Presentation and Status in Health Basket
1 X 3.6 mg/dose
Adults: One 3.6 mg depot injected subcutaneously into the anterior abdominal wall, every 28 days. No dosage adjustment is necessary for patients with renal or hepatic impairment or in the elderly. Endometriosis should be treated for a period of six months only, since at present there are no clinical data for longer treatment periods. Repeat courses should not be given due to concern about loss of bone mineral density. In patients receiving this product for the treatment of endometriosis, the addition of hormone replacement therapy (a daily oestrogenic agent and a progestogenic agent) has been shown to reduce bone mineral density loss and vasomotor symptoms. For use in endometrial thinning, four or eight weeks treatment. The second depot may be required for the patient with a large uterus or to allow flexible surgical timing. For women who are anaemic as a result of uterine fibroids: 3.6 mg depot with supplementary iron may be administered for up to three months before surgery.
Assisted reproduction: 3.6 mg is administered to downregulate the pituitary gland, as defined by serum oestradiol levels similar to those observed in the early follicular phase (approximately 150 pmol/l). This will usually take between 7 and 21 days. When downregulation is achieved, superovulation (controlled ovarian stimulation) with gonadotrophin is commenced. The downregulation achieved with a depot agonist is more consistent suggesting that, in some cases, there may be an increased requirement for gonadotrophin. At the appropriate stage of follicular development, gonadotrophin is stopped and human chorionic gonadotrophin (hCG) is administered to induce ovulation. Treatment monitor Treatment monitoring, oocyte retrieval and ing, oocyte retrieval and fertilisation techniques are performed according to the normal practice of the individual clinic. individual clinic.
Children: This product is not indicated for use in children.
Treatment of prostate cancer suitable for hormonal manipulation. Breast cancer in pre-menopausal women suitable for hormone manipulation. Endometriosis. Assisted reproduction: pituitary down regulation in preparion for superovulation.
Endometrial thinning: Zoladex is indicated for the prethinning of the utetine endometrium prior ro endometrial ablation or resection.
Uterine Fibroids: For reduction of fibroid size prior to surgery.
This product should not be given to patients with a known hypersensitivity to the active substance, to other LHRH analogues or to any of the excipients of this product. This product should not be used in pregnancy and lactation.
This product is not indicated for use in children, as safety and efficacy have not been established in this group of patients. There is an increased risk of incident depression (which may be severe) in patients undergoing treatment with GnRH agonists, such as Goserelin. Patients should be informed accordingly and treated as appropriate if symptoms occur. Initially, like other GnRH agonists, causes transient increases in serum levels of testosterone in men with prostate cancer, and estrogen in women with breast cancer. Transient worsening of symptoms, or the occurrence of additional signs and symptoms of prostate or breast cancer, may occasionally develop during the first few weeks of treatment. A small number of patients may experience a temporary increase in bone pain, which can be managed symptomatically.
Hypercalcemia: Hypercalcemia As with other GnRH agonists or hormonal therapies (antiestrogens, estrogens, etc.), hypercalcemia has been reported in some prostate and breast cancer patients with bone metastases after starting treatment. If hypercalcemia does occur, appropriate treatment measures should be initiated.
Males: The use in men at particular risk of developing ureteric obstruction or spinal cord compression should be considered carefully and the patients monitored closely during the first month of therapy. Consideration should be given to the initial use of an anti-androgen (eg. cyproterone acetate 300 mg daily for three days before and three weeks after commencement of this product) at the start of LHRH analogue therapy since this has been reported to prevent the possible sequelae of the initial rise in serum testosterone. If spinal cord compression or renal impairment due to ureteric obstruction are present or develop, specific standard treatment of these complications should be instituted. The use of LHRH agonists in men may cause a reduction in bone mineral density. In men, preliminary data suggest the use of a bisphosphonate in combination with an LHRH agonist may reduce bone mineral loss. Patients with known depression and patients with hypertension should be monitored carefully.
Hyperglycemia and Diabetes: Hyperglycemia and an increased risk of developing diabetes have been reported in men receiving GnRH agonists. Hyperglycemia may represent development of diabetes mellitus or worsening of glycemic control in patients with diabetes. Monitor blood glucose and/or glycosylated hemoglobin (HbA1c) periodically in patients receiving a GnRH agonist and manage with current practice for treatment of hyperglycemia or diabetes.
Cardiovascular Disease: Increased risk of developing myocardial infarction, sudden cardiac death and stroke has been reported in association with use of GnRH agonists in men. The risk appears low based on the reported odds ratios, and should be evaluated carefully along with cardiovascular risk factors when determining a treatment for patients with prostate cancer. Patients receiving a GnRH agonist should be monitored for symptoms and signs suggestive of development of cardiovascular disease and be managed according to current clinical practice.
Females: Females The use of LHRH agonists in women may cause a loss of bone mineral density. Following two years treatment for early breast cancer, the average loss of bone mineral density was 6.2% and 11.5% at the femoral neck and lumbar spine respectively. This loss has been shown to be partially reversible at the one year off treatment follow-up with recovery to 3.4% and 6.4% relative to baseline at the femoral 5 neck and lumbar spine respectively although this recovery is based on very limited data. In patients receiving this product for the treatment of endometriosis, the addition of hormone replacement therapy (a daily oestrogenic agent and a progestogenic agent) has been shown to reduce bone mineral density loss and vasomotor symptoms. This product should be used with caution in women with known metabolic bone disease. this productmay cause an increase in uterine cervical resistance, which may result in difficulty in dilating the cervix. Currently, there are no clinical data on the effect of treating benign gynaecological conditions with this product for periods in excess of six months. this product should only be administered as part of a regimen for assisted reproduction under the supervision of a specialist experienced in the area. As with other LHRH agonists, there have been reports of ovarian hyperstimulation syndrome (OHSS), associated with the use of 3.6 mg in combination with gonadotrophin. It has been suggested that the downregulation achieved with a depot agonist may lead, in some cases, to an increased requirement for gonadotrophin. The stimulation cycle should be monitored carefully to identify patients at risk of developing OHSS because its severity and incidence may be dependent on the dose regimen of gonadotrophin. Human chorionic gonadotrophin (hCG) should be withheld, if appropriate. It is recommended that this product is used with caution in assisted reproduction regimens in patients with polycystic ovarian syndrome as follicle recruitment may be increased. Patients with known depression and patients with hypertension should be monitored carefully. Treatment with Zoladex may lead to positive reactions in anti-doping tests.
The categories for adverse drug reactions (ADRs) were calculated based on reports from this product’s clinical trials and post-marketing sources.
For full details see prescribing information.
Pregnancy and Lactation
Pregnancy: Although reproductive toxicity in animals gave no evidence of teratogenic potential, this product should not be used in pregnancy as there is a theoretical risk of abortion or foetal abnormality if LHRH agonists are used during pregnancy. Potentially fertile women should be examined carefully before treatment to exclude pregnancy. Non hormonal methods of contraception should be employed during therapy and in the case of endometriosis should be continued until menses are resumed. Pregnancy should be excluded before this product is used for assisted reproduction. The clinical data from use in this setting are limited but the available evidence suggests there is no causal association between this product and any subsequent abnormalities of oocyte development or pregnancy and outcome.
Lactation: The use during breast feeding is not recommended.
There is limited experience of overdose in humans. In cases where this product has unintentionally been re-administered early or given at a higher dose, no clinically relevant adverse effects have been seen. Animal tests suggest that no effect other than the intended therapeutic effects on sex hormone concentrations and on the reproductive tract will be evident with higher doses. If overdose occurs, this should be managed symptomatically.