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Mechanism of Action
US Drug Names
2.5 mg PO 2 to 4 times per day. Dose range: 2.5 to 20 mg PO per day, given in divided doses, may be necessary. Use intermittently. The usual duration is 2 to 4 weeks, which may be repeated as needed. The dose and duration are adjusted to efficacy and tolerability. Adequate caloric and protein consumption is required.
The recommended dose is 5 mg PO twice daily. Use intermittently. The usual duration is 2 to 4 weeks, which may be repeated as needed. The dose and duration are adjusted to efficacy and tolerability. Adequate caloric and protein consumption is required.
0.1 mg/kg/day or less of body weight PO, given in divided doses 2 to 4 times per day (not to exceed max adult dosage of 20 mg/day). Use intermittently. Usual duration: 2 to 4 weeks; repeat as needed. Adjust to efficacy and tolerability. Adequate caloric and protein consumption is required.
Doses of 5—15 mg/day PO have been studied. The impact of oxandrolone on weight gain and muscle strength was determined in a randomized, placebo-controlled study of 63 men with AIDS-associated myopathy and wasting (greater than 10% loss of body weight). Weight gain over the 16 weeks was achieved with the 15-mg dose whereas weight maintenance and weight loss occurred in the 5 mg/day and placebo groups, respectively. Measurable improvements in muscle strength did not occur with any treatment.
Oxandrolone 0.1 mg/kg/day PO for 12 weeks has been studied in 9 HIV infected children aged 4—14 years with malnourishment or risk of malnourishment. Improvements such as increased weight gain, muscle mass, and body mass index occurred despite the absence of a prescribed exercise program and without a significant change in calorie or protein intake. Weight gain was maintained but a mild decrease in muscle mass occurred over 3 months after oxandrolone cessation.
In a pilot study, the effects of oxandrolone 0.1 mg/kg/day PO for 12 weeks on muscle strength were successful in 10 boys aged 6—9 years. A significant improvement in the mean muscle score was achieved with oxandrolone as compared to the expected decline. Significant improvement in muscle strength was also noted 4 weeks into the study.
In a randomized, placebo-controlled trial, oxandrolone 0.1 mg/kg/day PO for 1 year resulted in a significantly greater growth velocity as compared to placebo. Forty boys aged 11 to 14.7 years with delayed pubertal development and short stature were included in the study. Mean predicted adult heights did not differ between groups.
In combination with growth hormone, oxandrolone 0.05 mg/kg/day PO resulted in significant growth acceleration with a final height of at least 150 cm achieved in 75% of the 17 girls who were aged 9 to 16 years at the start of the study. A mean net gain of 8.5 cm over the projected final height was achieved. Concomitant oxandrolone and growth hormone resulted in better final height attainment than either concomitant oxandrolone, growth hormone, and ethinyl estradiol or initial oxandrolone followed by addition of growth hormone with or without ethinyl estradiol. Oxandrolone should only be used as adjunct therapy with growth hormone.
Maximum dosage information is not available.
Specific guidelines for dosage adjustments in hepatic impairment are not available; however, a reduced dose is reasonable for patients with impaired hepatic function.
Specific guidelines for dosage adjustments in renal impairment are not available; however, lower doses may be needed in patients with severe renal impairment.
Oxandrolone is an orally-administered synthetic testosterone derivative; the anabolic effects are greater than its androgenic effects due to the deletion of the methyl group from the C-19 position. The anabolic potency of oxandrolone is approximately 3 to 13 times that of testosterone and methyltestosterone. The drug is approved by the FDA as adjunctive therapy to offset the protein catabolism associated with prolonged administration of corticosteroids, and for the relief of the bone pain frequently accompanying osteoporosis. Anabolic effects require intake of adequate protein and calories. Oxandrolone has been used off-label to promote weight gain after burns or trauma and in certain disease states such as COPD and AIDS, but the beneficial effects on lean body mass are lost with drug discontinuance. Supportive data also exist for the treatment of patients with Duchenne's muscular dystrophy, constitutional delay of growth and puberty, HIV wasting syndrome/muscle weakness, and short stature associated with Turner's syndrome. Anabolic steroids have not been shown to enhance athletic ability and the NCAA and IOC currently prohibit their use by athletes. Oxandrolone is not ergogenic at labeled doses; however, athletes often use higher doses. Athletic use should be discouraged due to the risk for dyslipidemia, potential hepatotoxicity, and other serious side effects.
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Oxandrolone associated hepatotoxicity may be due to the development of peliosis hepatis, hepatoma formation leading to cholestasis and jaundice, or direct hepatic necrosis. The 17a-alkylation appears to be the etiology for hepatic effects with the exception of peliosis hepatis, which has also been seen with testosterone. The mechanism of peliosis hepatis development is unknown and there does not appear to be a dose or duration relationship. Jaundice due to cholestasis is dose and duration related; its development is rare with recommended use. Oxandrolone cessation usually resolves peliosis hepatis as well as jaundice. Hepatoma regression or growth cessation usually occurs with oxandrolone cessation, as the majority of tumors are benign and androgen dependent. However, hepatomas associated with androgens or anabolic steroids are much more vascular than other hepatic tumors and may be undetected until life-threatening intra-abdominal hemorrhage develops. Hepatocellular carcinoma has been associated rarely with long-term, high-dose anabolic steroid therapy and also may regress with drug cessation. Baseline liver function tests and exclusion of preexisting liver disease is recommended prior to therapy initiation. Underlying liver disease and concomitant use of other hepatotoxic drugs may potentiate or increase the severity of liver toxicity. Elderly patients may experience elevated hepatic enzymes more commonly than younger adults; a lower dose is recommended in elderly patients. Periodic assessment of liver function tests in all patients while on oxandrolone with drug discontinuation upon hepatic disease development is recommended. Other manifestations of hepatotoxicity can include elevated hepatic enzymes, hepatitis, or hepatic failure.
The androgenic effects of oxandrolone can affect both males and females. Manifestations include acne vulgaris, clitoromegaly, hirsutism, libido increase, penile enlargement, priapism, CNS depression, habituation, and CNS excitability including insomnia. Excessive sexual stimulation is more likely in geriatric males. Because irreversible virilization of women can occur, oxandrolone should be discontinued with the development of voice deepening or hoarseness, hirsutism, acne, or clitoromegaly. Male pattern baldness in females has been reported. Estrogen supplementation does not prevent oxandrolone induced virilizing changes and some changes may persist despite prompt drug discontinuation. Menstrual irregularity, amenorrhea, or oligomenorrhea can occur due to oxandrolone-induced suppression of gonadotropins.
Peripheral edema can occur with oxandrolone as the result of increased fluid retention (in association with sodium retention/ hypernatremia) and is manifested by weight gain. In the treatment of patients with impaired renal function or congestive heart failure, the fluid retention is of greater clinical significance. Geriatric patients may be more likely to experience fluid retention when compared to younger adult patients; a lower dose is recommended in older adult patients. Patients with moderate to severe COPD or COPD patients who are unresponsive to bronchodilators should be monitored closely for COPD exacerbation and fluid retention with oxandrolone. Other serum electrolytes (i.e., calcium (hypercalcemia), phosphate (hyperphosphatemia), and potassium (hyperkalemia)) are also retained. Hypercalcemia can also be a result of the stimulatory effect of oxandrolone on osteolytic bone resorption. Decreased glucose tolerance (e.g., hyperglycemia), increased creatinine excretion, and increased levels of creatinine phosphokinase (CPK) have been reported.
Prostate cancer as a new primary malignancy or prostatic hypertrophy can develop during prolonged therapy with oxandrolone especially in elderly men. Periodic assessment of prostate specific antigen is recommended especially for geriatric patients. Signs of acute epididymitis (e.g., fever, chills, pain in the inguinal region) or urinary urgency should prompt drug withdrawal and dosage reevaluation.
Male patients receiving oxandrolone may experience feminization due to gonadotrophin suppression. The feminizing effects are generally reversible with drug discontinuation. Impotence (erectile dysfunction), libido decrease, oligospermia, testicular atrophy, bladder irritation (bladder discomfort), gynecomastia, and epididymitis may occur.
Oxandrolone has the potential for teratogenesis (possible masculinization/virilization of the female fetus) and, thus, is contraindicated for use during pregnancy.
Periodic lipoprotein monitoring is recommended due to the possible development of hypercholesterolemia consisting of decreased high-density lipoproteins (HDL) and increased low-density lipoproteins. Alteration in the total cholesterol concentration may be minimal. The percentage decrease in HDL was 44% from one study of patients on 7.5 mg daily. There appears to be minimal to no dose relationship to the degree of HDL lowering. The nadir of HDL appears to occur in about seven days with reversal of these changes within one month of oxandrolone discontinuation. The magnitude of these changes can be significant especially for patients with preexisting cardiac disease. Periodic assessment of serum lipoprotein concentrations is recommended especially for patients with cardiovascular disease.
Anabolic steroids may cause suppression of clotting factors II, V, VII, and X. A clotting factor deficiency or coagulopathy may occur with oxandrolone. Bleeding has been reported in patients taking concomitant anticoagulant therapy.
Periodic measurement of hemoglobin and hematocrit is warranted in patients receiving high doses of oxandrolone due to the potential development of polycythemia.
Premature epiphyseal closure has been reported in pediaric patients receiving oxandrolone.
Oxandrolone is contraindicated for use during pregnancy. Masculinization of the fetus, infertility and teratogenic effects, including embryotoxicity and fetotoxicity, have been reported in female animal offspring when oxandrolone was given in doses 9-times the human dose. These are effects consistent with known effects of other anabolic and androgenic hormones. Oxandrolone should be used cautiously in females of child-bearing potential who may become pregnant. If oxandrolone is used during pregnancy, or if the patient becomes pregnant while taking this drug, the patient should be apprised of the potential hazard to the fetus.
It is unknown if oxandrolone is excreted into breast milk. Nursing discontinuation or oxandrolone cessation is recommended for mothers who are breast-feeding. Oxandrolone is a synthetic testosterone derivative. Significant exposure to this androgen via breast-feeding may have adverse androgenic effects on the infant and the drug may also interfere with proper establishment of lactation in the mother. Historically, testosterone/androgens have been used adjunctively for lactation suppression. Alternative methods to breast-feeding are recommended in lactating women receiving anabolic/androgenic therapy.
Oxandrolone can stimulate the growth of cancerous tissue and is contraindicated in male patients with known prostate cancer or breast cancer. Use is also contraindicated in any patient with hypercalcemia since androgenic anabolic steroids may stimulate osteolytic bone resorption. In female patients with breast cancer, anabolic steroid therapy may cause hypercalcemia by stimulating osteolysis. Women with disseminated breast cancer should have frequent determination of urine and serum calcium levels during the course of therapy. Oxandrolone therapy should be discontinued if hypercalcemia occurs. Males with prostatic hypertrophy should be treated with caution; periodic assessment of prostate specific antigen is recommended for older male patients.
Edema with or without congestive heart failure may be a serious complication in patients with pre-existing cardiac disease or heart failure during oxandrolone therapy. Concomitant administration of adrenal cortical steroid or ACTH may increase the edema. Patients with moderate to severe chronic obstructive pulmonary disease (COPD) or COPD patients who are unresponsive to bronchodilators should be monitored closely for COPD exacerbation and fluid retention. Anabolic steroids have been reported to increase low-density lipoproteins and decrease high-density lipoproteins. These levels revert to normal on discontinuation of treatment. The drug should be used cautiously in patients with hypercholesterolemia or hyperlipidemia; monitor serum lipid levels periodically during oxandrolone therapy and adjust therapy accordingly.
Oxandrolone should be used cautiously, if at all, in patients with pre-existing hepatic disease. Cholestatic hepatitis and jaundice may occur with 17-alpha-alkylated androgens at a relatively low dose. Edema due to androgen therapy may also be a serious complication in patients with pre-existing hepatic disease. Androgenic-anabolic steroids have been associated with the development of certain types of hepatic disease including peliosis hepatis (blood filled cysts in the liver and sometimes splenic tissue), benign and malignant liver tumors (e.g., hepatocellular cancer), cholestasis, cholestatic hepatitis, and jaundice. Rarely, hepatic failure has occurred. Because of the hepatotoxicity associated with the use of 17-alpha-alkylated androgens, liver function tests (LFTs) should be obtained periodically. If cholestatic hepatitis with jaundice appears or if LFTs become abnormal, oxandrolone should be discontinued and the etiology should be determined. Drug-induced jaundice is reversible when the medication is discontinued.
Edema may be a serious complication in patients with pre-existing renal disease during oxandrolone therapy. Concomitant administration of adrenal cortical steroid or ACTH may increase the edema. Due to the possible fluid retention, oxandrolone is contraindicated in patients with nephrosis (nephrotic syndrome), the nephrotic phase of glomerulonephritis.
Oxandrolone can inhibit the metabolism of oral antidiabetic agents and some androgens can lower blood glucose in patients with diabetes, which may cause hypoglycemia. Close monitoring of blood glucose concentrations in patients with diabetes mellitus taking oxandrolone is recommended.
Oxandrolone should generally be avoided in patients with polycythemia, as oxandrolone, especially in high doses, can cause further increases in the red cell mass. Periodic assessment of hemoglobin and hematocrit is recommended.
Oxandrolone at doses of 5 or 10 mg twice daily has been studied in 4 clinical trials that included patients 65 years of age and older. Mean weight gain was similar between geriatric and younger adults, with no differences in efficacy found between the 2 dosages; however, older adult patients (particularly geriatric women), were more likely to experience fluid retention and elevations in liver function tests (LFTs)/transaminases. Based on greater sensitivity to drug-induced fluid retention and transaminase elevations, a lower dose is recommended in the geriatric adult. Geriatric patients treated with androgenic anabolic steroids may be at an increased risk for the development of prostatic hypertrophy and prostatic carcinoma.
Androgenic anabolic steroid therapy should be used very cautiously in pediatric patients and only by specialists who are aware of the effects on bone maturation and the potential for growth inhibition. In children and adolescents, androgen therapy may accelerate bone maturation without producing compensatory gain in linear growth. This adverse effect results in compromised adult height. The younger the child, the greater the risk of compromising final mature height. The effect on bone maturation should be monitored by assessing bone age of the left wrist and hand every 6 months. This is usually accomplished via X-ray examinations to determine the rate of bone maturation and the effects of androgen therapy on the epiphyseal centers.
Laboratory test interference has been reported with the use of anabolic steroids such as oxandrolone. Anabolic steroids may decrease levels of thyroxine-binding globulin, resulting in decreased total T4 serum levels and increased resin uptake of T3 and T4. Free thyroid hormone levels remain unchanged. In addition, a decrease in protein-bound iodine test (PBI) and radioactive iodine uptake may occur.
Oxandrolone offsets the protein catabolism associated with prolonged administration of corticosteroids, and can help with the relief of bone pain frequently accompanying osteoporosis. Anabolic steroids such as oxandrolone are synthetic derivatives of testosterone. Certain clinical effects and adverse reactions demonstrate the androgenic properties of this class of drugs. Complete dissociation of anabolic and androgenic effects has not been achieved. The actions of anabolic steroids are therefore similar to those of male sex hormones with the possibility of causing serious disturbances of growth and sexual development if given to young children. Anabolic steroids suppress the gonadotropic functions of the pituitary and may exert a direct effect upon the testes. During exogenous administration of anabolic androgens, endogenous testosterone release is inhibited through inhibition of pituitary luteinizing hormone (LH). At large doses, spermatogenesis may be suppressed through feedback inhibition of pituitary follicle-stimulating hormone (FSH). Androgenic anabolic steroids stimulate osteolytic bone resorption. Anabolic steroids have been reported to increase low-density lipoproteins and decrease high-density lipoproteins. These levels revert to normal on discontinuation of treatment.
Oxandrolone is only administered orally. Plasma protein binding is 94 to 97%. Due to the 17-alpha-alkylation and absence of a 4-ene function in ring A, hepatic inactivation of oxandrolone is markedly retarded as compared to testosterone and other anabolic-androgenic steroids. Metabolism occurs in the liver by hydroxylation and sulfation, although the extent of hepatic inactivation is less with oxandrolone compared with other anabolic-androgenic steroids. The reduced metabolism results in a longer elimination half-life (10.4 hours in young individuals) and higher peak plasma concentrations than 17-2-methyltestosterone. Approximately 28% of an oral dose is excreted unchanged. Excretion of the parent drug and metabolites occurs primarily in the urine as unconjugated products.
Affected cytochrome P450 isoenzymes and drug transporters: None known
Absorption of oxandrolone is rapid and almost complete with an oral bioavailability of 97%.
Specific data are not available since patients with significant hepatic disease are not normally initiated on oxandrolone treatment; if liver function tests become abnormal during treatment, oxandrolone should be discontinued and the etiology should be determined.
Specific data are not available.
The mean elimination half-life is prolonged to 13.4 hours in geriatric patients; however, time to peak, peak plasma concentration, or AUC does not differ significantly between older adults and younger adult patients.
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