Metandienone
Metandienone, also known as methandienone or methandrostenolone and sold under the brand name Dianabol among others, is an androgen and anabolic steroid (AAS) medication which is mostly no longer used.[3][4][1][5] It is also used non-medically for physique- and performance-enhancing purposes.[1] It is often taken by mouth.[1]
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Side effects of metandienone include symptoms of masculinization like acne, increased hair growth, voice changes, and increased sexual desire, estrogenic effects like fluid retention and breast enlargement, and liver damage.[1] The drug is an agonist of the androgen receptor (AR), the biological target of androgens like testosterone and dihydrotestosterone (DHT), and has strong anabolic effects and moderate androgenic effects.[1] It also has moderate estrogenic effects.[1]
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Metandienone was originally developed in 1955 by CIBA and marketed in Germany and the United States.[1][6][3][7][8] As the CIBA product Dianabol, metandienone quickly became the first widely used AAS among professional and amateur athletes, and remains the most common orally active AAS for non-medical use.[9][7][10][11] It is currently a controlled substance in the United States[12] and United Kingdom[13] and remains popular among bodybuilders. Metandienone is readily available without a prescription in certain countries such as Mexico, and is also manufactured in some Asian countries.[5]
Methandienone Medical uses[edit]
Metandienone was formerly approved and marketed as a form of androgen replacement therapy for the treatment of hypogonadism in men, but has since been discontinued and withdrawn in most countries, including in the United States.[14][3][5]
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It was given at a dosage of 5 to 10 mg/day in men and 2.5 mg/day in women.[15][16][1]
Available forms[edit]
Metandienone was provided in the form of 2.5 and 5 mg oral tablets.[17][18][19][1]
Non-medical uses[edit]
Metandienone is used for physique- and performance-enhancing purposes by competitive athletes, bodybuilders, and powerlifters.[1] It is said to be the most widely used AAS for such purposes both today and historically.[1]
Side effects[edit]
Androgenic side effects such as oily skin, acne, seborrhea, increased facial/body hair growth, scalp hair loss, and virilization may occur.[1] Estrogenic side effects such as gynecomastia and fluid retention can also occur.[1] Case reports of gynecomastia exist.[20][21] As with other 17α-alkylated steroids, metandienone poses a risk of hepatotoxicity and use over extended periods of time can result in liver damage without appropriate precautions.[1]
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Pharmacology[edit]
Pharmacodynamics[edit]
Medication | Ratioa |
---|---|
Testosterone | ~1:1 |
Androstanolone (DHT) | ~1:1 |
Methyltestosterone | ~1:1 |
Methandriol | ~1:1 |
Fluoxymesterone | 1:1–1:15 |
Metandienone | 1:1–1:8 |
Drostanolone | 1:3–1:4 |
Metenolone | 1:2–1:30 |
Oxymetholone | 1:2–1:9 |
Oxandrolone | 1:3–1:13 |
Stanozolol | 1:1–1:30 |
Nandrolone | 1:3–1:16 |
Ethylestrenol | 1:2–1:19 |
Norethandrolone | 1:1–1:20 |
Notes: In rodents. Footnotes: a = Ratio of androgenic to anabolic activity. Sources: See template. |
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Metandienone binds to and activates the androgen receptor (AR) in order to exert its effects.[22] These include dramatic increases in protein synthesis, glycogenolysis, and muscle strength over a short space of time.[medical citation needed] While it can be metabolized by 5α-reductase into methyl-1-testosterone (17α-methyl-δ1-DHT), a more potent AAS, the drug has extremely low affinity for this enzyme and methyl-1-testosterone is thus produced in only trace amounts.[1][23] As such, 5α-reductase inhibitors like finasteride and dutasteride do not reduce the androgenic effects of metandienone.[1] Nonetheless, while the ratio of anabolic to androgenic activity of metandienone is improved relative to that of testosterone, the drug does still possess moderate androgenic activity and is capable of producing severe virilization in women and children.[1] As such, it is only really commonly used in men.[1]
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Metandienone is a substrate for aromatase and can be metabolized into the estrogen methylestradiol (17α-methylestradiol).[1] While the rate of aromatization is reduced relative to that for testosterone or methyltestosterone, the estrogen produced is metabolism-resistant and hence metandienone retains moderate estrogenic activity.[1] As such, it can cause side effects such as gynecomastia and fluid retention.[1] The co-administration of an antiestrogen such as an aromatase inhibitor like anastrozole or a selective estrogen receptor modulator like tamoxifen can reduce or prevent such estrogenic side effects.[1] Metandienone has no progestogenic activity.[1]
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As with other 17α-alkylated AAS, metandienone is hepatotoxic.[1]
Pharmacokinetics[edit]
Metandienone has high oral bioavailability.[1] It has very low affinity for human serum sex hormone-binding globulin (SHBG), about 10% of that of testosterone and 2% of that of DHT.[24] The drug is metabolized in the liver by 6β-hydroxylation, 3α- and 3β-oxidation, 5β-reduction, 17-epimerization, and conjugation among other reactions.[23] Unlike methyltestosterone, owing to the presence of its C1(2) double bond, metandienone does not produce 5α-reduced metabolites.[23][1][25] The elimination half-life of metandienone is about 3 to 6 hours.[1][2] It is eliminated in the urine.[23]
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Chemistry[edit]
Metandienone, also known as 17α-methyl-δ1-testosterone or as 17α-methylandrost-1,4-dien-17β-ol-3-one, is a synthetic androstane steroid and a 17α-alkylated derivative of testosterone.[6] It is a modification of testosterone with a methyl group at the C17α position and an additional double bond between the C1 and C2 positions.[6] The drug is also the 17α-methylated derivative of boldenone (δ1-testosterone) and the δ1 analogue of methyltestosterone (17α-methyltestosterone).[6]
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Detection in body fluids[edit]
Metandienone is subject to extensive hepatic biotransformation by a variety of enzymatic pathways. The primary urinary metabolites are detectable for up to 3 days, and a recently discovered hydroxymethyl metabolite is found in urine for up to 19 days after a single 5 mg oral dose.[26] Several of the metabolites are unique to metandienone. Methods for detection in urine specimens usually involve gas chromatography-mass spectrometry.[27][28]
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History[edit]
Metandienone was first described in 1955.[1] It was synthesized by researchers at the CIBA laboratories in Basel, Switzerland. CIBA filed for a U.S. patent in 1957,[29] and began marketing the drug as Dianabol in 1958 in the U.S.[1][30] It was initially prescribed to burn victims and the elderly. It was also prescribed off-label as a pharmaceutical performance enhancement to weight lifters and other athletes.[31] Early adopters included players for Oklahoma University and San Diego Chargers head coach Sid Gillman, who administered Dianabol to his team starting in 1963.[32]
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After the Kefauver Harris Amendment was passed in 1962, the U.S. FDA began the DESI review process to ensure the safety and efficacy of drugs approved under the more lenient pre-1962 standards, including Dianabol.[33] In 1965, the FDA pressured CIBA to further document its legitimate medical uses, and re-approved the drug for treating post-menopausal osteoporosis and pituitary-deficient dwarfism.[34] After CIBA’s patent exclusivity period lapsed, other manufacturers began to market generic metandienone in the U.S.
Following further FDA pressure, CIBA withdrew Dianabol from the U.S. market in 1983.[1] Generic production shut down two years later, when the FDA revoked metandienone’s approval entirely in 1985.[1][34][35] Non-medical use was outlawed in the U.S. under the Anabolic Steroids Control Act of 1990.[36] While metandienone is controlled and no longer medically available in the U.S., it continues to be produced and used medically in some other countries.[1]
Society and culture[edit]
Metandienone confiscated by the Drug Enforcement Administration (DEA) in 2008.
Generic names[edit]
Metandienone is the generic name of the drug and its INN, while methandienone is its BAN and métandiénone is its DCF.[6][3][4][5] It is also referred to as methandrostenolone and as dehydromethyltestosterone.[6][3][4][1][5] The former synonym should not be confused with methylandrostenolone, which is another name for a different AAS known as metenolone.[3]
Brand names[edit]
Metandienone was introduced and formerly sold primarily under the brand name Dianabol.[6][3][4][5][1] It has also been marketed under a variety of other brand names including Anabol, Averbol, Chinlipan, Danabol, Dronabol, Metanabol, Methandon, Naposim, Reforvit-B, and Vetanabol among others.[6][3][4][5][1]
Legal status[edit]
Metandienone, along with other AAS, is a schedule III controlled substance in the United States under the Controlled Substances Act.[37]
Doping in sports[edit]
There are many known cases of doping in sports with metandienone by professional athletes.
References[edit]
- ^ Jump up to:a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af agah ai aj ak Llewellyn W (2011). Anabolics. Molecular Nutrition Llc. pp. 444–454, 533. ISBN 978-0-9828280-1-4.
- ^ Jump up to:a b Pedro Ruiz; Eric C. Strain (2011). Lowinson and Ruiz’s Substance Abuse: A Comprehensive Textbook. Lippincott Williams & Wilkins. pp. 358–. ISBN 978-1-60547-277-5.
- ^ Jump up to:a b c d e f g h Swiss Pharmaceutical Society (2000). “Metandienone”. Index Nominum 2000: International Drug Directory. Taylor & Francis. p. 660. ISBN 978-3-88763-075-1.
- ^ Jump up to:a b c d e Morton IK, Hall JM (6 December 2012). Concise Dictionary of Pharmacological Agents: Properties and Synonyms. Springer Science & Business Media. pp. 177–. ISBN 978-94-011-4439-1.
- ^ Jump up to:a b c d e f g “Metandienone”. drugs.com.
- ^ Jump up to:a b c d e f g h Elks J (14 November 2014). The Dictionary of Drugs: Chemical Data: Chemical Data, Structures and Bibliographies. Springer. pp. 781–. ISBN 978-1-4757-2085-3.
- ^ Jump up to:a b Yesalis CE, Anderson WA, Buckley WE, Wright JE (1990). “Incidence of the nonmedical use of anabolic-androgenic steroids” (PDF). NIDA Research Monograph. 102: 97–112. PMID 2079979.
- ^ Fair JD (1993). “Isometrics or Steroids? Exploring New Frontiers Of Strength in the Early 1960s” (PDF). Journal of Sport History. 20 (1): 1–24. Archived from the original (PDF)on 2008-05-28.
- ^ Yesalis C, Bahrke M (2002). “History of Doping in Sport”(PDF). International Sports Studies. 24: 42–76. Archived from the original (PDF) on 2017-11-23. Retrieved 2017-01-14.
- ^ Lin GC, Erinoff L (1996-07-01). Anabolic Steroid Abuse. DIANE Publishing. p. 29. ISBN 978-0-7881-2969-8.
dianabol history.
- ^ Helms E (August 2014). “What can be achieved as a natural bodybuilder?” (PDF). Alan Aragon’s Research Review. Alan Aragon.
- ^ “Controlled Substances, Alphabetical Order” (PDF). United States Drug Enforcement Administration.
- ^ “List of most commonly encountered drugs currently controlled under the misuse of drugs legislation”. www.gov.uk. Retrieved 2017-01-14.
- ^ Barceloux DG (3 February 2012). Medical Toxicology of Drug Abuse: Synthesized Chemicals and Psychoactive Plants. John Wiley & Sons. pp. 275–. ISBN 978-1-118-10605-1.
- ^ Fruehan, Alice E. (1963). “Current Status of Anabolic Steroids”. JAMA: The Journal of the American Medical Association. 184 (7): 527–32. doi:10.1001/jama.1963.03700200049009. ISSN 0098-7484. PMID 13945852.
- ^ ABPI Data Sheet Compendium. Pharmind Pub. 1978.
- ^ National Drug Code Directory. Consumer Protection and Environmental Health Service, Public Health Service, U.S. Department of Health, Education, and Welfare. 1982. pp. 642–.
- ^ Federal Register. Office of the Federal Register, National Archives and Records Service, General Services Administration. 18 January 1983. pp. 2208–2209.
- ^ The National Formulary … American Pharmaceutical Association. 1974.
Tablets available — Methandrostenolone Tablets usually available contain the following amounts of methandrostenolone: 2.5 and 5 mg.
- ^ Ralph I. Dorfman (5 December 2016). Steroidal Activity in Experimental Animals and Man. Elsevier Science. pp. 70–. ISBN 978-1-4832-7300-6.
- ^ Laron, Zvi (1962). “Breast Development Induced by Methandrostenolone (Dianabol)”. The Journal of Clinical Endocrinology & Metabolism. 22 (4): 450–452. doi:10.1210/jcem-22-4-450. ISSN 0021-972X. PMID 14462467.
- ^ Roselli CE (May 1998). “The effect of anabolic-androgenic steroids on aromatase activity and androgen receptor binding in the rat preoptic area”. Brain Research. 792 (2): 271–6. doi:10.1016/S0006-8993(98)00148-6. PMID 9593936. S2CID 29441013.
- ^ Jump up to:a b c d Schänzer W, Geyer H, Donike M (April 1991). “Metabolism of metandienone in man: identification and synthesis of conjugated excreted urinary metabolites, determination of excretion rates and gas chromatographic-mass spectrometric identification of bis-hydroxylated metabolites”. The Journal of Steroid Biochemistry and Molecular Biology. 38 (4): 441–64. doi:10.1016/0960-0760(91)90332-y. PMID 2031859. S2CID 20197705.
- ^ Saartok T, Dahlberg E, Gustafsson JA (June 1984). “Relative binding affinity of anabolic-androgenic steroids: comparison of the binding to the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone-binding globulin”. Endocrinology. 114 (6): 2100–6. doi:10.1210/endo-114-6-2100. PMID 6539197.
- ^ Kicman AT (June 2008). “Pharmacology of anabolic steroids”. British Journal of Pharmacology. 154 (3): 502–21. doi:10.1038/bjp.2008.165. PMC 2439524. PMID 18500378.
- ^ Schänzer W, Geyer H, Fusshöller G, Halatcheva N, Kohler M, Parr MK, Guddat S, Thomas A, Thevis M (2006). “Mass spectrometric identification and characterization of a new long-term metabolite of metandienone in human urine”. Rapid Communications in Mass Spectrometry. 20 (15): 2252–8. Bibcode:2006RCMS…20.2252S. doi:10.1002/rcm.2587. PMID 16804957.
- ^ Baselt R (2008). Disposition of Toxic Drugs and Chemicals in Man (8th ed.). Foster City, CA: Biomedical Publications. pp. 952–4.
- ^ Fragkaki AG, Angelis YS, Tsantili-Kakoulidou A, Koupparis M, Georgakopoulos C (May 2009). “Schemes of metabolic patterns of anabolic androgenic steroids for the estimation of metabolites of designer steroids in human urine”. The Journal of Steroid Biochemistry and Molecular Biology. 115 (1–2): 44–61. doi:10.1016/j.jsbmb.2009.02.016. PMID 19429460. S2CID 10051396.
- ^ US granted 2900398, Wettstein A, Hunger A, Meystre C, Ehmann L, “Process for the manufacture of steroid dehydrogenation products”, issued 18 August 1959, assigned to Ciba Pharmaceutical Products, Inc.
- ^ Chaney M (16 June 2008). “Dianabol, the first widely used steroid, turns 50”. NY Daily News. Retrieved 2017-01-14.
- ^ Peters J (2005-02-18). “The Man Behind the Juice”. Slate. ISSN 1091-2339. Retrieved 2017-01-14.
- ^ Quinn TJ (2009-02-01). “OTL: Football’s first steroids team? The ’63 Chargers”. ESPN. Retrieved 2017-01-14.
- ^ Fourcroy J (2006). “Designer steroids: past, present and future”. Current Opinion in Endocrinology, Diabetes and Obesity. 13 (3): 306–309. doi:10.1097/01.med.0000224812.46942.c3. S2CID 87333977.
- ^ Jump up to:a b Llewellyn W (2011-01-01). Anabolics. Molecular Nutrition Llc. ISBN 978-0-9828280-1-4.
- ^ Roach R (2017-01-14). Muscle, Smoke and Mirrors. AuthorHouse. ISBN 978-1-4670-3840-9.
- ^ Diversion Control Division. “Implementation of the Anabolic Steroid Control Act of 2004”. United States Department of Justice. Retrieved 2017-01-14.
- ^ Karch SB (21 December 2006). Drug Abuse Handbook(Second ed.). CRC Press. pp. 30–. ISBN 978-1-4200-0346-8.
- Tertiary alcohols
- Androgens and anabolic steroids
- Androstanes
- Bodybuilding
- Doping in sport
- Hepatotoxins
- Enones
- Synthetic estrogens
- Testosterone
- Veterinary drugs
- World Anti-Doping Agency prohibited substances
Methandienone
Methandienone International Programme on Chemical Safety Poisons Information Monograph 905 Pharmaceutical This monograph does not contain all of the sections completed. This mongraph is harmonised with the Group monograph on Anabolic Steroids (PIM G007). 1. NAME 1.1 Substance Methandienone 1.2 Group ATC Classification: A14 (Anabolic Agents for Systemic Use) A14A (Anabolic steroids) 1.3 Synonyms Metandienone (pINN); Methandrostenolone; NSC-42722; Métandiénone; Dehydromethyltestosterone; Metandienonum; Methandienone; Methandrostenolone 1.4 Identification numbers 1.4.1 CAS number 72-63-9 1.4.2 Other numbers 1.5 Main brand names, main trade names 1.6 Main manufacturers, main importers 2. SUMMARY 2.1 Main risks and target organs There is no serious risk from acute poisoning, but chronic use can cause harm. The main risks are those of excessive androgens: menstrual irregularities and virilization in women and impotence, premature cardiovascular disease and prostatic hypertrophy in men. Both men and women can suffer liver damage with oral anabolic steroids containing a substituted 17-alpha-carbon. Psychiatric changes can occur during use or after cessation of these agents. 2.2 Summary of clinical effects Acute overdosage can produce nausea and gastrointestinal upset. Chronic usage is thought to cause an increase in muscle bulk, and can cause an exageration of male characteristics and effects related to male hormones. Anabolic steroids can influence sexual function. They can also cause cardiovascular and hepatic damage. Acne and male- pattern baldness occur in both sexes; irregular menses, atrophy of the breasts, and clitoromegaly in women; and testicular atrophy and prostatic hypertrophy in men. 2.3 Diagnosis The diagnosis depends on a history of use of oral or injected anabolic steroids, together with signs of increased muscle bulk, commonly seen in "body-builders". Biochemical tests of liver function are often abnormal in patients who take excessive doses of oral anabolic steroids. Laboratory analyses of urinary anabolic steroids and their metabolites can be helpful in detecting covert use of these drugs. 2.4 First aid measures and management principles Supportive care is the only treatment necessary or appropriate for acute intoxication. Chronic (ab)users can be very reluctant to cease abuse, and may require professional help as with other drug misuse. 3. PHYSICO-CHEMICAL PROPERTIES 3.1 Origin of the substance Naturally-occuring anabolic steroids are synthesised in the testis, ovary and adrenal gland from cholesterol via pregnenolone. Synthetic anabolic steroids are based on the principal male hormone testosterone, modified in one of three ways: alkylation of the 17-carbon esterification of the 17-OH group modification of the steroid nucleus (Murad & Haynes, 1985). 3.2 Chemical structure Chemical Name: 17beta-Hydroxy-17alpha-methylandrosta-1,4-dien-3-one. Molecular Formula: C20H28O2 Molecular Weight: 300.4 3.3 Physical properties 3.3.1 Colour 3.3.2 State/form 3.3.3 Description 3.4 Other characteristics 3.4.1 Shelf-life of the substance 3.4.2 Storage conditions Protect from light. Vials for parenteral administration should be stored at room temperature (15 to 30°C). Visual inspection for particulate and/or discoloration is advisable. 4. USES 4.1 Indications 4.1.1 Indications Anabolic agent; systemic Anabolic steroid Androstan derivative; anabolic steroid Estren derivative; anabolic steroid Other anabolic agent Anabolic agent for systemic use; veterinary Anabolic steroid; veterinary Estren derivative; veterinary 4.1.2 Description The only legitimate therapeutic indications for anabolic steroids are: (a) replacement of male sex steroids in men who have androgen deficiency, for example as a result of loss of both testes (b) the treatment of certain rare forms of aplastic anaemia which are or may be responsive to anabolic androgens. (ABPI Data Sheet Compendium, 1993) (c) the drugs have been used in certain countries to counteract catabolic states, for example after major trauma. 4.2 Therapeutic dosage 4.2.1 Adults 4.2.2 Children Not applicable 4.3 Contraindications Known or suspected cancer of the prostate or (in men) breast. Pregnancy or breast-feeding. Known cardiovascular disease is a relative contraindication. 5. ROUTES OF EXPOSURE 5.1 Oral Anabolic steroids can be absorbed from the gastrointestinal tract, but many compounds undergo such extensive first-pass metabolism in the liver that they are inactive. Those compounds in which substitution of the 17- carbon protects the compound from the rapid hepatic metabolism are active orally (Murad and Haynes, 1985). There are preparations of testosterone that can be taken sublingually. 5.2 Inhalation Not relevant 5.3 Dermal No data available 5.4 Eye Not relevant 5.5 Parenteral Intramuscular or deep subcutaneous injection is the principal route of administration of all the anabolic steroids except the 17-alpha-substituted steroids which are active orally. 5.6 Other Not relevant 6. KINETICS 6.1 Absorption by route of exposure The absorption after oral dosing is rapid for testosterone and probably for other anabolic steroids, but there is extensive first-pass hepatic metabolism for all anabolic steroids except those that are substituted at the 17-alpha position. The rate of absorption from subcutaneous or intramuscular depots depends on the product and its formulation. Absorption is slow for the lipid-soluble esters such as the cypionate or enanthate, and for oily suspensions. 6.2 Distribution by route of exposure The anabolic steroids are highly protein bound, and is carried in plasma by a specific protein called sex-hormone binding globulin. 6.3 Biological half-life by route of exposure The metabolism of absorbed drug is rapid, and the elimination half-life from plasma is very short. The duration of the biological effects is therefore determined almost entirely by the rate of absorption from subcutaneous or intramuscular depots, and on the de-esterification which precedes it (Wilson, 1992). 6.4 Metabolism Free (de-esterified) anabolic androgens are metabolized by hepatic mixed function oxidases (Wilson, 1992). 6.5 Elimination by route of exposure After administration of radiolabelled testosterone, about 90% of the radioactivity appears in the urine, and 6% in the faeces; there is some enterohepatic recirculation (Wilson, 1992). 7. PHARMACOLOGY AND TOXICOLOGY 7.1 Mode of action 7.1.1 Toxicodynamics The toxic effects are an exaggeration of the normal pharmacological effects. 7.1.2 Pharmacodynamics Anabolic steroids bind to specific receptors present especially in reproductive tissue, muscle and fat (Mooradian & Morley, 1987). The anabolic steroids reduce nitrogen excretion from tissue breakdown in androgen deficient men. They are also responsible for normal male sexual differentiation. The ratio of anabolic ("body-building") effects to androgenic (virilizing) effects may differ among the members of the class, but in practice all agents possess both properties to some degree. There is no clear evidence that anabolic steroids enhance overall athletic performance (Elashoff et al, 1991). 7.2 Toxicity 7.2.1 Human data 7.2.1.1 Adults No data available. 7.2.1.2 Children No data available. 7.2.2 Relevant animal data No data available. 7.2.3 Relevant in vitro data No data 7.3 Carcinogenicity Anabolic steroids may be carcinogenic. They can stimulate growth of sex-hormone dependent tissue, primarily the prostate gland in men. Precocious prostatic cancer has been described after long-term anabolic steroid abuse (Roberts & Essenhigh, 1986). Cases where hepatic cancers have been associated with anabolic steroid abuse have been reported (Overly et al, 1984). 7.4 Teratogenicity Androgen ingestion by a pregnant mother can cause virilization of a female fetus (Dewhurst & Gordon, 1984). 7.5 Mutagenicity No data available. 7.6 Interactions No data available. 7.7 Main adverse effects The adverse effects of anabolic steroids include weight gain, fluid retention, and abnormal liver function as measured by biochemical tests. Administration to children can cause premature closure of the epiphyses. Men can develop impotence and azoospermia. Women are at risk of virilization. 8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS 8.1 Material sampling plan 8.1.1 Sampling and specimen collection 8.1.1.1 Toxicological analyses 8.1.1.2 Biomedical analyses 8.1.1.3 Arterial blood gas analysis 8.1.1.4 Haematological analyses 8.1.1.5 Other (unspecified) analyses 8.1.2 Storage of laboratory samples and specimens 8.1.2.1 Toxicological analyses 8.1.2.2 Biomedical analyses 8.1.2.3 Arterial blood gas analysis 8.1.2.4 Haematological analyses 8.1.2.5 Other (unspecified) analyses 8.1.3 Transport of laboratory samples and specimens 8.1.3.1 Toxicological analyses 8.1.3.2 Biomedical analyses 8.1.3.3 Arterial blood gas analysis 8.1.3.4 Haematological analyses 8.1.3.5 Other (unspecified) analyses 8.2 Toxicological Analyses and Their Interpretation 8.2.1 Tests on toxic ingredient(s) of material 8.2.1.1 Simple Qualitative Test(s) 8.2.1.2 Advanced Qualitative Confirmation Test(s) 8.2.1.3 Simple Quantitative Method(s) 8.2.1.4 Advanced Quantitative Method(s) 8.2.2 Tests for biological specimens 8.2.2.1 Simple Qualitative Test(s) 8.2.2.2 Advanced Qualitative Confirmation Test(s) 8.2.2.3 Simple Quantitative Method(s) 8.2.2.4 Advanced Quantitative Method(s) 8.2.2.5 Other Dedicated Method(s) 8.2.3 Interpretation of toxicological analyses 8.3 Biomedical investigations and their interpretation 8.3.1 Biochemical analysis 8.3.1.1 Blood, plasma or serum 8.3.1.2 Urine 8.3.1.3 Other fluids 8.3.2 Arterial blood gas analyses 8.3.3 Haematological analyses 8.3.4 Interpretation of biomedical investigations 8.4 Other biomedical (diagnostic) investigations and their interpretation 8.5 Overall Interpretation of all toxicological analyses and toxicological investigations Biomedical analysis The following tests can be relevant in the investigation of chronic anabolic steroid abuse: a) full blood count b) electrolytes and renal function tests c) hepatic function tests d) testosterone e) Lutenizing hormone f) prostatic acid phosphatase or prostate related antigen g) blood glucose concentration h) cholesterol concentration Toxicological analysis -urinary analysis for anabolic steroids and their metabolites Other investigations -electrocardiogram 8.6 References 9. CLINICAL EFFECTS 9.1 Acute poisoning 9.1.1 Ingestion Nausea and vomiting can occur. 9.1.2 Inhalation Not relevant 9.1.3 Skin exposure Not relevant 9.1.4 Eye contact Not relevant 9.1.5 Parenteral exposure Patients are expected to recover rapidly after acute overdosage, but there are few data. "Body- builders" use doses many times the standard therapeutic doses for these compounds but do not suffer acute toxic effects. 9.1.6 Other Not relevant 9.2 Chronic poisoning 9.2.1 Ingestion Hepatic damage, manifest as derangement of biochemical tests of liver function and sometimes severe enough to cause jaundice; virilization in women; prostatic hypertrophy, impotence and azoospermia in men; acne, abnormal lipids, premature cardiovascular disease (including stroke and myocardial infarction), abnormal glucose tolerance, and muscular hypertrophy in both sexes; psychiatric disturbances can occur during or after prolonged treatment (Ferner & Rawlins, 1988; Kennedy, 1992; Ross & Deutch, 1990; Ryan, 1981; Wagner, 1989). 9.2.2 Inhalation Not relevant 9.2.3 Skin exposure Not relevant 9.2.4 Eye contact Not relevant 9.2.5 Parenteral exposure Virilization in women; prostatic hypertrophy, impotence and azoospermia in men; acne, abnormal lipids, premature cardiovascular disease (including stroke and myocardial infarction), abnormal glucose tolerance, and muscular hypertrophy in both sexes. Psychiatric disturbances can occur during or after prolonged treatment. Hepatic damage is not expected from parenteral preparations. 9.2.6 Other Not relevant 9.3 Course, prognosis, cause of death Patients with symptoms of acute poisoning are expected to recover rapidly. Patients who persistently abuse high doses of anabolic steroids are at risk of death from premature heart disease or cancer, especially prostatic cancer. Non-fatal but long-lasting effects include voice changes in women and fusion of the epiphyses in children. Other effects are reversible over weeks or months. 9.4 Systematic description of clinical effects 9.4.1 Cardiovascular Chronic ingestion of high doses of anabolic steroids can cause elevations in blood pressure, left ventricular hypertrophy and premature coronary artery disease (McKillop et al., 1986; Bowman, 1990; McNutt et al., 1988). 9.4.2 Respiratory Not reported 9.4.3 Neurological 9.4.3.1 Central nervous system Stroke has been described in a young anabolic steroid abuser (Frankle et al., 1988). Pope & Katz (1988) described mania and psychotic symptoms of hallucination and delusion in anabolic steroid abusers. They also described depression after withdrawal from anabolic steroids. There is also considerable debate about the effects of anabolic steroids on aggressive behaviour (Schulte et al., 1993) and on criminal behaviour (Dalby, 1992). Mood swings were significantly more common in normal volunteers during the active phase of a trial comparing methyltestosterone with placebo (Su et al., 1993). 9.4.3.2 Peripheral nervous system No data available 9.4.3.3 Autonomic nervous system No data available 9.4.3.4 Skeletal and smooth muscle No data available 9.4.4 Gastrointestinal Acute ingestion of large doses can cause nausea and gastrointestinal upset. 9.4.5 Hepatic Orally active (17-alpha substituted) anabolic steroids can cause abnormalities of hepatic function, manifest as abnormally elevated hepatic enzyme activity in biochemical tests of liver function,and sometimes as overt jaundice. The histological abnormality of peliosis hepatis has been associated with anabolic steroid use (Soe et al., 1992). Angiosarcoma (Falk et al, 1979) and a case of hepatocellular carcinoma in an anabolic steroid user has been reported (Overly et al., 1984). 9.4.6 Urinary 9.4.6.1 Renal Not reported 9.4.6.2 Other Men who take large doses of anabolic steroids can develop prostatic hypertrophy. Prostatic carcinoma has been described in young men who have abused anabolic steroids (Roberts & Essenhigh, 1986). 9.4.7 Endocrine and reproductive systems Small doses of anabolic steroids are said to increase libido, but larger doses lead to azoospermia and impotence. Testicular atrophy is a common clinical feature of long-term abuse of anabolic steroids, and gynaecomastia can occur (Martikainen et al., 1986; Schurmeyer et al., 1984; Spano & Ryan, 1984). Women develop signs of virilism, with increased facial hair, male pattern baldness, acne, deepening of the voice, irregular menses and clitoral enlargement (Malarkey et al., 1991; Strauss et al., 1984). 9.4.8 Dermatological Acne occurs in both male and female anabolic steroids abusers. Women can develop signs of virilism, with increased facial hair and male pattern baldness. 9.4.9 Eye, ear, nose, throat: local effects Changes in the larynx in women caused by anabolic steroids can result in a hoarse, deep voice. The changes are irreversible. 9.4.10 Haematological Anabolic androgens stimulate erythropoesis. 9.4.11 Immunological No data available 9.4.12 Metabolic 9.4.12.1 Acid-base disturbances No data available. 9.4.12.2 Fluid and electrolyte disturbances Sodium and water retention can occur, and result in oedema; hypercalcaemia is also reported (Reynolds, 1992). 9.4.12.3 Others Insulin resistance with a fall in glucose tolerance (Cohen & Hickman, 1987), and hypercholesterolaemia with a fall in high density lipoprotein cholesterol, have been reported (Cohen et al., 1988; Glazer, 1991; Webb et al., 1984). 9.4.13 Allergic reactions No data available 9.4.14 Other clinical effects No data available 9.4.15 Special risks Risk of abuse 9.5 Other No data available 9.6 Summary 10. MANAGEMENT 10.1 General principles The management of acute overdosage consists of supportive treatment, with fluid replacement if vomiting is severe. Chronic abuse should be discouraged, and psychological support may be needed as in the treatment of other drug abuse. The possibility of clinically important depression after cessation of usage should be borne in mind. 10.2 Life supportive procedures and symptomatic/specific treatment Not relevant 10.3 Decontamination Not usually required. 10.4 Enhanced elimination Not indicated 10.5 Antidote treatment 10.5.1 Adults None available 10.5.2 Children None available 10.6 Management discussion Not relevant 11. ILLUSTRATIVE CASES 11.1 Case reports from literature A 38-year old man presented with acute urinary retention, and was found to have carcinoma of the prostate. He had taken anabolic steroids for many years, and worked as a "strong-man" (Roberts and Essenhigh, 1986). A 22-year old male world-class weight lifter developed severe chest pain awaking him from sleep, and was shown to have myocardial infarction. For six weeks before, he had been taking high doses of oral and injected anabolic steroids. Total serum cholesterol was 596 mg/dL (HDL 14 mg/dL, LDL 513 mg/dL) (McNutt et al., 1988). Values of total cholesterol concentration above 200 mg/dL are considered undesirable. A 22-year old body builder took two eight-week courses of anabolic steroids. He became severely depressed after the second course, and when the depression gradually receded, he had prominent paranoid and religious delusions (Pope and Katz, 1987). A 19-year old American college footballer took intramuscular testosterone and oral methandrostenolone over 4 months. He became increasingly aggressive with his wife and child. After he severely injured the child, he ceased using anabolic steroids, and his violence and aggression resolved within 2 months (Schulte et al, 1993). 12. Additional information 12.1 Specific preventive measures Anabolic steroid abuse amongst athletes, weight lifters, body builders and others is now apparently common at all levels of these sports. Not all abusers are competitive sportsmen. There is therefore scope for a public health campaign, for example, based on gymnasia, to emphasize the dangers of anabolic steroid abuse and to support those who wish to stop using the drugs.
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