Oxandrolone is 17β-hydroxy-17α-methyl-2-oxa-5α-androstan-3-one. Inactive ingredients include cornstarch, lactose, magnesium stearate, and hydroxypropyl methylcellulose.
Anabolic steroids 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).
Anabolic steroids have been reported to increase low-density lipoproteins and decrease high-density lipoproteins. These levels revert to normal on discontinuation of treatment.
In a single dose pharmacokinetic study of Oxandrin in elderly subjects, the mean elimination half-life was 13.3 hours. In a previous single dose pharmacokinetic study in younger volunteers, the mean elimination half-life was 10.4 hours. No significant differences between younger and elderly volunteers were found for time to peak, peak plasma concentration or AUC after a single dose of Oxandrin. The correlation between plasma level and therapeutic effect has not been defined.
Indications and usage:
Oxandrin is indicated as adjunctive therapy to promote weight gain after weight loss following extensive surgery, chronic infections, or severe trauma, and in some patients who without definite pathophysiologic reasons fail to gain or to maintain normal weight, to offset the protein catabolism associated with prolonged administration of corticosteroids, and for the relief of the bone pain frequently accompanying osteoporosis.
Dosage and administration:
Therapy with anabolic steroids is adjunctive to and not a replacement for conventional therapy. The duration of therapy with Oxandrin (oxandrolone) will depend on the response of the patient and the possible appearance of adverse reactions. Therapy should be intermittent.
Adults: The response of individuals to anabolic steroids varies. The daily adult dosage is 2.5 mg to 20 mg given in 2 to 4 divided doses. The desired response may be achieved with as little as 2.5 mg or as much as 20 mg daily. A course of therapy of 2 to 4 weeks is usually adequate. This may be repeated intermittently as indicated.
Children: For children the total daily dosage of Oxandrin is ≤0.1 mg per kilogram body weight or ≤0.045 mg per pound of body weight. This may be repeated intermittently as indicated.
Geriatric Use: Recommended dose for geriatric patients is 5 mg bid.
1. Known or suspected carcinoma of the prostate or the male breast.
2. Carcinoma of the breast in females with hypercalcemia (androgenic anabolic steroids may stimulate osteolytic bone resorption).
3. Pregnancy, because of possible masculinization of the fetus. Oxandrin has been shown to cause embryotoxicity, fetotoxicity, infertility, and masculinization of female animal offspring when given in doses 9 times the human dose.
4. Nephrosis, the nephrotic phase of nephritis.
Warnings and precautions:
Cholestatic hepatitis and jaundice may occur with 17-alpha-alkylated androgens at a relatively low dose. If cholestatic hepatitis with jaundice appears or if liver function tests become abnormal, oxandrolone should be discontinued and the etiology should be determined. Drug-induced jaundice is reversible when the medication is discontinued.
In patients with breast cancer, anabolic steroid therapy may cause hypercalcemia by stimulating osteolysis. Oxandrolone therapy should be discontinued if hypercalcemia occurs.
Edema with or without congestive heart failure may be a serious complication in patients with pre-existing cardiac, renal, or hepatic disease. Concomitant administration of adrenal cortical steroid or ACTH may increase the edema.
In children, 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.
Anabolic steroids may decrease levels of thyroxine-binding globulin, resulting in decreased total T4serum levels and increased resin uptake of T3 and T4. Free thyroid hormone levels remain unchanged. In addition, a decrease in PBI and radioactive iodine uptake may occur.
Pregnancy and lactation:
Teratogenic effects-Pregnancy Category X Nursing mothers
It is not known whether anabolic steroids are excreted in human milk. Because of the potential of serious adverse reactions in nursing infants from oxandrolone, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother.
Anabolic agents may accelerate epiphyseal maturation more rapidly than linear growth in children and the effect may continue for 6 months after the drug has been stopped. Therefore, therapy should be monitored by x-ray studies at 6-month intervals in order to avoid the risk of compromising adult height. Androgenic anabolic steroid therapy should be used very cautiously in children and only by specialists who are aware of the effects on bone maturation.
Patients with moderate to severe COPD or COPD patients who are unresponsive to bronchodilators should be monitored closely for COPD exacerbation and fluid retention.
The following adverse reactions have been associated with use of anabolic steroids: Hepatic: Cholestatic jaundice with, rarely, hepatic necrosis and death. Hepatocellular neoplasms and peliosis hepatis with long-term therapy. Reversible changes in liver function tests also occur including increased bromsulfophthalein (BSP) retention, changes in alkaline phosphatase and increases in serum bilirubin, aspartate aminotransferase (AST, SGOT) and alanine aminotransferase (ALT, SGPT)
Prepubertal: Phallic enlargement and increased frequency or persistence of erections.
Postpubertal: Inhibition of testicular function, testicular atrophy and oligospermia, impotence, chronic priapism, epididymitis, and bladder irritability.
Clitoral enlargement, menstrual irregularities.
CNS: Habituation, excitation, insomnia, depression, and changes in libido.
Hematologic: Bleeding in patients on concomitant oral anticoagulant therapy.
Larynx: Deepening of the voice in females.
Hair: Hirsutism and male pattern baldness in females.
Skin: Acne (especially in females and prepubertal males).
Skeletal: Premature closure of epiphyses in children.
Fluid and electrolytes: Edema, retention of serum electrolytes (sodium chloride, potassium, phosphate, calcium).
Metabolic/Endocrine: Decreased glucose tolerance, increased creatinine excretion, increased serum levels of creatinine phosphokinase (CPK). Masculinization of the fetus. Inhibition of gonadotropin secretion.
There have been no reports of acute overdosage with anabolics.
Store in cool dry place below 30℃. Protect from light.