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Anabolic Steroids - Topic Overview

anabolic steroids medscape

Treatment for misuse of anabolic steroids has not been studied much. In most clinical scenarios, the association of protein-calorie malnutrition increases the morbidity and mortality of the primary disease state. The most apparent and common adverse effect is the growth of tender, estrogen-sensitive tissue under the male nipple.

Dosing & Uses

In the suicides, AAS-related impulsive behavior characterized by violent rage, mood swings, and propensity to depression was also noted. Therapy does not increase adult stature. A placebo-controlled randomized trial. After this process is complete, the receptor complex dissociates and is recycled along with the hormone, to repeat this process multiple times prior to metabolism. Relative importance of 5alpha reduction for the androgenic and LH-inhibiting activities of deltaketosteroids.

Pediatrics Premature closure of epiphyses. Unknown if excreted; not recommended Pregnancy Categories A: Pharmacology Mechanism of Action Anabolic steroid; promotes body tissue building, increases production of erythropoietin in patients with anemia resulting from bone marrow failure or from deficient red cell production.

Print without Office Info. Print with Office Info. Formulary Formulary Patient Discounts. Create Your List of Plans. View explanations for tiers and restrictions. Tier Description 1 This drug is available at the lowest co-pay. Most commonly, these are generic drugs. Most commonly, these are "preferred" on formulary brand drugs.

Most commonly, these are "non-preferred" brand drugs. Most commonly, these are "non-preferred" brand drugs or specialty prescription products. This restriction requires that specific clinical criteria be met prior to the approval of the prescription.

QL Quantity Limits Drugs that have quantity limits associated with each prescription. This restriction typically limits the quantity of the drug that will be covered. ST Step Therapy Drugs that have step therapy associated with each prescription.

This restriction typically requires that certain criteria be met prior to approval for the prescription. OR Other Restrictions Drugs that have restrictions other than prior authorization, quantity limits, and step therapy associated with each prescription. Non-Medicare Plans Medicare Plans. Medscape prescription drug monographs are based on FDA-approved labeling information, unless otherwise noted, combined with additional data derived from primary medical literature.

What would you like to print? Print this section Print the entire contents of. This website also contains material copyrighted by 3rd parties. This website uses cookies to deliver its services as described in our Cookie Policy. By using this website, you agree to the use of cookies. Need a Curbside Consult? Share cases and questions with Physicians on Medscape consult. This drug is available at a middle level co-pay. Testosterone is produced under a negative feedback loop between the hypothalamus, the anterior pituitary, and the testes.

Testosterone, dihydrotestosterone, and estrogen all act at the hypothalamus to exert negative feedback inhibition upon gonadotropin-releasing hormone GnRH.

Since GnRH stimulates follicle-stimulating hormone FSH and LH release in the pituitary, this negative feedback can be seen to inhibit subsequent testosterone production and effect spermatogenesis. Testosterone activity is mediated via an androgen receptor that is present in various tissues throughout the human body.

Testosterone binds to an intracellular receptor found in the cytosol of cells, forming a receptor complex that migrates into the nucleus, where it binds to specific deoxyribonucleic acid DNA segments. This, in turn, activates specific messenger ribonucleic acid mRNA to increase transcription, leading to an increased rate of protein synthesis; in the case of muscle cells, this means increased production of the proteins actin and myosin.

After this process is complete, the receptor complex dissociates and is recycled along with the hormone, to repeat this process multiple times prior to metabolism. These anabolic actions of testosterone are thought to be primarily due to testosterone acting upon the androgen receptor in anabolic-responsive tissues.

Androgenic effects are likely mediated via the same androgen receptor in androgen-responsive tissues under the influence of dihydrotestosterone DHT , which is produced by the interaction of 5-alpha reductase 5AR with testosterone and the subsequent reduction of the C double bond. Additionally, DHT cannot undergo further reduction, nor is it a substrate for aromatase; thus, it is not converted to estrogenic metabolites. DHT has been shown to bind avidly to receptors in tissues, such as skin, scalp, and prostate, and to exert times the androgenic effect of testosterone.

Thus, the primary hormone mediating the androgenic effects of testosterone is actually the 5-alpha reduced DHT. At physiologic testosterone levels, nearly all androgen receptors are engaged. Therefore, supraphysiologic doses of testosterone or AASs would have no increased anabolic effect in healthy athletes unless other mechanisms of action existed. Because there are many agents in production and literally hundreds more that have been synthesized, this discussion focuses on the basics involving the steroid ring substitutions and how these substitutions affect the properties of the drug.

Detailed analysis is limited to those agents that are available or have been approved for use in the United States. Anabolic-androgenic steroid AAS development was centered on the need for agents that exhibited different characteristics than did testosterone. In general, the goal was to develop agents that were more anabolic and less androgenic than testosterone, that were capable of being administered orally, and that had less effect upon the hypothalamic-pituitary-gonadal axis.

Most AASs are derived from 3 compounds: The third compound is structurally identical to testosterone except for the deletion of the 19th carbon hence its name. These parent compounds offer different properties with regard to action and metabolism that are generally constant throughout the entire family of compounds. One of the first changes made to the testosterone molecule was the addition of a methyl group or an ethyl group to the carbon position.

This addition was noted to inhibit the hepatic degradation of the molecule, greatly extending the molecule's half-life and making it active when administered orally. Prior to this, testosterone, dihydrotestosterone, and nortestosterone all required parenteral administration due to hepatic metabolism of ketosteroids; this metabolism occurred on the first pass, when the drugs were administered orally.

However, adding a methyl group or an ethyl group did not produce a drug with the exact properties of the parent compound. The alteration of hepatic metabolism was noted to cause strain on the liver, and indeed all oral compounds with this C addition were found to cause dose-related hepatotoxicity.

This small change was also found to lower these agents' interaction with aromatase. Testosterone esters have increasingly been used in replacement therapy, but abuse of these compounds has risen as well.

A feature that all testosterone esters have in common is a testosterone molecule with a carboxylic acid group ester linkage attached to the beta hydroxyl group. These esters differ in structural shape and size; they function only to determine the rate at which the testosterone is released from tissue. Generally, the shorter the ester chain, the shorter the drug's half-life and quicker the drug enters the circulation. Once in the circulation, the ester is cleaved, leaving free testosterone.

Methyltestosterone is a very basic anabolic-androgenic steroid AAS , with the only addition being a methyl group at C This eliminates first-pass degradation in the liver, making oral dosing possible. It also causes dose-related hepatotoxicity. Methyltestosterone is metabolized by aromatase to the potent estrogen alpha methyl estradiol and is also reduced by 5AR to alpha methyl dihydrotestosterone.

This compound exhibits very strong androgenic and estrogenic side effects and is generally a poor choice for most, if not all, uses. Methandrostenolone has an added cis- 1 to cis- 2 double bond that reduces estrogenic and androgenic properties. However, it does undergo aromatization to the rather potent estrogen alpha methyl estradiol, but curiously, it does not show the in-vivo propensity for reduction by 5AR to alpha dihydromethandrostenolone to any large degree.

This steroid was first commercially manufactured in by Ciba under the brand name Dianabol and quickly became the most used and abused steroid worldwide, remaining so to date. It jokingly came to be known as "the breakfast of champions" in sports circles. This agent is very anabolic, with a half-life of approximately 4 hours.

The methyl group at C makes this AAS an oral preparation and potentially hepatotoxic. Ciba, as well as generic firms in the United States, discontinued methandrostenolone in the late s, but over 15 countries worldwide still produce it in generic form. Fluoxymesterone is a potent androgen that is produced under the brand name Halotestin. With the addition of a 9-fluoro group, it is a very potent androgen that has little anabolic activity.

An added beta hydroxyl group inhibits its aromatization. Again, the C methyl group makes oral administration possible, but with hepatic concerns. Nandrolone decanoate is simply a nortestosterone molecule in which a carbon decanoate ester has been added to the beta hydroxyl group. This addition extends the half-life of the drug considerably. Nandrolone is a potent anabolic with a relatively favorable safety profile.

Nandrolone is reduced by 5AR in target tissues to the less potent androgen dihydronandrolone. Its affinity for aromatization to estrogen is low, being perhaps times less than that of testosterone. Nandrolone and its several esters decanoate, phenylpropionate differ only in their half-lives, due to the difference in ester properties.

Nandrolone is a relatively safe drug with minimal androgenic concerns and ample anabolic action at therapeutic doses. Nandrolone decanoate is an intramuscular IM preparation and lacks the hepatotoxic C group; however, this agent is one of the most widely abused AASs, due to its efficacy, safety profile, and worldwide manufacture. Ethylestrenol is an oral nortestosterone derivative and was marketed in the United States under the brand name Maxibolin, but it has since been discontinued.

This agent differs from nandrolone by the addition of a alpha ethyl group to reduce first-pass metabolism, as well as by the deletion of the 3-keto group. This latter omission seems to reduce androgen receptor binding. Ethylestrenol is a mild AAS, having very little anabolic or androgenic effect at therapeutic doses. Trenbolone is a derivative of nandrolone with several additions. The addition of a cis- 9 to cis- 10 double bond inhibits aromatization, while a cis- 11 to cis- 12 double bond greatly enhances androgen receptor binding.

This drug is androgenically and anabolically potent. It is comparably more androgenic than nandrolone due to its lack of conversion to a weaker androgen by 5AR, as is seen with nandrolone.

Trenbolone is a European drug with a very high abuse record. In the United States, it is used in veterinary preparations as trenbolone acetate; as such, it has found its way into the hands of persons who wish to exploit its androgenic and anabolic potential. The second carbon substitution with oxygen is thought to increase the stability of the 3-keto group and greatly increase its anabolic component. This AAS is very anabolic, with little androgenic effect at a therapeutic dose.

First marketed by Searle, DHT was discontinued in the mids. Due to its mild androgenic properties, oxandrolone is one of the few agents to be routinely abused by female athletes. Athletes, from weightlifters to boxers, use oxandrolone, seeking to increase strength without experiencing additional weight gain. Stanozolol is an active AAS, due to the stability afforded by the 3,2 pyrazole group on the A-ring, which greatly enhances androgen receptor binding. The C methyl group enhances oral availability.

Stanozolol is highly active in androgen- and anabolic-sensitive tissue. It is a weaker androgen than DHT and exerts comparatively less androgenic effect. It will not aromatize to estrogenic metabolites. Athletes, many in track and field, have abused it. In , Canadian sprinter Ben Johnson was stripped of his Olympic gold medal after testing positive for stanozolol.

This quite potent AAS is a unique agent. Oxymetholone is C methylated and, thus, is an oral agent. The 3-keto stability added by the 2-hydroxymethylene group greatly enhances the drug's anabolic properties. The action of this agent in androgen-sensitive tissues is much like that of DHT and is quite androgenic.

Oxymetholone is the only AAS to date to be considered a carcinogen. Like this entire class, oxymetholone does not aromatize. It is thought to activate estrogen receptors via the 2-hydroxymethylene group, and it can exert many estrogenic side effects.

Oxymetholone is marketed in the United States as Anadrol and has been abused the world over by weight lifters and strength athletes for its strong anabolic and pronounced androgenic effects. The use of anabolic-androgenic steroids AASs to improve performance and acquire more muscular bodies is on the rise worldwide.

In the US, it is estimated that between 2. Men use AASs significantly more than women, although use among females is increasing. The global lifetime prevalence for males is 6. The chronic use of AASs can cause various pathologic alterations, which are related to dose, frequency, and patterns of use.

Adverse effects include the hepatic, cardiovascular, reproductive, musculoskeletal, endocrine, renal, immunologic, and hematologic systems, as well as psychological and psychiatric effects. An increase in suicide and violent death has been demonstrated in individuals with a history of long-term AAS use. In the suicides, AAS-related impulsive behavior characterized by violent rage, mood swings, and propensity to depression was also noted.

Most of the adverse effects of anabolic-androgenic steroid AAS use are dose dependent, and some are reversible with cessation of the offending agent or agents.

Vital signs, including heart rate and blood pressure, and basic chemistries, such as sodium, potassium, hemoglobin, hematocrit, BUN blood urea nitrogen , creatinine, hepatic, and lipid profiles, must be monitored carefully. Monitoring these parameters will help the clinician to determine drug choice, treatment dose, and duration, and will help to alert the prescriber to potentially serious adverse effects that necessitate the discontinuation of therapy. The most common deleterious effects of AAS use on the cardiovascular system include increased heart rate, increased blood pressure, and changes in lipid metabolism, including lowered high-density lipoprotein HDL and increased low-density lipoprotein LDL.

The increase in heart rate is thought to be more profound with the androgens, especially those resistant to aromatase, and is believed to be due to the inhibition of monoamine oxidase MAO. This effect, when combined with the increased renal recovery of ions, such as sodium, causing subsequent fluid retention, can lead to dramatic increases in blood pressure.

Combine this with a tendency to lower HDL and raise LDL, and the stage is set for untoward atherogenic and cardiac effects. Anabolic steroid users can have a lower left ventricle ejection fraction. Anabolic steroid abuse has been associated with ventricular arrhythmias. The changes made to C to inhibit hepatic degradation make nearly all oral preparations hepatotoxic. Levels approaching times baseline are often set as upper limits of reference ranges when administering oral AASs, but the risk-to-benefit ratio must be constantly evaluated.

Another life-threatening, albeit rare, adverse effect that is seen in the liver and sometimes in the spleen is peliosis hepatitis, which is characterized by the appearance of blood-filled, cystic structures. These cysts, which may rupture and bleed profusely, have been found in patients with near-normal liver function test LFT values, as well as in individuals who are in liver failure.

Fortunately, drug cessation usually results in complete recovery. Primary liver tumors have been reported, most of which are benign, androgen-dependent growths that regress with the discontinuation of AAS therapy. Other hepatic adverse effects associated with AAS abuse include subcellular changes of hepatocytes, hepatocellular hyperplasia, and general hepatic damage determined by increased liver enzymes: The endocrine system has a remarkable array of checks and balances that ensure the human body is at or near homeostasis at any point in time.

Interruption of one feedback system has been shown to produce changes in other hormone feedback systems via direct receptor changes, as well as through competition for common enzymes and metabolic pathways. Studies have shown that AASs bind to glucocorticoid, progesterone, and estrogen receptors and exert multiple effects. Discussions exist as to how the endogenous testosterone and spermatogenic functions of the testes are inhibited by the use of testosterone and AASs.

By suppressing FSH, spermatogenic function should be reduced. An up-regulation of sex-hormone binding globulin, with a concomitant decrease in TBG, is thought to cause the changes in total T4 levels. The male prostate is very sensitive to androgens, especially those that are reduced in prostatic tissue to dihydrotestosterone DHT or DHT analogues.

In response to this stimulation, the prostate grows in size, potentially causing or exacerbating benign prostatic hyperplasia BPH. Worsening BPH may indeed cause severe bladder and secondary renal damage. In addition, the use of AASs in patients with underlying carcinoma of the prostate is absolutely contraindicated due to the potential for hormone-sensitive tumor growth.

However, a 3-year study of hypogonadal men on testosterone replacement therapy failed to show significant differences between the group and the controls in urinary symptoms, urine flow rate, or urine postvoid residual. The most apparent and common adverse effect is the growth of tender, estrogen-sensitive tissue under the male nipple. This unsightly growth is termed gynecomastia and can be treated medically or surgically. Other adverse effects include impotence, priapism, and infertility.

Direct clotting factors may be reduced with an increase in prothrombin time. In patients on concomitant anticoagulant therapy, this increase could cause bleeding. AASs cause increases in hemoglobin and hematocrit and are used in many cases of anemia, although the clinician must be aware of the potential for polycythemia.

Skin, especially the face and scalp, has a high degree of androgen receptors and 5AR. DHT is known to cause increases in sebum production, leading to clinical acne. Also, male pattern baldness is related to scalp DHT production and binding, along with genetic factors influencing hair growth. Male pattern baldness is greatly exacerbated by most AASs in susceptible individuals. There is preliminary evidence that long-term AAS abuse may cause neurotoxicity, particularly in brain regions associated with visuospatial memory.

These preliminary findings raise the ominous possibility that long-term, high-dose AAS exposure may cause cognitive deficits, notably in visuospatial memory. These investigators also speculated that AAS abuse might facilitate the onset or progression of neurodegenerative diseases. The impact of AAS abuse on affective behaviors is the constellation of symptoms called 'roid rage,' including poor impulse control, extreme mood swings, and abnormal levels of aggression.

Additionally, it was found that AAS users were more likely to have abused other illicit drugs. However, the study was not able to determine the cause and effect relationship between the mental health problems and steroid use.

Clearly, hormone replacement therapy is the most common use of testosterone. Anabolic-androgenic steroids AASs have many other potential clinical uses. In most clinical scenarios, the association of protein-calorie malnutrition increases the morbidity and mortality of the primary disease state. By preventing this loss of lean body mass, the clinician can hope to prevent many of the adverse effects caused by the disease and, perhaps, by other treatments that have been enacted.

In all clinical cases, with the exception of cancer, AASs have shown efficacy in weight gain. Commonly used AASs include oxandrolone , nandrolone, and oxymetholone. All 3 agents have been studied for increased LBM and weight gain.

Iamges: anabolic steroids medscape

anabolic steroids medscape

The alterations to the female reproductive system are caused by the artificial increase in testosterone levels, which are normally present in females in small amounts. Distinguishing constitutional delay of growth and puberty from isolated hypogonadotropic hypogonadism:

anabolic steroids medscape

Many forms of anemia. Because of the way these medications are metabolized, the need to have recovery time, and to prevent detection, steroids are often taken in cycles in which they are used for a few days at a time, then stopped and the cycle repeated again days or weeks later. Your list will be saved and can be edited at any time.

anabolic steroids medscape

Effect of growth hormone treatment on adult height in peripubertal children with idiopathic short stature: Men use AASs significantly more than anabolic steroids medscape, sterooids use among females is increasing. What Are the Common Street Names? Medscape App Get fast, accurate answers for point-of-care decision making. Effect of testosterone treatment on bone mineral density in men over 65 years of age. Business of Medicine Anabolic steroids medscape the anadrol empty stomach business, legal, and ethical arenas towards building and maintaining a successful medical practice.