Oxandrolone-LA® 10mg (30 tabs)

Description : Oxandrolone® oral tablets contain 5 mg and 10 mg of the anabolic steroid oxandrolone. Oxandrolone is 17β-hydroxy-17α-methyl-2-oxa-5α-androstan-3-one. Inactive ingredients include cornstarch, lactose, magnesium stearate, and hydroxypropyl methylcellulose.

Comment from Expert

Chemical name “ Oxandrolone” Oxandrolne is a weak steroid with only slight androgenic component : There is any rarely side effect. It developed mostly for women and children, it does not cause an early stunting of growth in children since this “ it does not premature close epiphyseal growth” Oxandrolone – cause a strong strength gain by stimulating the phosphocreatine synthesis in the muscle cell without deposit liquid water in the joint of the muscle It does not aromatize in any dosage (not change to estrogen) Even high dosage this compound does not. Influence the body's own testosterone (not suppress) Dosage daily 10 – 15 mg. Can using with any of the following : - Halotestin 20–30 mg daily very effective muscle look harder. - Clenbuterol 120 – 140 mcg. /day - Deca – Nan 200 mg 2 time/ week. - Propionate 200 mg/ week - Andriol 280 mg

CLINICAL PHARMACOLOGY Anabolic steroids are synthetic derivatives of testosterone.Certain clinical effects and adverse reactions demonstratethe 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.

INDICATIONS AND USAGE Oxandrolone® 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 (See DOSAGE AND ADMINISTRATION).

DRUG ABUSE AND DEPENDENCE Oxandrolone® is classified as a controlled substance under the Anabolic Steroids Control Act of 1990 and has been as signed to Schedule III (non-narcotic).

CONTRAINDICATIONS 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. Oxandrolone® 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. 5. Hypercalcemia.

WARNINGS PELIOSIS HEPATIS, A CONDITION IN WHICH LIVER AND SOMETIMES SPLENIC TISSUE IS REPLACED WITH BLOOD-FILLED CYSTS, HAS BEEN REPORTED IN PATIENTS RECEIVING ANDROGENIC ANABOLIC STEROID THERAPY. THESE CYSTS ARE SOMETIMES PRESENT WITH MINIMAL HEPATIC DYSFUNCTION, BUT AT OTHER TIMES THEY HAVE BEEN ASSOCIATED WITH LIVER FAILURE. THEY ARE OFTEN NOT RECOGNIZED UNTIL LIFE-THREATENING LIVER FAILURE OR INTRA-ABDOMINAL HEMORRHAGE DEVELOPS. WITHDRAWAL OF DRUG USUALLY RESULTS IN COMPLETE DISAPPERANCE OF LESIONS.

LIVER CELL TUMORS ARE ALSO REPORTED. MOST OFTEN THESE TUMORS ARE BENIGN AND ANDROGEN DEPENDENT, BUT FATAL MALIGNANT TUMORS HAVE BEEN REPORTED. WITHDRAWAL OF DRUG OFTEN RESULTS IN REGRESSION OR CESSATION OF PROGRESSION OF THE TUMOR. HOWEVER, HEPATIC TUMORS ASSOCIATED WITH ANDROGENS OR ANABOLIC STEROIDS ARE MUCH MORE VASCULAR THAN OTHER HEPATIC TUMORS AND MAY BE SILENT UNTIL LIFE-THREATENING INTRA-ABDOMINAL HEMORRHAGE DEVELOPS. BLOOD LIPID CHANGES THAT ARE KNOWN TO BE ASSOCIATED WITH INCREASED RISK OF ATHEROSCLEROSIS ARE SEEN IN PATIENTS TREATED WITH

ANDROGENS AND ANABOLIC STEROIDS. THESE CHANGES INCLUDE DECREASED HIGH-DENSITY LIPOPROTEIN AND SOMETIMES INCREASED LOW-DENSITY LIPOPROTEIN. THE CHANGES MAY BE VERY MARKED AND COULD HAVE A SERIOUS IMPACT ON THE RISK OF ATHEROSCLEROSIS AND CORONARY ARTERY DISEASE.

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 fuction 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.

PRECAUTIONS: Laboratory tests). Geriatric patients treated with androgenic anabolic steroids may be at an increased risk for the development of prostatic hypertrophy and prostatic carcinoma.

ANABOLIC STEROIDS HAVE NOT BEEN SHOWN TO ENHANCE ATHLETIC ABILITY.

PRECAUTIONS General: Women should be observed for signs of virilization (deepening of the voice, hirsutism, acne, clitoromegaly). Discontinuation of drug therapy at the time of evidence of mild virilism is necessary to prevent irreversible virilization. Some virilizing changes in women are irreversible even after prompt discontinuance of therapy and are not prevented by concomitant use of estrogens. Menstrual irregularities may also occur. Anabolic steroids may cause suppression of clotting factors II, V, VII, and X, and an increase in prothrombin time.

Information for patients: The physician should instruct patients to report any of the following side effects of androgens: Males: Too frequent or persistent erections of the penis, appearance or aggravation of acne. Females: Hoarseness, acne, changes in menstrual periods, or more facial hair. All patients: Nausea, vomiting, changes in skin color, or ankle swelling.

Laboratory tests: Women with disseminated breast carcinoma should have frequent determination of urine and serum calcium levels during the course of therapy (See WARNINGS). Because of the hepatotoxicity associated with the use of 17-alpha-alkylated androgens, liver function tests should be obtained periodically.

Periodic (every 6 months) x-ray examinations of bone age should be made during treatment of children to determine the rate of bone maturation and the effects of androgen therapy on the epiphyseal centers.

Serum lipids and high-density lipoprotein cholesterol determinations should be done periodically as androgenic anabolic steroids have been reported to increase low-density lipoproteins. Serum cholesterol levels may increase during therapy. Therefore, caution is required when administering these agents to patients with a history of myocardial infarction or coronary artery disease. Serial determination serum cholesterol should be made and therapy adjusted accordingly.

Hemoglobin and hematocrit should be checked periodic for polycythemia in patients who are receiving high dose anabolic steroids.

Drug interactions Anticoagulants: Anabolic steroids may increase sensitivity to oral anticoagu-lants. Dosage of the anticoagulant may have to be decreased in order to maintain desired prothrombin time. Patients re-ceiving oral anticoagulant therapy require close monitoring especially when anabolic steroids are started or stopped.

Oral hypoglycemic agents: Oxandrolone® may inhibit the metabolism of oral hypoglyce-mic agents.

Adrenal steroids or ACTH: In patients with edema, concomitant administration with adrenal cortical steroids or ACTH may increase the edema

Drug/Laboratory test interactions: 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 PBI and radioactive iodine uptake may occur.

Carcinogenesis, mutagenesis, impairments of fertility Animal data: Oxandrolone® has not been tested in laboratory animals for carcinogenic or mutagenic effects. In 2-year chronic orally to studies, a dose-related reduction of spermatogenesis and de-creased organ weights (testes, prostate, seminal vesicle, ovaries, uterus, adrenals, and pituitary) were shown.

Human data: Liver cell tumors have been reported in patients receiving long-term therapy with androgenic anabolic steroids in high doses (See WARNINGS). Withdrawal of the drugs did not lead to regression of the tumors in all cases.Geriatric patients treated with androgenic anabolic steroids may be at an increased risk for the development of prostatic hypertrophy and prostatic carcinomal.

Pregnancy: Teratogenic effects-Pregnancy Category X (See CONTRA-

INDICATIONS). Nursing mother: It is not known whether anabolic steroids are excreted in human milk. Because of the potential of serious adverse re-actions 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.

Pediatric use: Anabolic agents may accelerate epiphyseal maturation more rapidly than linear growth in children and the effects may continue for 6 months after the drug has been stopped.Therefore, therapy should be monitored by x-ray studies 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

(See WARNINGS). ADVERSE REACTIONS 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 hepatic with long-term therapy

(See WARNINGS). Reversible changes in liver function tests also occur including increased bromsulfophthalein (BSP) retention, and increase in serum bilirubin, aspartate aminotransferase (AST SGOT) and alkaline phosphatase. In males: 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. In females:

Clitoral enlargement, menstrual irregularities. CNS: Habituation, excitation, insomnia, depression, and changes in libido. Hematologic: Bleeding in patients on concomitant anticoag- ulant therapy. Breast: Gynecomastia. 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

(See PRECAUTIONS: Pediatric use). Fluid and electrolytes:Edema, retention of serum electro-lytes (sodium chloride, potassium, phosphate, calcium) Metabolic/Endocrine: Decreased glucose tolerance

(See PRECAUTIONS: Laboratory tests), increased creatinine excretion, increased serum levels of creatiinine phosphoki-nase (CPK). Masculinization of the fetus. Inhibition of go-nadotropin secretion.

OVERDOSAGE No symptoms or signs associated with overdosage have been reported. It is possible that sodium and water reten-tion may occur. The oral LD50 of oxandrolone in mice and dogs is greater than 5,000 mg/kg. No specific antidote is known, but gastric lavage may be used.

DOSAGE AND ADMINISTRATION Therapy with anabolic steroids is adjunctive to and not a replacement for conventional therapy. The duration of therapy with Oxandrolone® will depend on the response of the patient and the possible appearance of adverse reaction. Therapy should be intermittent.

Adults: The usual adult dosage of Oxandrolone® is one 2.5mg 2 to 4 times daily. However, the response of individual to anabolic steroids varies, and a daily dosage of as little as 2.5 mg or as much as 20 mg may be required to achieve the desired response. 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 Oxandrolone® is 0.1 mg per kilogram body weight or 0.045 mg per pound of body weight. This may be repeated intermittently as indicated.

HOW SUPPLIED Oxandrolone® 5 mg is supplied in bottle of 50 white tablets Oxandrolone® 10 mg is supplied in bottle of 30 green tablets

Do not store above 30°C or 86°F

Manufactured by LA pharma S.r.l.

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