25mg/ tab, 100tabs
Oxymetholone tablet contains 25 mg of Oxymetholone. Practically insoluble in water; freely soluble in chloroform; sparingly soluble in alcohol and in acetone.
Oxymetholone appears to be well-absorbed with oral administration. Oxymetholone has very low affinity for human serum sex hormone-binding globulin (SHBG), less than 5% of that of testosterone and less than 1% of that of DHT. The drug is metabolized in the liver by oxidation at the C2 position, reduction at the C3 position, hydroxylation at the C17 position, and conjugation. The C2 hydroxymethylene group of Oxymetholone can be cleaved to form mestanolone (17 α-methyl-DHT), which may contribute to the effects of Oxymetholone. The elimination half-life of Oxymetholone is unknown. Oxymetholone and its metabolites are eliminated in the urine.
Indications and Usage
Indications of Oxymetholone as adjunctive therapy are to promote weight gain after weight loss following extensive surgery, chronic infections, or severe trauma and in some patients who fail to gain or maintain normal weight without definite pathophysiologic reasons, to offset the protein catabolism associated with prolonged administration of corticosteroids, and to relief osteoporosis bone pain.
Therapy with anabolic steroids is adjunctive to and not a replacement for conventional therapy. The duration of Oxymetholone therapy depends on the response of a patient and appearance of adverse reactions. Therapy should be intermittent. Adults-The response of individuals to anabolic steroids varies.
The daily adult dosage is 50 mg to 100 mg given. A 2-4 weeks therapy course is usually adequate. A course can be repeated if indicated. Geriatric Use-Recommended dose for geriatric patients is 25 mg.
Cholestatic hepatitis and jaundice may occur with 17-alpha-alkylated androgens at a relatively low dose. If cholestatic hepatitis with jaundice appears or liver function tests become abnormal, Oxymetholone 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. Oxymetholone therapy should be discontinued if hypercalcemia occurs. Edema with or without congestive heart failure is a serious complication in patients with pre-existing cardiac, renal, or hepatic disease. Concomitant administration of corticosteroids 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 Geriatric male patients treated with androgenic anabolic steroids
may be at an increased risk for the development of prostate hypertrophy and prostatic carcinoma.
Anabolic steroids may increase sensitivity to oral anticoagulants. Dosage of the anticoagulant may have to be adjusted in order to maintain the prothrombin time at the desired therapeutic level. Patients receiving oral anticoagulant therapy require close monitoring, especially when starting or stopping taking anabolic steroids.
There have been no reports of acute overdosing with this substance. Symptomatic treatment should be provided
– Male patients with carcinoma of the breast or with known or suspected prostate tumor
– Brest carcinoma in females with hypercalcemia: androgenic anabolic steroids may stimulate osteolytic resorption of bones.
– Pregnancy, because of masculinization of the fetus.
– Nephrosis or the nephrotic phase of nephritis
Cholestatic jaundice is associated with therapeutic use of the anabolic and the androgenic steroids. Edema may occur occasionally with or without congestive heart failure. Concomitant administration of corticosteroids, ACTH may add to the edema. In children, anabolic steroid treatment may accelerate bone maturation without producing compensatory gain in linear growth. This adverse effect may result in compromised adult stature. The younger the child is, the greater the risk of compromising final mature height might be. The effect on bone maturation should be monitored by assessing bone age of the wrist and hand every six months.
Hepatic Hepatocellular neoplasms have been reported in association with long-term androgenic anabolic steroid therapy.
Prepubertal: Phallic enlargement and increased frequency of erections.
Postpubertal: Inhibition of testicular function, testicular atrophy and oligospermia, impotence, chronic priapism, epididymitis and bladder irritation.
Clitoral enlargement, menstrual irregularities.
In both genders: Increased or decreased libido.
CNS: Habituation, excitation, insomnia, depression.
Gastrointestinal: Nausea, vomiting, diarrhea.
Hematologic: Bleeding in patients on concomitant anticoagulant therapy
Larynx: Deepening of the voice in women.
Hair: Hirsutism and male pattern of baldness in women.
Skin: Acne (especially in women and prepubertal boys.)
Fluid and Electrolytes: Edema, retention of serum electrolytes (sodium, chloride, potassium, phosphate, calcium). Metabolic/Endocrine: Decreased glucose tolerance, increased serum levels of low-density lipoprotein and decreased levels of high-density lipoprotein, increased creatine and creatinine excretion, increased serum levels of creatinine phosphokinase (CPK).
Some virilizing changes in women are irreversible even after prompt discontinuance of therapy and are not prevented by concomitant use of estrogens.
Store in a dark, dry place. Keep away from children.
Tablet in vial, or pvc-alu blisters