Methyltestosterone
| 1. NAME |
| 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. SUMMARY |
| 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. USES |
| 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. KINETICS |
| 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 |
| 7.2.1.1 Adults |
| 7.2.1.2 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 |
| 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 |
| 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 |
| 9.4.3.1 Central nervous system |
| 9.4.3.2 Peripheral nervous system |
| 9.4.3.3 Autonomic nervous system |
| 9.4.3.4 Skeletal and smooth muscle |
| 9.4.4 Gastrointestinal |
| 9.4.5 Hepatic |
| 9.4.6 Urinary |
| 9.4.6.1 Renal |
| 9.4.6.2 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 |
| 9.4.12.1 Acid-base disturbances |
| 9.4.12.2 Fluid and electrolyte disturbances |
| 9.4.12.3 Others |
| 9.4.13 Allergic reactions |
| 9.4.14 Other clinical effects |
| 9.4.15 Special risks |
| 9.5 Other |
| 9.6 Summary |
| 10. MANAGEMENT |
| 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 |
| 13. REFERENCES |
| 14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESS(ES) |
Methyltestosterone
International Programme on Chemical Safety
Poisons Information Monograph 908
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
Methyltestosterone
1.2 Group
ATC Classification:
A14 (Anabolic Agents for Systemic Use)
A14A (Anabolic steroids)
1.3 Synonyms
Methyltestosteronum; NSC-9701; Methyltestosterone (Rec.INN);
Methyltestosteron; Methyltestosteronum; Metiltestosterone
1.4 Identification numbers
1.4.1 CAS number
58-18-4
1.4.2 Other numbers
1.5 Main brand names, main trade names
Android(R) (Brown, USA); Android(R) (ICN, USA);
Androteston(R) (Organon);
Gynosterone(R) (Sam-On, Israel);
Hormobin(R) (Münir Sahin, Turkey);
Malestrone(R) (Kirk, USA);
Mesteron(R) (Polfa, Poland);
Metandren(R) (Ciba-Geigy, Canada);
Neo-Hombreol(R) (Organon);
Neo-Hombreol(R) M (Organon);
Orchisterone(R) (Negroni, Italy);
Oreton(R) Methyl(R) (Schering, USA);
Seksfort(R) (Uranium, Turkey);
Synandrets(R) (Pfizer);
Synandrotabs(R) (Pfizer);
Testipron(R) (Kwizda, Austria);
Testomet(R) (Protea, Australia);
Testosteron lingvalete(R) (Galenika, Yugoslavia);
Testotonic B(R) (Sam-On, Israel);
Testovis(R) (SIT, Italy);
Testred(R) (ICN, USA);
Virilon(R) (Star, USA)
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-methylandrost-4-en-3-one
Molecular Formula: C20H30O2
Molecular Weight: 302.5
3.3 Physical properties
3.3.1 Colour
White or slightly yellowish-white
3.3.2 State/form
Solid-crystals
3.3.3 Description
Odourless, slightly hygroscopic.
Practically insoluble in water; freely soluble in
chloroform; soluble in methyl alcohol; sparingly
soluble in vegetable oils; the British Pharmacopoeia
states that it is freely soluble in alcohol and
slightly soluble in ether, while the US Pharmacopoeia
has soluble in alcohol and in ether.
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.
12.2 Other
No data available.
13. REFERENCES
ABPI Data Sheet Compendium (1993) Datapharm Publications,
London.
Bowman S. (1990) Anabolic steroids and infarction. Br Med J;
300:
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:
49-56.
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.
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
2; 1120-1123.
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14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
ADDRESS(ES)
Author: Dr R. E. Ferner,
West Midlands Centre for Adverse Drug Reaction
Reporting,
City Hospital Dudley Road,
Birmingham B18 7QH
England.
Tel: +44-121-5074587
Fax: +44-121-5236125
Email: fernerre@bham.ac.uk
Date: 1994
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