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Description
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as a form of androgen replacement therapy for the treatment of hypogonadism in men, but has since been discontinued and withdrawn in most countries, including in the United States.[14][3][5]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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