Genotropin Special Precautions

Diagnosis and therapy with somatropin should be initiated and monitored by physicians who are appropriately qualified and experienced in the diagnosis and management of patients with the therapeutic indication of use.
Myositis is a very rare adverse event that may be related to the preservative m-cresol. If myalgia or disproportionate pain at injection site develops, myositis should be considered and, if confirmed, a presentation of somatropin without m-cresol should be used.
Somatropin may induce a state of insulin resistance and, in some patients, hyperglycemia. Therefore, patients should be observed for evidence of glucose intolerance. In rare cases, therapy with somatropin may produce sufficient glucose intolerance to meet the diagnostic criteria for Type 2 diabetes mellitus. The risk of developing diabetes during treatment with somatropin is greatest in those patients with other risk factors for Type 2 diabetes mellitus, such as obesity, family history of diabetes, treatment with steroids, or prior impaired glucose tolerance. In patients with pre-existing diabetes mellitus, the dose of anti-diabetic therapy might require adjustment when somatropin is instituted.
In general, peripheral thyroid hormone levels remain within the normal reference range during treatment with somatropin. However, there is an enhanced conversion of T4 to T3 that may result in a reduction in serum T4 and an increase in serum T3 concentrations. This effect may be of clinical relevance for patients with central subclinical hypothyroidism in whom hypothyroidism may theoretically develop. Conversely, mild hyperthyroidism may occur in patients receiving replacement therapy with thyroxin. It is therefore, advisable to test thyroid function shortly after the start of treatment with somatropin, and after dose adjustments.
Introduction of somatropin treatment may result in inhibition of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD-1) and reduced serum cortisol concentrations. 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 Interactions).
If a woman taking somatropin begins oral estrogen therapy, the dose of somatropin may need to be increased to maintain the serum insulin-like growth factor-I (IGF-I) levels within the normal age-appropriate range. Conversely, if a woman on somatropin discontinues oral estrogen therapy, the dose of somatropin may need to be reduced to avoid excess of growth hormone and/or side effects (see Interactions).
In patients with growth hormone deficiency secondary to treatment of malignant disease, it is recommended to monitor for signs of relapse of the malignancy.
In patients with endocrine disorders, including growth hormone deficiency, slipped epiphyses of the hip may occur more frequently than in the general population. Children who develop a limp during treatment with somatropin should be evaluated (see Adverse Reactions).
In case of severe or recurrent headache, visual problems, nausea, or vomiting, a funduscopy for papilledema is recommended. If papilledema is confirmed, a diagnosis of benign intracranial hypertension should be considered and, if appropriate, growth hormone treatment should be discontinued. At present, there is insufficient evidence to guide the decision of whether or not to reintroduce growth hormone therapy in patients with resolved intracranial hypertension. If growth hormone treatment is restarted, careful monitoring for symptoms of intracranial hypertension is necessary.
Progression of scoliosis can occur in patients who experience rapid growth. Because growth hormone increases growth rate, physicians should be alert to this abnormality, which may manifest during growth hormone therapy.
Experience in patients above 60 years is limited.
In patients with chronic renal insufficiency, renal function should be below 50% of normal before institution of therapy with somatropin. To verify growth disturbance, growth should be followed for a year preceding institution of therapy. Conservative treatment for renal insufficiency should have been established and should be maintained during therapy with growth hormone. Somatropin should be discontinued at renal transplantation.
If patients who are receiving growth hormone replacement therapy become acutely critically ill, the potential benefit of continued treatment with somatropin should be weighed against the potential risk (see Contraindications).
Somatropin is ineffective for growth promotion in children with closed epiphyses.
Effects on ability to drive and use machines: No effects on the ability to drive and use machines have been observed.