Description

Overview of Danazol Capsules

Dosage Strengths of Danazol Capsules

Compounded: 25 mg, 75 mg

Commercial: 50 mg

Danazol is a synthetic steroid derived from ethisterone (ethinyl testosterone). Danazol is antiestrogenic and weakly androgenic. Danazol is used in the treatment of endometriosis, unless the process has advanced to the stage of surgical correction. Danazol also is used in the palliative treatment of fibrocystic breast disease. Hereditary angioedema in both males and females also has been successfully treated with danazol. Frequency of attacks can be limited by careful dose reduction after the initial response has been achieved. Danazol was approved by the FDA in 1976.

Through its action on the pituitary, danazol indirectly reduces estrogen production by lowering the output of follicle-stimulating hormone and luteinizing hormone. There is also evidence that danazol binds to sex hormone receptors in target tissues, thereby exibiting anabolic, antiestrognic and weakly androgenic activity. With higher doses, amenorrhea generally occurs after about 6 weeks of therapy; ovulation and cyclic bleeding returns to normal 60—90 days after therapy is discontinued. Danazol is used to treat endometriosis because it causes atrophy of ectopic endometrial tissue, which relieves symptoms completely. It also decreases the growth rate of abnormal breast tissue, making it useful in fibrocystic breast disease. Heriditary angioedema is an inherited disorder characterized by a deficiency in C1 esterase inhibitor (C1 INH), a serum inhibitor of the activated first component of complement. Danazol increases circulating levels of C1 INH and therby increases C4 of the complement system, which also is deficient in hereditary angioedema. Consequently, danazol prevents attacks of hereditary angioedema in both males and females. The exact mechanism by which danazol increases C1 INH is not known. Danazol does not possess any progestogenic activity, and does not suppress normal pituitary release of corticotropin, or release of cortisol by the adrenal glands.

Danazol is administered orally. Distribution data are limited, but extensive hepatic metabolism produces the primary metabolite, 2-hydroxymethylethisterone. Danazol is excreted in the urine and has an elimination half-life of 4—5 hours.

Route-Specific Pharmacokinetics:

Oral Route: The bioavailability of danazol is not directly dose-related; dosage increases are not proportional to increases in plasma concentrations. For example, doubling the dose may yield only a 30—40% increase in plasma concentration. Peak concentrations occur within 2 hours, but the onset of a therapeutic effect (anovulation or amenorrhea) does not occur for approximately 6—8 weeks after taking daily doses. Pain reduction in fibrocystic breast disease will begin to be realized at 1 month, with a peak effect at 2—3 months.

Danazol should be used with caution in patients with seizure disorder, migraine headaches, cardiac disease, or renal impairment because the drug can increase fluid retention, which can exacerbate these conditions. Danazol should not be used in patients with severe cardiac disease or severe renal disease (including renal failure).

Do not use danazol in patients with severe hepatic disease. Danazol should be used with caution, if at all, in patients with milder grades of hepatic disease. Danazol use can cause hepatic dysfunction including cholestatic jaundice, peliosis of the liver, and benign hepatic adenoma. Peliosis and adenoma may not be apparent until patients present with life-threatening intra-abdominal hemorrhage. Regular liver function tests (LFTs) should be carried out in all patients.

Danazol can induce ALA synthetase activity and porphyrin metabolism. For this reason, danazol should not be used in patients with acute intermittent porphyria because it can precipitate an attack.

Danazol is contraindicated during pregnancy (FDA pregnancy category X), so care should be taken to ensure that the patient is not pregnant or becomes pregnant during therapy. Teratogenic effects have been associated with danazol treatment. In addition, androgens have caused virilization of the external genitalia of the female fetus, including clitoromegaly, abnormal vaginal development, and fusion of genital folds to form a scrotal-like structure. The degree of masculinization is dependent on the amount of drug given and the age of the fetus; these effects are most likely to occur in the female fetus when the drugs are given in the first trimester. Females of childbearing potential should use adequate methods of contraception, and should commence therapy during menstrua5tion when possible to ensure a nonpregnant state. If pregnancy occurs, the drug should be immediately discontinued and the patient should be counseled concerning the potential risks to the fetus.

Danazol is excreted into human breast milk. Because of androgenic effects on the infant, its use is contraindicated during breast-feeding. An alternative method to breast-feeding should be found if the drug must be used.

Danazol can cause menstrual irregularity, breakthrough bleeding and other adverse reactions in women that could exacerbate or mask preexisting vaginal conditions. Therefore, danazol use is contraindicated in undiagnosed vaginal bleeding.

Danazol should not be used for the treatment of fibrocystic breast disease until the possibility of breast cancer has been eliminated. If nodules persist or become enlarged during treatment, the possibility of cancer should be investigated.

Geriatric patients should be treated with danazol cautiously as safety and effectiveness has not been determined in patients >= 65 years during clinical studies. Elderly male patients may be at risk of developing prostatic hypertrophy.

Danazol has been associated with cases of pseudotumor cerebri (benign increased intracranial pressure). Early signs and symptoms include headache, nausea/vomiting, visual disturbances, and papilledema. Patients with these signs and symptoms should be examined for papilledema, and if present, should discontinue the drug immediately and be referred for neurologic evaluation.

Thromboembolic disease such as thromboembolism or thrombotic events have occurred during danazol therapy. Cases of sagittal sinus thrombosis and fatal or life-threatening stroke have been reported.This list may not include all possible contraindications.

Danazol is contraindicated during pregnancy (FDA pregnancy category X), so care should be taken to ensure that the patient is not pregnant or becomes pregnant during therapy. Teratogenic effects have been associated with danazol treatment. In addition, androgens have caused virilization of the external genitalia of the female fetus, including clitoromegaly, abnormal vaginal development, and fusion of genital folds to form a scrotal-like structure. The degree of masculinization is dependent on the amount of drug given and the age of the fetus; these effects are most likely to occur in the female fetus when the drugs are given in the first trimester. Females of childbearing potential should use adequate methods of contraception, and should commence therapy during menstruation when possible to ensure a nonpregnant state. If pregnancy occurs, the drug should be immediately discontinued and the patient should be counseled concerning the potential risks to the fetus.

Danazol is excreted into human breast milk. Because of androgenic effects on the infant, its use is contraindicated during breastfeeding. An alternative method to breast-feeding should be found if the drug must be used.

NOTE: Danazol inhibits the cytochrome P450 system isoenzyme CYP3A4, and may reduce the hepatic metabolism of CYP3A4 substrates.

Danazol can decrease hepatic synthesis of procoagulant factors, increasing the possibility of bleeding when used concurrently with anticoagulants, platelet inhibitors, or thrombolytic agents. Coadministration of warfarin and danazol has been reported to increase the prothrombin time, with some cases resulting in serious bleeding. Avoid this combination when possible. If danazol therapy is necessary, consider reduction of the warfarin dosage when danazol is initiated, and monitor the anticoagulant response.

The risk of myopathy and rhabdomyolysis is increased if danazol is used with simvastatin or lovastatin. The use of simvastatin with danazol is contraindicated due to an increased risk of myopathy and rhabdomyolysis. If concurrent use of lovastatin and danazol is desired, carefully weigh the benefits of the ‘statin’ against the risk of myopathy and rhabdomyolysis. When coadministered with danazol, the initial lovastatin dose should not exceed 10 mg/day PO, and the total lovastatin dose should not exceed 20 mg/day PO. A single case report has documented the onset of myositis which progressed to rhabdomyolysis with myoglobinuria after danazol was added to a regimen containing lovastatin. Although other drugs were in use concurrently, a drug interaction between danazol and lovastatin is suspected since danazol (CYP3A4 inhibitor) is known to inhibit lovastatin metabolism. Other inhibitors of lovastatin metabolism (e.g., erythromycin) have been reported to increase the risk of lovastatin myopathy. Until more data are available, danazol should be used very cautiously, if at all, in patients receiving lovastatin or other HMG Co-A reductase inhibitors metabolized by CYP3A4 isozymes (e.g., atorvastatin, cerivastatin). Since compounds in red yeast rice claim to have HMG-CoA reductase inhibitor activity, red yeast rice should not be used in combination with danazol.

The use of ezetimibe; simvastatin with danazol is contraindicated due to an increased risk of myopathy and rhabdomyolysis. A single case report has documented the onset of myositis which progressed to rhabdomyolysis with myoglobinuria after danazol was added to a regimen containing lovastatin.7 Although other drugs were in use concurrently, a drug interaction between danazol and lovastatin is suspected since danazol (CYP3A4 inhibitor) is known to inhibit lovastatin metabolism.

The use of niacin; simvastatin with danazol is contraindicated due to an increased risk of myopathy and rhabdomyolysis. A single case report has documented the onset of myositis that progressed to rhabdomyolysis with myoglobinuria after danazol was added to a regimen containing lovastatin. Although other drugs were in use concurrently, a drug interaction between danazol and lovastatin is suspected, as danazol (CYP3A4 inhibitor) is known to inhibit lovastatin metabolism.

Danazol may increase concentrations of cyclosporine. Danazol is an inhibitor of and cyclosporine a substrate of CYP3A4. In a patient stabilized on cyclosporine, the addition of danazol 200 mg every 8 hours yielded a 38% increase in the cyclosporine blood concentration and necessitated a cyclosporine dosage reduction from 250 mg twice daily to 200 mg twice daily. Close monitoring of cyclosporine concentrations is required when danazol is given concurrently with cyclosporine.

Danazol is a CYP3A4 inhibitor and can decrease the hepatic metabolism of some drugs. Danazol has been noted to inhibit carbamazepine metabolism. Patients receiving carbamazepine should be closely monitored for toxicity if danazol is added to therapy. Conversely, a dose adjustment of carbamazepine may be necessary if danazol therapy is discontinued.

Danazol is a CYP3A4 inhibitor and can decrease the hepatic metabolism of some drugs. Danazol has also been reported to increase tacrolimus whole blood concentrations. Patients receiving tacrolimus should be closely monitored for toxicity if danazol is added to therapy. Conversely, a dose adjustment of tacrolimus may be necessary if danazol therapy is discontinued.

Danazol is a CYP3A4 inhibitor and can decrease the hepatic metabolism of CYP3A4 substrates. Examples of CYP3A4 substrates with potential for a narrow therapeutic index include: amiodarone, astemizole, benzodiazepines metabolized by oxidation (e.g., alprazolam, chlordiazepoxide, clonazepam, clorazepate, diazepam, estazolam, flurazepam, midazolam, prazepam, quazepam, triazolam), buspirone, calcium-channel blockers, certain opiates (e.g., alfentanil, fentanyl, methadone, sufentanil), cilostazol, cisapride, disopyramide, dofetilide, ergot alkaloids, ethosuximide, halofantrine lidocaine paricalcitol, pimozide, quinidine, sildenafil, sirolimus, terfenadine, vinca alkaloids, ziprasidone zonisamide, and others. This list is not inclusive of all agents metabolized by CYP3A4.

In vitro, both genistein and daidzein inhibit 5 alpha-reductase isoenzyme II, resulting in decreased conversion of testosterone to the potent androgen 5-alpha-dihydrotestosterone (DHT) and a subsequent reduction in testosterone-dependent tissue proliferation. The action is similar to that of finasteride, but is thought to be less potent. Theoretically, because the soy isoflavones appear to inhibit type II 5-alpha-reductase, the soy isoflavones may counteract the activity of the androgens. Danazol is weakly androgenic.

Aprepitant, fosaprepitant is a substrate of CYP3A4. Danazol is a CYP3A4 inhibitor. Coadministration may lead to increased aprepitant concentrations, although the clinical significance of this interaction is not known. Aprepitant, fosaprepitant generally appears to be well-tolerated at a broad dosage range and is indicated for short-term use at a fixed dosage schedule.

Doxercalciferol is converted in the liver to 1,25-dihydroxyergocalciferol, the major active metabolite, and 1-alpha, 24-dihydroxyvitamin D2, a minor metabolite. Although not specifically studied, cytochrome P450 enzyme inhibitors including danazol may inhibit the 25-hydroxylation of doxercalciferol, thereby decreasing the formation of the active metabolite and thus, decreasing efficacy. Patients should be monitored for a decrease in efficacy if danazol is coadministered with doxercalciferol.

The concomitant use of systemic tretinoin, ATRA and danazol should be done cautiously due to the potential for increased intracranial pressure and an increased risk of pseudotumor cerebri (benign intracranial hypertension). Early signs and symptoms of pseudotumor cerebri include papilledema, headache, nausea, vomiting, and visual disturbances.

Plasma concentrations of orally administered budesonide may increase during coadministration with CYP3A4 inhibitors; a budesonide dose reduction should be considered. Toxicity may occur, particularly excessive HPA-axis suppression. Theoretically, inhibition of CYP3A4 may be clinically significant for inhaled forms of budesonide, including budesonide nasal spray.

Danazol is a CYP3A4 inhibitor, and may reduce the hepatic metabolism of CYP3A4 substrates. Moderate or potent CYP3A4 inhibitors are contraindicated for use with ranolazine, a CYP3A4 substrate. Inhibition of ranolazine metabolism could lead to increased ranolazine plasma concentrations and associated QTc prolongation. Avoid coadministration of ranolazine with danazol due to the potential for reduced metabolism of ranolazine and the risk of QT prolongation.

Concurrent administration of sunitinib with inhibitors of cytochrome P450 3A4 such as danazol results in increased concentrations of sunitinib and its primary active metabolite. Whenever possible selection of an alternative concomitant medication with no or minimal enzyme inhibition potential is recommended. If an alternative therapy is not available, monitor patients closely for increased adverse reactions to sunitinib; a reduction in the dose of sunitinib may be required.

Danazol is a CYP3A4 inhibitor, and may reduce the hepatic metabolism of CYP3A4 substrates. Although not studied, danazol may increase the risk of toxicity from CYP3A4 substrates such as bosentan. Excessive bosentan dosage can result in hypotension or elevated hepatic enzymes. It is important to review all the medications taken concurrently with bosentan. According to the manufacturer, coadministration of bosentan with a potent CYP2C9 inhibitor plus a CYP3A4 inhibitor is not recommended; large increases in bosentan plasma concentrations are expected with such combinations.

In vitro studies indicate ambrisentan is a substrate of CYP3A, although in vivo studies with ketoconazole, a CYP3A4 inhibitor, did not demonstrate a clinically significant drug-drug interaction. Although data are lacking, significant CYP3A4 inhibitors, such as danazol could potentially increase ambrisentan plasma concentrations via CYP3A4 inhibition; the clinical significance of this potential interaction is unknown, but an increase in adverse effects is possible. If these drugs are coadministered, patients should be monitored for increased toxicity as well as increased therapeutic effect.

Danazol is an inhibitor of CYP3A4. Nilotinib is a substrate of CYP3A4. Coadminister these drugs with caution. Altered nilotinib serum concentrations may occur leading to an increased risk of nilotinib-related adverse reactions (including QT interval prolongation).

The cytochrome P450 3A4 (CYP3A4) isoenzyme is involved in the metabolism of quetiapine. Danazol may increase plasma concentrations of quetiapine through CYP3A4 inhibition. The manufacturer of quetiapine recommends a reduced dosage during concurrent administration of CYP3A4 inhibitors.

Concentrations of telithromycin may be increased with concomitant use of danazol. Telithromycin is a substrate of CYP3A4 and danazol is a CYP3A4 inhibitor.

Danazol is an inhibitor of CYP3A4, one of the isoenzymes responsible for the metabolism of haloperidol. Mild to moderate increases in haloperidol plasma concentrations have been reported during concurrent use of haloperidol and inhibitors of CYP3A4. Elevated haloperidol concentrations occurring through inhibition of CYP3A4 may increase the risk of adverse effects, including QT prolongation. Until more data are available, it is advisable to closely monitor for adverse events when these medications are co-administered.

Avoid concomitant use of danazol, a moderate CYP3A4 inhibitor, with ibrutinib, a CYP3A4 substrate, unless the benefit outweighs the possible risk of ibrutinib toxicity. Simulations using physiologically-based pharmacokinetic (PBPK) models suggest that moderate CYP3A4 inhibitors may increase the ibrutinib AUC 6 to 9-fold. If the use of both agents is necessary, reduce the dose of ibrutinib and monitor patients for signs of increased ibrutinib toxicity.

Danazol may reduce the hypoglycemic effects of insulins. Patients receiving insulin should be closely monitored for changes in diabetic control when hormone therapy is instituted or discontinued. Exogenously administered androgens have variable effects on blood glucose control in patients with diabetes mellitus. In general, low testosterone concentrations are associated with insulin resistance. Further, when hypogonadal men (with or without diabetes) are administered exogenous androgens, glycemic control typically improves as indicated by significant reductions in fasting plasma glucose concentrations and HbA1C. Conversely, the administration of large doses of anabolic steroids has decreased glucose tolerance, possibly through inducing insulin resistance. While data are conflicting, it would be prudent to monitor all patients with type 2 diabetes on antidiabetic agents receiving androgens for changes in glycemic control. Hypoglycemia or hyperglycemia can occur; dosage adjustments of the antidiabetic agent may be necessary.

Androgenic effects can occur during therapy with danazol in females and can be irreversible, even upon discontinuation of the drug. These effects include weight gain, acne vulgaris, seborrhea, hirsutism, edema, alopecia, deepening of the voice, pharyngitis, or hoarseness. Rarely, clitoral hypertrophy or testicular atrophy can occur. In male patients, modest spermatogenesis inhibition may be evident; abnormalities in semen volume, viscosity, sperm count (oligospermia), and motility may also occur in patients receiving long-term therapy.

Hypoestrogenic effects also commonly result from danazol use in females. These effects can be manifested by menstrual irregularity, breakthrough bleeding, reduction in breast size, ovulatory changes including anovulation, vaginal dryness, emotional lability, flushing, and diaphoresis, and these effects are generally are reversible. Amenorrhea occurs in about half of the female patients treated and may not resolve for a prolonged period, even upon discontinuation of the drug. In most patients, menstruation usually returns in 2—3 months following the discontinuation of the drug. In addition, hematuria and nipple discharge (breast discharge) have been reported in patients receiving danazol; a direct causal relationship to danazol use has neither been confirmed or refuted.Danocrine (danazol) package insert. Bridgewater, New Jersey: sanofi-aventis U.S. LLC; 2011 Dec.

Danazol is associated with hepatotoxicity. Reversible elevated hepatic enzymes have been reported in patients receiving >= 400 mg of danazol. Serious toxicity can lead to cholestasis, jaundice, peliosis hepatis or adenoma. Therapy should entail the use of the lowest possible adequate dose and regular monitoring of hepatic function. Malignant hepatic tumors (hepatoma) have been reported in rare instances, after long-term use; a direct causal relationship to danazol use has neither been confirmed or refuted.

Gastrointestinal adverse effects have been reported in patients receiving danazol, including gastroenteritis, nausea, vomiting, constipation, and rarely, pancreatitis and splenic peliosis. A direct causal relationship to danazol use has neither been confirmed or refuted.

Hypercholesterolemia, specifically, an increase in LDL cholesterol and a decrease in HDL cholesterol has been reported in patients on danazol therapy. This effect can be marked, and must be considered in patients with coronary artery disease or other risk factors. It should be noted, however, that laboratory test abnormalities can occur during therapy with danazol, including lipids, lipoproteins, CPK, glucose tolerance, glucagon, thyroid binding globulin, sex hormone binding globulin, and other plasma proteins. Patients with diabetes should be made aware that increased insulin has been required due to hyperglycemia in some patients receiving danazol, but a direct causal relationship to danazol use has neither been confirmed or refuted.

Allergic reactions to danazol can be manifested by urticaria, pruritus, purpura, petechiae, vesicular rash, and papular or maculopapular rash. Erythema multiforme (including Stevens-Johnson syndrome), photosensitivity, nasal congestion, and Guillain-Barre syndrome have also been reported, but a direct causal relationship to danazol use has neither been confirmed or refuted.

Thromboembolism or thrombotic events have occurred during danazol therapy. Cases of sagittal sinus thrombosis and stroke have been reported. In addition, myocardial infarction, palpitations, sinus tachycardia, and elevation in blood pressure have been reported, but a direct causal relationship to danazol use has neither been confirmed or refuted.

Teratogenesis is a serious concern with danazol; this agent should not be administered during pregnancy. Limited data describing inadvertent use of danazol during pregnancy report the occurrence of female pseudohermaphroditism. No adverse effects in male fetuses have been reported.

Central nervous system effects that have been reported with danazol include nervousness, dizziness and fainting, depression, fatigue, sleep disorders, headache, tremor, paresthesias, weakness, anxiety, changes in appetite, and chills. Convulsions and benign intracranial hypertension have been reported rarely; a direct causal relationship to danazol use has neither been confirmed or refuted. Benign intracranial hypertension (pseudotumor cerebri) produces headache, papilledema, nausea/vomiting, and visual impairment.

Musculoskeletal adverse reactions have been reported in patients receiving danazol, including muscle cramps or spasms, pelvic pain, joint pain, joint lockup, joint swelling, back pain, neck or extremity pain, and rarely, carpal tunnel syndrome which may be secondary to fluid retention. A direct causal relationship to danazol use has neither been confirmed or refuted.

Hematologic reactions have been reported in patients receiving danazol, including eosinophilia, leukopenia, thrombocytopenia, and increases in red cell and platelet count. Reversible erythrocytosis, leukocytosis or polycythemia may be provoked. A direct causal relationship to danazol use has neither been confirmed or refuted.

Interstitial pneumonitis has been reported in patients receiving danazol therapy. Cataracts, bleeding gums, and fever have been rarely reported. A direct causal relationship to danazol use has neither been confirmed or refuted.

This list may not include all possible adverse reactions or side effects. Call your health care provider immediately if you are experiencing any signs of an allergic reaction: skin rash, itching or hives, swelling of the face, lips, or tongue, blue tint to skin, chest tightness, pain, difficulty breathing, wheezing, dizziness, red, a swollen painful area/areas on the leg.

Store this medication at 68°F to 77°F (20°C to 25°C) and away from heat, moisture and light. Keep all medicine out of the reach of children. Throw away any unused medicine after the beyond use date. Do not flush unused medications or pour down a sink or drain.

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