| 1.1 Substance|
| 1.2 Group|
| 1.3 Synonyms|
| 1.4 Identification numbers|
| 1.4.1 CAS number|
| 1.4.2 Other numbers|
| 1.5 Main brand names, main trade names|
| 1.6 Main manufacturers, main importers|
| 2.1 Main risks and target organs|
| 2.2 Summary of clinical effects|
| 2.3 Diagnosis|
| 2.4 First aid measures and management principles|
|3. PHYSICO-CHEMICAL PROPERTIES|
| 3.1 Origin of the substance|
| 3.2 Chemical structure|
| 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|
| 4.1 Indications|
| 4.1.1 Indications|
| 4.1.2 Description|
| 4.2 Therapeutic dosage|
| 4.2.1 Adults|
| 4.2.2 Children|
| 4.3 Contraindications|
|5. ROUTES OF EXPOSURE|
| 5.1 Oral|
| 5.2 Inhalation|
| 5.3 Dermal|
| 5.4 Eye|
| 5.5 Parenteral|
| 5.6 Other|
| 6.1 Absorption by route of exposure|
| 6.2 Distribution by route of exposure|
| 6.3 Biological half-life by route of exposure|
| 6.4 Metabolism|
| 6.5 Elimination by route of exposure|
|7. PHARMACOLOGY AND TOXICOLOGY|
| 7.1 Mode of action|
| 7.1.1 Toxicodynamics|
| 7.1.2 Pharmacodynamics|
| 7.2 Toxicity|
| 7.2.1 Human data|
| 126.96.36.199 Adults|
| 188.8.131.52 Children|
| 7.2.2 Relevant animal data|
| 7.2.3 Relevant in vitro data|
| 7.3 Carcinogenicity|
| 7.4 Teratogenicity|
| 7.5 Mutagenicity|
| 7.6 Interactions|
| 7.7 Main adverse effects|
|8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS|
| 8.1 Material sampling plan|
| 8.1.1 Sampling and specimen collection|
| 184.108.40.206 Toxicological analyses|
| 220.127.116.11 Biomedical analyses|
| 18.104.22.168 Arterial blood gas analysis|
| 22.214.171.124 Haematological analyses|
| 126.96.36.199 Other (unspecified) analyses|
| 8.1.2 Storage of laboratory samples and specimens|
| 188.8.131.52 Toxicological analyses|
| 184.108.40.206 Biomedical analyses|
| 220.127.116.11 Arterial blood gas analysis|
| 18.104.22.168 Haematological analyses|
| 22.214.171.124 Other (unspecified) analyses|
| 8.1.3 Transport of laboratory samples and specimens|
| 126.96.36.199 Toxicological analyses|
| 188.8.131.52 Biomedical analyses|
| 184.108.40.206 Arterial blood gas analysis|
| 220.127.116.11 Haematological analyses|
| 18.104.22.168 Other (unspecified) analyses|
| 8.2 Toxicological Analyses and Their Interpretation|
| 8.2.1 Tests on toxic ingredient(s) of material|
| 22.214.171.124 Simple Qualitative Test(s)|
| 126.96.36.199 Advanced Qualitative Confirmation Test(s)|
| 188.8.131.52 Simple Quantitative Method(s)|
| 184.108.40.206 Advanced Quantitative Method(s)|
| 8.2.2 Tests for biological specimens|
| 220.127.116.11 Simple Qualitative Test(s)|
| 18.104.22.168 Advanced Qualitative Confirmation Test(s)|
| 22.214.171.124 Simple Quantitative Method(s)|
| 126.96.36.199 Advanced Quantitative Method(s)|
| 188.8.131.52 Other Dedicated Method(s)|
| 8.2.3 Interpretation of toxicological analyses|
| 8.3 Biomedical investigations and their interpretation|
| 8.3.1 Biochemical analysis|
| 184.108.40.206 Blood, plasma or serum|
| 220.127.116.11 Urine|
| 18.104.22.168 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|
| 8.6 References|
|9. CLINICAL EFFECTS|
| 9.1 Acute poisoning|
| 9.1.1 Ingestion|
| 9.1.2 Inhalation|
| 9.1.3 Skin exposure|
| 9.1.4 Eye contact|
| 9.1.5 Parenteral exposure|
| 9.1.6 Other|
| 9.2 Chronic poisoning|
| 9.2.1 Ingestion|
| 9.2.2 Inhalation|
| 9.2.3 Skin exposure|
| 9.2.4 Eye contact|
| 9.2.5 Parenteral exposure|
| 9.2.6 Other|
| 9.3 Course, prognosis, cause of death|
| 9.4 Systematic description of clinical effects|
| 9.4.1 Cardiovascular|
| 9.4.2 Respiratory|
| 9.4.3 Neurological|
| 22.214.171.124 Central nervous system|
| 126.96.36.199 Peripheral nervous system|
| 188.8.131.52 Autonomic nervous system|
| 184.108.40.206 Skeletal and smooth muscle|
| 9.4.4 Gastrointestinal|
| 9.4.5 Hepatic|
| 9.4.6 Urinary|
| 220.127.116.11 Renal|
| 18.104.22.168 Other|
| 9.4.7 Endocrine and reproductive systems|
| 9.4.8 Dermatological|
| 9.4.9 Eye, ear, nose, throat: local effects|
| 9.4.10 Haematological|
| 9.4.11 Immunological|
| 9.4.12 Metabolic|
| 22.214.171.124 Acid-base disturbances|
| 126.96.36.199 Fluid and electrolyte disturbances|
| 188.8.131.52 Others|
| 9.4.13 Allergic reactions|
| 9.4.14 Other clinical effects|
| 9.4.15 Special risks|
| 9.5 Other|
| 9.6 Summary|
| 10.1 General principles|
| 10.2 Life supportive procedures and symptomatic/specific treatment|
| 10.3 Decontamination|
| 10.4 Enhanced elimination|
| 10.5 Antidote treatment|
| 10.5.1 Adults|
| 10.5.2 Children|
| 10.6 Management discussion|
|11. ILLUSTRATIVE CASES|
| 11.1 Case reports from literature|
|12. ADDITIONAL INFORMATION|
| 12.1 Specific preventive measures|
| 12.2 Other|
|14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESS(ES)|
International Programme on Chemical Safety
Poisons Information Monograph 519
A14 (Anabolic Agents for Systemic Use)
A14A (Anabolic steroids)
Testosteroid; testosteron; testostosterone;
1.4 Identification numbers
1.4.1 CAS number
1.4.2 Other numbers
NIOSH/RTECS XA 3030000
Testosterone Cypionate (CAS 58-20-8)
Testosterone Enanthate (CAS 315-37-7)
Testosterone Isocaproate (CAS 15262-86-9)
Testosterone Phenylpropionate (CAS 1255-49-8)
Testosterone Propioponate (CAS 57-85-2)
1.5 Main brand names, main trade names
Androderm; Andropatch; Histerone; Malogen Aqueous (FM);
Sterile Testosterone Suspension USP 23; Tesamone; Testandro;
Testoderm; Testopel; Testosterone Implants; Testosterone
Implants BP 1993; Testotop; Homosten (FM)
1.6 Main manufacturers, main importers
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
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.
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
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
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-Hydroxyandrost-4-en-3-one
-delta (sup 4) -androsten-17 (beta)-ol-3-
-17-beta-Hydroxy-delta (sup 4)-androsten-
Molecular Formula: C19H28O2
Molecular Weight: 288.4
The following salts also are available:
Testosterone Cypionate C27H40O3.
Testosterone Enanthate C26H40O3.
Testosterone Isocaproate C25H3803.
Testosterone Phenylpropionate C28H36O3.
Testosterone Propionate C22H32O3.
Testosteron Undecanoate C29H48O3.
3.3 Physical properties
White or slightly creamy-white
Odourless or almost odourless, crystals or
crystalline powder. Practically insoluble in water;
freely soluble in alcohol; soluble 1 in 6 of
dehydrated alcohol, 1 in 2 of chloroform, and 1 in 100
of ether; slightly soluble in ethyl oleate; soluble in
dioxan and vegetable oils.
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
Anabolic agent; systemic
Androstan derivative; anabolic steroid
Estren derivative; anabolic steroid
Other anabolic agent
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
(ABPI Data Sheet Compendium, 1993)
(c) the drugs have been used in certain countries to
counteract catabolic states, for example after major
4.2 Therapeutic dosage
testosterone undecanoate up to 160 mg/day
testosterone esters 150 to 300 mg/week
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
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
No data available
Intramuscular or deep subcutaneous injection is the
principal route of administration of all the anabolic
steroids except the 17-alpha-substituted steroids which are
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
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.
Testosterone esters, prepared for parenteral administration
are less polar than the free steroids. Therefore, they are
absorbed more slowly being effective if given with 1 to 3
weeks intervals. Some preparations are effective even when
given at 12 week intervals (Wilson, 1992).
6.2 Distribution by route of exposure
The anabolic steroids are highly protein bound, and are
carried in plasma by a specific protein called sex-hormone
After absorption, only two per cent of testosterone is found
free in plasma with 98% becoming bound. The testosterone
esters are hydrolyzed prior to action. In the tissues, it is
transformed by steroid 5-alphareductase to
dihydrotestosterone, the more active compound (Prod. Info.,
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).
Free (de-esterified) anabolic androgens are metabolized
by hepatic mixed function oxidases in the liver (Wilson,
1992). Conversion of testosterone to androstenedione involves
oxidation of the 17-OH group. Androsterone and
androstenedione are formed by reducing metabolic
6.5 Elimination by route of exposure
After administration of radiolabelled testosterone,
about 90% of the radioactivity appears in the urine as
glucuronic or sulfate conjugates, and 6% % of the
unconjugated testosterone in the faeces; there is some
enterohepatic recirculation (Wilson, 1992). Small amounts of
androstenediol and estrogens are excreted in the urine.
7. PHARMACOLOGY AND TOXICOLOGY
7.1 Mode of action
The toxic effects are an exaggeration of the
normal pharmacological effects.
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).
7.2.1 Human data
No data available.
No data available.
7.2.2 Relevant animal data
No data available.
7.2.3 Relevant in vitro data
No data available
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).
Androgen ingestion by a pregnant mother can cause
virilization of a female fetus (Dewhurst & Gordon,
No data available.
The main clinically important drug-drug interactions of
testosterone are related to the increase in the anticoagulant
effects of coumarinic drugs. Therefore, if these drugs are
used together the anticoagulant response should be carefully
monitored. Decreased anticoagulant tolerance has been
described when oxymetholone is administered together with
warfarin (Edwards & Curtis, 1971).
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
8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
8.1 Material sampling plan
8.1.1 Sampling and specimen collection
184.108.40.206 Toxicological analyses
220.127.116.11 Biomedical analyses
18.104.22.168 Arterial blood gas analysis
22.214.171.124 Haematological analyses
126.96.36.199 Other (unspecified) analyses
8.1.2 Storage of laboratory samples and specimens
188.8.131.52 Toxicological analyses
184.108.40.206 Biomedical analyses
220.127.116.11 Arterial blood gas analysis
18.104.22.168 Haematological analyses
22.214.171.124 Other (unspecified) analyses
8.1.3 Transport of laboratory samples and specimens
126.96.36.199 Toxicological analyses
188.8.131.52 Biomedical analyses
184.108.40.206 Arterial blood gas analysis
220.127.116.11 Haematological analyses
18.104.22.168 Other (unspecified) analyses
8.2 Toxicological Analyses and Their Interpretation
8.2.1 Tests on toxic ingredient(s) of material
22.214.171.124 Simple Qualitative Test(s)
126.96.36.199 Advanced Qualitative Confirmation Test(s)
188.8.131.52 Simple Quantitative Method(s)
184.108.40.206 Advanced Quantitative Method(s)
8.2.2 Tests for biological specimens
220.127.116.11 Simple Qualitative Test(s)
18.104.22.168 Advanced Qualitative Confirmation Test(s)
22.214.171.124 Simple Quantitative Method(s)
126.96.36.199 Advanced Quantitative Method(s)
188.8.131.52 Other Dedicated Method(s)
8.2.3 Interpretation of toxicological analyses
8.3 Biomedical investigations and their interpretation
8.3.1 Biochemical analysis
184.108.40.206 Blood, plasma or serum
220.127.116.11 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
8.5 Overall Interpretation of all toxicological analyses and
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
e) Lutenizing hormone
f) prostatic acid phosphatase or prostate related antigen
g) blood glucose concentration
h) cholesterol concentration
-urinary analysis for anabolic steroids and their metabolites
9. CLINICAL EFFECTS
9.1 Acute poisoning
Nausea and vomiting can occur.
9.1.3 Skin exposure
9.1.4 Eye contact
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.
9.2 Chronic poisoning
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).
9.2.3 Skin exposure
9.2.4 Eye contact
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.
9.3 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
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).
18.104.22.168 Central nervous system
Stroke has been described in a young
anabolic steroid abuser (Frankle et al.,
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).
22.214.171.124 Peripheral nervous system
No data available
126.96.36.199 Autonomic nervous system
No data available
188.8.131.52 Skeletal and smooth muscle
No data available
Acute ingestion of large doses can cause nausea
and gastrointestinal upset.
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.,
Angiosarcoma (Falk et al, 1979) and a case of
hepatocellular carcinoma in an anabolic steroid user
has been reported (Overly et al., 1984).
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).
Acne occurs in both male and female anabolic
steroids abusers. Women can develop signs of
virilism, with increased facial hair and male pattern
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.
Anabolic androgens stimulate erythropoesis.
No data available
184.108.40.206 Acid-base disturbances
No data available.
220.127.116.11 Fluid and electrolyte disturbances
Sodium and water retention can
occur, and result in oedema; hypercalcaemia
is also reported (Reynolds, 1992).
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
No data available
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
10.2 Life supportive procedures and symptomatic/specific treatment
Not usually required.
10.4 Enhanced elimination
10.5 Antidote treatment
10.6 Management discussion
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
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
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.
No data available.
ABPI Data Sheet Compendium (1993) Datapharm Publications,
Bowman S. (1990) Anabolic steroids and infarction. Br Med J;
Cohen JC & Hickman R. (1987) Insulin Resistance and diminished
glucose tolerance in powerlifters ingesting anabolic steroids. J
Clin Endocrinol Metab 64: 960.
Cohen JC, Noakes TD, & Spinnler Benade AJ. (1988)
Hypercholesterolemia in male power lifters using Anabolic
Androgenic Steroids. The Physician and Sports medicine 16:
Dalby JT. (1992) Brief anabolic steroid use and sustained
behavioral reaction. Am J Psychiatry 149: 271-272.
Dewhurst J. & Gordon RR (1984). Fertility following change of
sex: a follow-up. Lancet: ii: 1461-2.
Edwards, MS & Curtis, JR (1971) Decreased anticoagulant tolerance
with oxymetholone. Lancet; 2: 221.
Elashoff JD, Jacknow AD, Shain SG, & Braunstein GD. (1991) Effects
of anabolic-androgenic steroids on muscular strength. Annals Inter
Med 115: 387-393.
Falk H, Thomas LB, Popper H, Ishak KG. (1979). Hepatic
angiosacroma associated with androgenic-anabolic steroids. Lancet
Ferner RE & Rawlins MD (1988) Anabolic steroids: the power and the
glory? Br Med J 1988; 297: 877-878.
Frankle MA, Eichberg R, & Zacharian SB. (1988) Anabolic Androgenic
steroids and stroke in an athlete: case report. Arch Phys Med
Rehabil 1988; 69: 632-633.
Glazer G. (1991) Atherogenic effects of anabolic steroids on serum
lipid levels. Arch Intern Med 151: 1925-1933.
Kennedy MC. (1992). Anabolic steroid abuse and toxicology. Aust NZ
J Med 22: 374-381.
Malarkey WB, Strauss RH, Leizman DJ, Liggett M, & Demers LM.
(1991). Endocrine effects in femal weight lifters who self-
administer testosterone and anabolic steroids. Am J Obstet
Gynecol 165: 1385-1390.
Martikainen H, Alen M, Rahkila P, & Vihko R. (1986) Testicular
responsiveness to human chorionic gonadotrophin during transient
hypogonadotrophic hypogondasim induced by androgenic/anabolic
steroids in power athletes. Biochem 25: 109-112.
McKillop G, Todd IC, Ballantyne D. (1986) Increased left
ventricular mass in a body builder using anabolic steroids. Brit J
Sports Med 20: 151-152.
McNutt RA, Ferenchick GS, Kirlin PC, & Hamlin NJ. (1988) Acute
myocardial infarction in a 22 year old world class weight lifter
using anabolic steroids. Am J Cardiol 62: 164.
Mooradian JE, Morley JE, Korenman SG. (1987) Biological actions
of androgens. Endocrine Reviews 8:1-27.
Murad F, & Haynes RC. (1985). Androgens. in. Ed: Goodman Gilman
A, Goodman L S, Roll T W, Murad F. The Pharmacological Basis of
Therapeutics, 7th edition, Macmillan, New York: 1440-1458
Overly WL et al. (1984). Androgens and hepatocellular carcinoma in
an athlete. Ann Int Med 100: 158-159.
Pope GR,, & Katz DL. (1988). Affective and psychotic symptoms
associated with anabolic steroid use. Am J Psychiatry 145:
Product Information- Deposteron (R) - Novaquomica,(1994).
Reynolds Ed. (1992) Martindale-The Extra Pharmacopeia. The
Pharmaceutical Press. London.
Roberts JT, & Essenhigh DM. (1986) Adenocarcinoma of prostate in
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14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
Author: Staff of the Poison Control Center of Rio de
Sylvana do Valle Costa , MD
Denir Gomes Nogueira, Pharm. D.; MSc.
Carlos Alberto Guimares Reis; MD.
Marcia Matos Silva; Pharm D.
Jaderson Socrates Lima; MD, MSc.
Poison Control Center of Rio de Janeiro
University Hospital - Federal University of Rio de
Av Brig. Trompovsky,
SN - 21940-590-
Rio de Janeiro - Brazil
Reviewed: INTOX 9, Cardif, Wales, September, 1996
This monograph has been harmonised with the Group Monograph (G007)
on Anabolic Steroids written by Dr R. Ferner:
Dr R. E. Ferner,
West Midlands Centre for Adverse Drug Reaction
City Hospital Dudley Road,
Birmingham B18 7QH
Peer review: INTOX Meeting, Sao Paulo, Brazil, September 1994
(Drs P.Kulling, R.McKuowen, A.Borges, R.Higa,
R.Garnier, Hartigan-Go, E.Wickstrom)
Editor: Dr M.Ruse, March 1998