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Norditropin SimpleXx 15 mg/ ml - Summary of Product Characteristics (SmPC) - (eMC)
Patients with childhood onset GHD should be re-evaluated for growth hormone secretory capacity after growth completion. Pronounced GHD in known hypothalamic-pituitary disease, cranial irradiation, and traumatic brain injury.
GHD should be associated with one other deficient axis, other than prolactin. GHD should be demonstrated by one provocative test after institution of adequate replacement therapy for any other deficient axis. In adults, the insulin tolerance test is the provocative test of choice. When the insulin tolerance test is contraindicated, alternative provocative tests must be used. The combined arginine-growth hormone releasing hormone is recommended.
An arginine or glucagon test may also be considered; however these tests have less established diagnostic value than the insulin tolerance test.
Norditropin should only be prescribed by doctors with special knowledge of the therapeutic indication of use. The dosage is individual and must always be adjusted in accordance with the individual's clinical and biochemical response to therapy. When GHD persists after growth completion, growth hormone treatment should be continued to achieve full somatic adult development including lean body mass and bone mineral accrual for guidance on dosing, see Replacement therapy in adults.
A dose of 0. In patients with childhood onset GHD, the recommended dose to restart is 0. In patients with adult onset GHD, it is recommended to start treatment with a low dose: It is recommended to increase the dosage gradually at monthly intervals based on the clinical response and the patient's experience of adverse events.
Serum IGF-I can be used as guidance for the dose titration. Women may require higher doses than men, with men showing an increasing IGF-I sensitivity over time. This means that there is a risk that women, especially those on oral oestrogen replacement are under-treated while men are over-treated. Dose requirements decline with age. Maintenance dosages vary considerably from person to person, but seldom exceed 1.
Generally, daily subcutaneous administration in the evening is recommended. The injection site should be varied to prevent lipoatrophy. Somatropin must not be used when there is any evidence of activity of a tumour. Intracranial tumours must be inactive and antitumour therapy must be completed prior to starting growth hormone GH therapy. Treatment should be discontinued if there is evidence of tumour growth.
Somatropin should not be used for longitudinal growth promotion in children with closed epiphyses. Patients with acute critical illness suffering complications following open heart surgery, abdominal surgery, multiple accidental trauma, acute respiratory failure, or similar conditions should not be treated with somatropin see section 4.
In children with chronic renal disease, treatment with Norditropin SimpleXx and Norditropin NordiFlex should be discontinued at renal transplantation. Children treated with somatropin should be regularly assessed by a specialist in child growth. Somatropin treatment should always be instigated by a physician with special knowledge of growth hormone insufficiency and its treatment.
This is true also for the management of Turner syndrome, chronic renal disease, and SGA. Data of final adult height following the use of Norditropin for children with chronic renal disease are not available. The stimulation of longitudinal growth in children can only be expected until epiphyseal closure. There have been reports of sudden death after initiating somatropin therapy in patients with Prader- Willi syndrome, who had one or more of the following risk factors: Severe obesity, history of upper airway obstruction or sleep apnoea, or unidentified respiratory infection.
In short children born SGA other medical reasons or treatments that could explain growth disturbance should be ruled out before starting treatment. 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. Monitoring of growth of hands and feet in Turner syndrome patients treated with somatropin is recommended and a dose reduction to the lower part of the dose range should be considered if increased growth is observed.
Girls with Turner syndrome generally have an increased risk of otitis media, which is why otological evaluation is recommended on at least an annual basis. The dosage in children with chronic renal disease is individual and must be adjusted according to the individual response to therapy see section 4. The growth disturbance should be clearly established before somatropin treatment by following growth on optimal treatment for renal disease over one year.
Conservative management of uraemia with customary medicinal product, and if needed, dialysis should be maintained during somatropin therapy. Patients with chronic renal disease normally experience a decline in renal function as part of the natural course of their illness. However, as a precautionary measure during somatropin treatment, renal function should be monitored for an excessive decline, or increase in the glomerular filtration rate which could imply hyperfiltration.
Scoliosis may progress in any child during rapid growth. Signs of scoliosis should be monitored during treatment. However, somatropin treatment has not been shown to increase the incidence or severity of scoliosis. In Turner syndrome and SGA children it is recommended to measure fasting insulin and blood glucose before start of treatment and annually thereafter.
In patients with increased risk of diabetes mellitus e. If overt diabetes occurs, somatropin should not be administered. Somatropin has been found to influence carbohydrate metabolism, therefore, patients should be observed for evidence of glucose intolerance.
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. Growth hormone deficiency in adults is a lifelong disease and needs to be treated accordingly, however, experience in patients older than 60 years and in patients with more than five years of treatment in adult growth hormone deficiency is still limited. There is no evidence for increased risk of new primary cancers in children or in adults treated with somatropin.
In patients in complete remission from tumours or malignant disease, somatropin therapy has not been associated with an increased relapse rate. An overall slight increase in second neoplasms has been observed in childhood cancer survivors treated with growth hormone, with the most frequent being intracranial tumours. The dominant risk factor for second neoplasms seems to be prior exposure to radiation. Patients who have achieved complete remission of malignant disease should be followed closely for relapse after commencement of somatropin therapy.
Leukaemia has been reported in a small number of growth hormone deficient patients, some of whom have been treated with somatropin.
However, there is no evidence that leukaemia incidence is increased in somatropin recipients without predisposition factors. If papilloedema is confirmed, a diagnosis of benign intracranial hypertension should be considered, and if appropriate, the somatropin treatment should be discontinued.
At present there is insufficient evidence to guide clinical decision making in patients with resolved intracranial hypertension. If somatropin treatment is restarted, careful monitoring for symptoms of intracranial hypertension is necessary.
Patients with growth hormone deficiency secondary to an intracranial lesion should be examined frequently for progression or recurrence of the underlying disease process. Somatropin increases the extrathyroidal conversion of T4 to T3 and may, as such, unmask incipient hypothyroidism. Monitoring of thyroid function should therefore be conducted in all patients. In patients with hypopituitarism, standard replacement therapy must be closely monitored when somatropin therapy is administered.
Patients with Turner syndrome have an increased risk of developing primary hypothyroidism associated with anti-thyroid antibodies. As hypothyroidism interferes with the response to somatropin therapy, patients should have their thyroid function tested regularly and should receive replacement therapy with thyroid hormone when indicated.
Because somatropin may reduce insulin sensitivity, patients should be monitored for evidence of glucose intolerance see section 4. For patients with diabetes mellitus, the insulin dose may require adjustment after somatropin containing product therapy is instituted. Patients with diabetes or glucose intolerance should be monitored closely during somatropin therapy. As with all somatropin containing products, a small percentage of patients may develop antibodies to somatropin.
The binding capacity of these antibodies is low and there is no effect on growth rate. Testing for antibodies to somatropin should be carried out in any patient who fails to respond to therapy. In patients treated with somatropin, previously undiagnosed central secondary hypoadrenalism may be unmasked and glucocorticoid replacement may be required. In addition, patients treated with glucocorticoid replacement therapy for previously diagnosed hypoadrenalism may require an increase in their maintenance or stress doses, following initiation of somatropin treatment see section 4.
If a woman taking somatropin begins oral oestrogen therapy, the dose of somatropin may need to be increased to maintain the serum IGF-1 levels within the normal age-appropriate range. Two placebo-controlled clinical trials of patients in intensive care units have demonstrated an increased mortality among patients suffering from acute critical illness due to complications following open heart or abdominal surgery, multiple accidental trauma or acute respiratory failure, who were treated with somatropin in high doses 5.
The safety of continuing somatropin treatment in patients receiving replacement doses for approved indications who concurrently develop these illnesses has not been established. Therefore, the potential benefit of treatment continuation with somatropin in patients having acute critical illnesses should be weighed against the potential risk.
One open-label, randomised clinical trial dose range 0. Concomitant treatment with glucocorticoids inhibits the growth-promoting effects of Norditropin. Patients with ACTH deficiency should have their glucocorticoid replacement therapy carefully adjusted to avoid any inhibitory effect on growth. Growth hormone decreases the conversion of cortisone to cortisol and may unmask previously undiscovered central hypoadrenalism or render low glucocorticoid replacement doses ineffective see section 4.
In women on oral oestrogen replacement, a higher dose of growth hormone may be required to achieve the treatment goal see section 4. Data from an interaction study performed in growth hormone deficient adults, suggest that somatropin administration may increase the clearance of compounds known to be metabolised by cytochrome P isoenzymes.
The clearance of compounds metabolised by cytochrome P 3A4 e. The clinical significance of this is unknown. The effect of somatropin on final height can also be influenced by additional therapy with other hormones, e. In insulin treated patients adjustment of insulin dose may be needed after initiation of somatropin treatment see section 4.
Animal studies are insufficient with regard to effects on pregnancy, embryofoetal development, parturition, or postnatal development. No clinical data on exposed pregnancies are available. Therefore, somatropin containing products are not recommended during pregnancy and in women of childbearing potential not using contraception.
There have been no clinical studies conducted with somatropin containing products in breast-feeding women. It is not known whether somatropin is excreted in human milk. Therefore caution should be exercised when somatropin containing products are administered to breast-feeding women. Norditropin SimpleXx and Norditropin NordiFlex has no or negligible influence on the ability to drive and use machines.