PDR SearchThe information at Drugs. Always consult your doctor or pharmacist. In general, total doses above mg per month are not required because of the prolonged action of the preparation. Injections more frequently than every two weeks are delatestryl injection dosage celatestryl. Use of a wet needle or delatestryl injection dosage syringe may cause the solution to become cloudy; however this does not affect the potency of the material. Parenteral drug products should be inspected visually for dianabol tablets suppliers matter and discoloration prior to administration, whenever solution and container permit. As replacement therapy, i.
DELATESTRYL (Testosterone enanthate) dosage, indication, interactions, side effects | EMPR
In their active form, androgens have a beta-hydroxy group. Esterification of the beta-hydroxy group increases the duration of action of testosterone; hydrolysis to free testosterone occurs in vivo. Each mL of sterile, colorless to pale yellow solution provides mg testosterone enanthate in sesame oil with 5 mg chlorobutanol chloral derivative as a preservative. Endogenous androgens are responsible for the normal growth and development of the male sex organs and for maintenance of secondary sex characteristics.
These effects include growth and maturation of prostate, seminal vesicles, penis, and scrotum; development of male hair distribution, such as beard, pubic, chest, and axillary hair; laryngeal enlargement; vocal chord thickening; alterations in body musculature; and fat distribution.
Androgens also cause retention of nitrogen, sodium, potassium, and phosphorus, and decreased urinary excretion of calcium. Androgens have been reported to increase protein anabolism and decrease protein catabolism. Nitrogen balance is improved only when there is sufficient intake of calories and protein. Androgens are responsible for the growth spurt of adolescence and for the eventual termination of linear growth which is brought about by fusion of the epiphyseal growth centers.
In children, exogenous androgens accelerate linear growth rates but may cause a disproportionate advancement in bone maturation.
Use over long periods may result in fusion of the epiphyseal growth centers and termination of the growth process. Androgens have been reported to stimulate the production of red blood cells by enhancing the production of erythropoietic stimulating factor.
During exogenous administration of androgens, endogenous testosterone release is inhibited through feedback inhibition of pituitary luteinizing hormone LH. At large doses of exogenous androgens, spermatogenesis may also be suppressed through feedback inhibition of pituitary follicle stimulating hormone FSH.
There is a lack of substantial evidence that androgens are effective in fractures, surgery, convalescence, and functional uterine bleeding. Testosterone esters are less polar than free testosterone. Testosterone esters in oil injected intramuscularly are absorbed slowly from the lipid phase; thus testosterone enanthate can be given at intervals of two to four weeks.
Testosterone in plasma is 98 percent bound to a specific testosterone-estradiol binding globulin, and about two percent is free.
Generally, the amount of this sex-hormone binding globulin SHBG in the plasma will determine the distribution of testosterone between free and bound forms, and the free testosterone concentration will determine its half-life. About 90 percent of a dose of testosterone is excreted in the urine as glucuronic and sulfuric acid conjugates of testosterone and its metabolites; about six percent of a dose is excreted in the feces, mostly in the unconjugated form.
Inactivation of testosterone occurs primarily in the liver. Testosterone is metabolized to various keto steroids through two different pathways. There are considerable variations of the half-life of testosterone as reported in the literature, ranging from 10 to minutes. In responsive tissues, the activity of testosterone appears to depend on reduction to dihydrotestosterone DHT , which binds to cytosol receptor proteins.
The steroid-receptor complex is transported to the nucleus where it initiates transcription events and cellular changes related to androgen action. Primary hypogonadism congenital or acquired — Testicular failure due to cryptorchidism, bilateral torsion, orchitis, vanishing testis syndrome, or orchidectomy. Hypogonadotropic hypogonadism congenital or acquired — Gonadotropin or luteinizing hormone-releasing hormone LHRH deficiency, or pituitary-hypothalamic injury from tumors, trauma, or radiation.
Appropriate adrenal cortical and thyroid hormone replacement therapy are still necessary, however, and are actually of primary importance. If the above conditions occur prior to puberty, androgen replacement therapy will be needed during the adolescent years for development of secondary sexual characteristics. Prolonged androgen treatment will be required to maintain sexual characteristics in these and other males who develop testosterone deficiency after puberty.
These patients usually have a familial pattern of delayed puberty that is not secondary to a pathological disorder; puberty is expected to occur spontaneously at a relatively late date. Brief treatment with conservative doses may occasionally be justified in these patients if they do not respond to psychological support. The potential adverse effect on bone maturation should be discussed with the patient and parents prior to androgen administration.
Primary goals of therapy in these women include ablation of the ovaries. This treatment has also been used in premenopausal women with breast cancer who have benefited from oophorectomy and are considered to have a hormone-responsive tumor. Judgment concerning androgen therapy should be made by an oncologist with expertise in this field.
Androgens are contraindicated in men with carcinomas of the breast or with known or suspected carcinomas of the prostate and in women who are or may become pregnant. When administered to pregnant women, androgens cause virilization of the external genitalia of the female fetus. This virilization includes clitoromegaly, abnormal vaginal development, and fusion of genital folds to form a scrotal-like structure. The degree of masculinization is related to the amount of drug given and the age of the fetus and is most likely to occur in the female fetus when the drugs are given in the first trimester.
If the patient becomes pregnant while taking androgens, she should be apprised of the potential hazard to the fetus. This preparation is also contraindicated in patients with a history of hypersensitivity to any of its components. In patients with breast cancer and in immobilized patients, androgen therapy may cause hypercalcemia by stimulating osteolysis.
In patients with cancer, hypercalcemia may indicate progression of bony metastasis. If hypercalcemia occurs, the drug should be discontinued and appropriate measures instituted. Peliosis hepatis can be a life-threatening or fatal complication. If cholestatic hepatitis with jaundice appears or if liver function tests become abnormal, the androgen should be discontinued and the etiology should be determined. Drug-induced jaundice is reversible when the medication is discontinued.
Geriatric patients treated with androgens may be at an increased risk for the development of prostatic hypertrophy and prostatic carcinoma. Evaluate patients who report symptoms of pain, edema, warmth and erythema in the lower extremity for DVT and those who present with acute shortness of breath for PE. Long term clinical safety trials have not been conducted to assess the cardiovascular outcomes of testosterone replacement therapy in men.
To date, epidemiologic studies and randomized controlled trials have been inconclusive for determining the risk of major adverse cardiovascular events MACE , such as non-fatal myocardial infarction, non-fatal stroke, and cardiovascular death, with the use of testosterone compared to non-use.
Some studies, but not all, have reported an increased risk of MACE in association with use of testosterone replacement therapy in men. Testosterone has been subject to abuse, typically at doses higher than recommended for the approved indication and in combination with other anabolic steroids.
If testosterone abuse is suspected, check serum testosterone concentrations to ensure they are within therapeutic range. However, testosterone levels may be in the normal or subnormal range in men abusing synthetic testosterone derivatives.
Counsel patients concerning the serious adverse reactions associated with abuse of testosterone and anabolic steroids. Conversely, consider the possibility of testosterone and anabolic steroid abuse in suspected patients who present with serious cardiovascular or psychiatric adverse events. Due to sodium and water retention, edema with or without congestive heart failure may be a serious complication in patients with preexisting cardiac, renal, or hepatic disease.
In addition to discontinuation of the drug, diuretic therapy may be required. If the administration of testosterone enanthate is restarted, a lower dose should be used. Gynecomastia frequently develops and occasionally persists in patients being treated for hypogonadism. Androgen therapy should be used cautiously in healthy males with delayed puberty.
The effect on bone maturation should be monitored by assessing bone age of the wrist and hand every six months. In children, androgen 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 the greater the risk of compromising final mature height. Women should be observed for signs of virilization deepening of the voice, hirsutism, acne, clitoromegaly, and menstrual irregularities. Discontinuation of drug therapy at the time of evidence of mild virilism is necessary to prevent irreversible virilization.
Such virilization is usual following androgen use at high doses and is not prevented by concomitant use of estrogens. A decision may be made by the patient and the physician that some virilization will be tolerated during treatment for breast carcinoma.
Because androgens may alter serum cholesterol concentration, caution should be used when administering these drugs to patients with a history of myocardial infarction or coronary artery disease. Serial determinations of serum cholesterol should be made and therapy adjusted accordingly.
A causal relationship between myocardial infarction and hypercholesterolemia has not been established. Male adolescent patients receiving androgens for delayed puberty should have bone development checked every six months. Adult or adolescent males — too frequent or persistent erections of the penis.
Women — hoarseness, acne, changes in menstrual periods, or more facial hair. All patients — any nausea, vomiting, changes in skin color, or ankle swelling. Current studies do not assess whether testosterone use increases risks of prostate cancer, prostate hyperplasia, and cardiovascular disease in the geriatric population.
Care should be taken to slowly inject the preparation deeply into the gluteal muscle, being sure to follow the usual precautions for intramuscular administration, such as the avoidance of intravascular injection.
Women with disseminated breast carcinoma should have frequent determination of urine and serum calcium levels during the course of androgen therapy see WARNINGS. Periodic every six months X-ray examinations of bone age should be made during treatment of pre-pubertal males to determine the rate of bone maturation and the effects of androgen therapy on the epiphyseal centers.
Hemoglobin and hematocrit should be checked periodically for polycythemia in patients who are receiving high doses of androgens. Anticoagulants, oral — C substituted derivatives of testosterone, such as methandrostenolone, have been reported to decrease the anticoagulant requirement.
Patients receiving oral anticoagulant therapy require close monitoring especially when androgens are started or stopped. Antidiabetic drugs and insulin — In diabetic patients, the metabolic effects of androgens may decrease blood glucose and insulin requirements. ACTH and corticosteroids — Enhanced tendency toward edema. Use caution when giving these drugs together, especially in patients with hepatic or cardiac disease. Oxyphenbutazone — Elevated serum levels of oxyphenbutazone may result.
Androgens may decrease levels of thyroxine-binding globulin, resulting in decreased total T 4 serum levels and increased resin uptake of T 3 and T 4. Free thyroid hormone levels remain unchanged, however, and there is no clinical evidence of thyroid dysfunction. Testosterone has been tested by subcutaneous injection and implantation in mice and rats. The implant induced cervical-uterine tumors in mice, which metastasized in some cases. There is suggestive evidence that injection of testosterone into some strains of female mice increases their susceptibility to hepatoma.
Testosterone is also known to increase the number of tumors and decrease the degree of differentiation of chemically induced carcinomas of the liver in rats. There are rare reports of hepatocellular carcinoma in patients receiving long-term therapy with androgens in high doses.
Withdrawal of the drugs did not lead to regression of the tumors in all cases. It is not known whether androgens are excreted in human milk. Because many drugs are excreted in human milk and because of the potential for serious adverse reactions in nursing infants from androgens, 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.