartons of 1 and 10 vials with diluent (5 mL Bacteriostatic Sodium Chloride Injection, USP).

Each vial of sterile, nonpyrogenic, lyophilized powder for reconstitution contains: somatropin 8.8 mg. Nonmedicinal ingredients: phosphoric acid, sodium hydroxide and sucrose. 1 vial of SAIZEN product and 1 cartridge of bacteriostatic solvent pre-assembled in 1 reconstitution device (click.easy) comprising of the main body, the cap assembly and the sterile transfer cannula. 5 vials of SAIZEN product and 5 cartridges of bacteriostatic solvent pre-assembled in 5 reconstitution devices (click.easy) comprising each of the main body, the cap assembly and sterile transfer cannula. The DIN 2R 3 mL vials of SAIZEN and the cartridges of the solvent are of neutral glass (Type I). There is no latex in the components of the vial, cartridge or reconstitution device.

Not indicated for treatment in the geriatric population.

Serum levels of inorganic phosphorus, alkaline phosphatase, and IGF-1 may increase with SAIZEN therapy.

Carcinogenicity studies have not been conducted. Mutagenicity studies showed no mutagenic activity with SAIZEN.

Leukemia has been reported in a small number of growth hormone deficient patients, treated with growth hormone. Based on the current evidence, experts cannot conclude that growth hormone therapy is responsible for these occurrences.

SAIZEN treatment should be carried out under regular guidance of a physician experienced in the diagnosis and management of growth disorders.

In clinical studies in non-growth hormone deficient adult patients, a significant increase in mortality has been reported among somatropin treated patients with acute critical illness in intensive care units due to complications following cardiac surgery, abdominal surgery, multiple accident trauma or acute respiratory failure (see Contraindications). In 2 clinical studies with another somatropin and in published articles, where growth hormone was given at doses much higher than those used in the SAIZEN trials (approximately double to triple the dosage), the death rate in this patient population doubled (41.9%) relative to placebo (19.3%). The safety of continuing somatropin treatment in patients receiving replacement doses for approved indications who concurrently develop acute or critical illnesses has not been established. Therefore, the potential benefit of treatment continuation with growth hormone in patients having such an illness should be weighted against the potential risks.

Slipped capital femoral epiphysis is often associated with endocrine disorders such as GHD and hypothyroidism, and growth spurts. In children treated with growth hormone, slipped capital femoral epiphysis may either be due to underlying endocrine disorders or to the increased growth velocity caused by treatment. Physicians and parents should be alert to the development of a limp or complaints of hip or knee pain in children treated with SAIZEN.

Concomitant glucocorticoid therapy may inhibit the response to SAIZEN and should not exceed 10-15 mg hydrocortisone equivalent/m² body surface area during SAIZEN treatment.

Injection sites should be varied to prevent localized lipoatrophy, in particular in the case of long-term, subcutaneous administrations of SAIZEN.

Scoliosis has also been reported in patients treated with growth hormone.

Patients with growth failure due to chronic renal failure should be regularly examined and monitored for progression of renal osteodystrophy. Slipped capital femoral epiphysis or avascular necrosis of the femoral head may occur in children with advanced renal osteodystrophy and it is uncertain whether these complications are affected by growth hormone therapy. In these patients, radiograms of the hips and laboratory exams (serum calcium, phosphorus, alkaline phosphatase and PTH) should be made prior to initiating growth hormone therapy and regularly followed subsequently. Physicians and parents should be alert to the development of a limp or complaints of hip or knee pain (as knee pain may be referred hip pain) in patients treated with growth hormone therapy.

Bone age should be monitored periodically during SAIZEN administration especially in patients who are pubertal and/or receiving concomitant thyroid replacement therapy. Under these circumstances, epiphyseal maturation may progress rapidly.

Patients with growth hormone deficiency secondary to an intracranial lesion should be examined frequently for progression or recurrence of the underlying disease process.

Patients with an intra or extracranial neoplasia in remission who are receiving treatment with growth hormone should be examined carefully and at regular intervals by the physician. Patients developing neoplasia should be reported to Health Canada by the treating physician.

In short children born SGA other medical reasons or treatments that could explain growth disturbance should be ruled out before starting treatment.

For SGA patients, it is recommended to measure IGF-I level before start of treatment and twice a year thereafter. If on repeated measurements IFG-I levels exceed +2 SD compared to references for age and pubertal status, the IGF-I/GFBP-3 ratio could be taken into account to consider dose adjustment.

Experience in initiating treatment in SGA patients near onset of puberty is limited. It is therefore not recommended to initiate treatment near onset of puberty. Experience with SGA patients with Silver-Russel syndrome is limited.

Some of the height gain obtained with treating short children born SGA with somatropin may be lost if treatment is stopped before final height is reached.

In case of persistent oedema or severe paraesthesia the dosage should be decreased in order to avoid the development of carpal tunnel syndrome. Growth hormone deficiency in the Adult is a lifelong condition and should be treated accordingly, however experience with patients over sixty years and experience with prolonged treatment is limited.

Growth hormone administration is followed by a transient phase of hypoglycemia of approximately 2 hours, then from 2-4 hours onward by an increase in blood glucose levels despite high insulin concentrations. To detect insulin resistance, patients should be monitored for evidence of glucose intolerance.

Idiopathic intracranial hypertension has been recognized as a complication (early in treatment usually) of growth hormone treatment. The diagnosis is made on the basis of clinical symptoms such as severe, persistent or recurrent headache, visual problems, nausea and/or vomiting, papilloedema and temporal relationship to growth hormone. Physicians and parents should be attentive to relevant symptoms such as headache and visual problems in patients under SAIZEN therapy. Fundoscopic examination should be performed routinely before initiating treatment with SAIZEN to exclude pre-existent papilloedema and repeated if there is any clinical suspicion. If papilloedema is confirmed by fundoscopy, SAIZEN treatment should be stopped. It can be restarted at a lower dose after idiopathic-intracranial hypertension has resolved which occurs rapidly when treatment is withdrawn. If growth hormone treatment is restarted, careful monitoring for symptoms of intracranial hypertension is necessary, and treatment should be discontinued if intracranial hypertension recurs. At present, there is insufficient evidence to guide clinical decision making in patients with resolved intracranial hypertension.

Because human growth hormone may induce a state of insulin-resistance, SAIZEN patients should be monitored for evidence of glucose intolerance. SAIZEN should be used with caution in patients with diabetes mellitus (adjustment of their antidiabetic therapy may be required) or a family history of diabetes mellitus. SGA patients are a subgroup of patients at higher risk of developing diabetes in whom fasting insulin and blood glucose should be closely monitored before initiating and during treatment with SAIZEN. SAIZEN administration is followed by a transient phase of hypoglycemia of approximately 2 hours, then from 2-4 hours onward by an increase in blood glucose levels despite high insulin concentrations. To detect insulin resistance, patients should be monitored for evidence of glucose intolerance.

Hypothyroidism may develop during SAIZEN therapy. Growth hormone can affect the metabolism of thyroid hormones by increasing the extrathyroidal conversion of T4 to T3 and this lowering effect on T4 may unmask incipient central hypothyroidism in hypopituitary patients. Therefore, thyroid function should be evaluated before starting SAIZEN therapy and regularly assessed during treatment, not less frequently than annually. If hypothyroidism is diagnosed in the course of SAIZEN therapy, it should be corrected because untreated hypothyroidism will jeopardize the response to growth hormone.

There have been reports of fatalities after initiating therapy with growth hormone in pediatric patients with Prader-Willi syndrome who had one or more of the following risk factors: severe obesity, history of upper airway obstruction or sleep apnea, or unidentified respiratory infection. Male patients with one or more of these factors may be at greater risk than females. Patients with Prader Willi syndrome should be evaluated for signs of upper airway obstruction and sleep apnea before initiation of treatment with growth hormone. If during treatment with growth hormone, patients show signs of upper airway obstruction (including onset of or increased snoring) and/or new onset of sleep apnea, treatment should also be interrupted. All patients with Prader-Willi syndrome treated growth hormone should also have effective weight control and be monitored for signs of respiratory infection, which should be diagnosed as early as possible and treated aggressively (see Contraindications). Unless patients with Prader-Willi syndrome also have a diagnosis of growth hormone deficiency, SAIZEN is not indicated for the long-term treatment of pediatric patients who have growth failure due to genetically-confirmed Prader-Willi syndrome.

SAIZEN does not interfere with the patient’s ability to drive or use machinery.

Patients who are sensitive to the preservative metacresol, found in the diluent, should consider using SAIZEN supplied with bacteriostatic diluent containing benzyl alcohol as preservative.

Reproduction studies have not been conducted. It is not known whether somatropin can cause fetal harm when administered to a pregnant woman or can affect reproduction capacity. Somatropin should only be given to a pregnant woman if the benefits outweigh the risks.

SAIZEN is indicated for use in children (see Indications and Clinical Use).

It is not known whether this drug is excreted in human milk. Due to the large molecular weight, it is unlikely that it would be passed intact into the maternal milk and absorption of intact protein from the gastrointestinal tract of the infant is also unlikely. However, secretion of breakdown products of the drug in breast milk has not been studied. Because many drugs are excreted in human milk, caution should be exercised when somatropin is administered to a nursing mother.

The recommended diluents for reconstitution are:

3.33 mg Vial: Sodium Chloride Injection, USP and Bacteriostatic Sodium Chloride Injection, USP.

5 mg Vial: Water for Injection, USP and Bacteriostatic Water for Injection, USP.

When reconstituted with Bacteriostatic Sodium Chloride Injection, USP, the reconstituted solution may be stored at 2-8°C for up to 21 days.

When reconstituted with Sodium Chloride Injection, USP, the reconstituted solution should be administered immediately (within 3 hours). Any unused solution should be discarded.

To prevent possible contamination of the vial, wipe the rubber stopper with an antiseptic solution before puncturing it with the needle.

After determining appropriate patient dose, reconstitute each 5 mg vial of SAIZEN with 1-3 mL of Bacteriostatic Water for Injection, USP (Benzyl Alcohol preserved), each 3.33 mg vial of SAIZEN with up to 5 mL of Bacteriostatic Sodium Chloride Injection, USP (Benzyl Alcohol preserved).

To reconstitute SAIZEN, inject the diluent into the vial of SAIZEN aiming the liquid against the glass vial wall. Swirl the vial with a gentle rotary motion until contents are dissolved completely. Do not shake. If shaken, the solution will appear opalescent; however, this opalescence does not indicate any decrease in potency. Parenteral drug products should be inspected visually prior to administration. Do not inject if the reconstituted product contains particulate matter or is discoloured. For use in patients sensitive to the diluent see Warnings and Precautions.

When reconstituted with 1 mL to 5 mL Bacteriostatic Water for Injection, USP, the reconstituted solution may be stored at 2-8°C for up to 14 days.

When reconstituted with Water for Injection, USP, the reconstituted solution should be administered immediately (within 3 hours). Any unused solution should be discarded.

SAIZEN should not be mixed with other drugs.

Store at room temperature (25°C or below) in original package. Do not freeze. Store reconstituted product at 2-8°C in the cartridge for up to 28 days. Keep in a safe place out of the reach of children. Do not use after expiry date.

3.33 mg Vial: Store SAIZEN lyophilized product under refrigeration at 2-8°C.

5 mg Vial: Store SAIZEN lyophilized product at room temperature.

Do not use SAIZEN after the expiry date shown on label.

SAIZEN is indicated for children with chronic renal failure (see Indications and Clinical Use). No other studies have been conducted with special populations and conditions.

The measurable increase in growth (body length) after somatropin treatment results from its effect on cartilaginous growth areas of the long bones. It is known that somatropin's effect is mediated by a sulfation factor, IGF-1, which permits the incorporation of sulfate into cartilage. IGF-1 is present in low concentration in the serum of growth hormone deficient patients and increases during somatropin therapy.

Connective tissue metabolism is affected by somatropin's ability to stimulate the synthesis of chondroitin sulfate and collagen as well as the urinary excretion of hydroxyproline.

Somatropin is a polypeptide hormone consisting of 191 amino acid residues and its structure is identical to that of growth hormone extracted from human pituitary glands. It is produced by recombinant (rDNA) technology in a mammalian cell expression system. Somatropin is also therapeutically equivalent to human growth hormone of pituitary origin.

SAIZEN provides an exogenous supply of human growth hormone for those patients lacking the ability to produce adequate endogenous supplies.

Somatropin brings about cellular growth as demonstrated by an increase in the muscular, visceral and red cell mass. In muscle tissue, the increase in mass is associated with a corresponding increase in both number and dimension of muscular fibre cells.

Lipid metabolism is also affected by somatropin. This occurs when intracellular lipolysis is stimulated, thus increasing the plasma concentration of free fatty acids and stimulating the oxidation of fatty acids. In the diabetic patient, somatropin has been shown to accentuate ketogenesis.

Somatropin affects mineral metabolism by inducing the net retention of phosphorus and potassium and to a lesser degree sodium. Somatropin induces the increased intestinal absorption of calcium and the increased renal tubular reabsorption of phosphorus with increased serum and inorganic phosphate. Increased serum alkaline phosphatase may also be observed during somatropin therapy.

Somatropin stimulates linear growth in patients with pituitary growth hormone deficiency, Turner’s syndrome and chronic renal failure. Treatment of these patients with SAIZEN results in increased growth rates and IGF-1 levels similar to those seen for children treated with growth hormone of pituitary origin.

Somatropin has an effect on carbohydrate metabolism. The diabetogenic effect of somatropin is well-known in clinical medicine. Acromegalic patients often suffer from diabetes mellitus while hypopituitary children experience hypoglycemia. In healthy patients, very large doses of somatropin may interfere with glucose tolerance. A simultaneous increase in the plasma insulin level is observed upon somatropin administration.

The diabetogenic activity of somatropin is perhaps due to several concomitant factors:

1. Reduced transport of glucose into peripheral tissues.

   
   

2. Increased release of glucose from the liver.

   
   

3. Reduced concentration of insulin at the muscular level.

   
   

4. Reduced glycolysis from the block of the enzyme triose phosphate dehydrogenase, mediated by non-esterified fatty acids.

Somatropin has an effect on protein metabolism. Somatropin is an anabolic agent that stimulates intracellular transport of amino acids, net retention of nitrogen and protein synthesis which can be quantified by observing the decline in urinary nitrogen excretion and BUN.

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