Drostanolone
Drostanolone, or dromostanolone, is an anabolic–androgenic steroid (AAS) of the dihydrotestosterone (DHT) group which was never marketed.[1][2][3] An androgen ester prodrug of drostanolone, drostanolone propionate, was formerly used in the treatment of breast cancer in women under brand names such as Drolban, Masteril, and Masteron.[1][2][3][4] This ester has also been used non-medically for physique- or performance-enhancing purposes.[3]
Drostanolone 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. |
Like other AAS, drostanolone is an agonist of the androgen receptor (AR).[3] It is not a substrate for 5α-reductase and is a poor substrate for 3α-hydroxysteroid dehydrogenase (3α-HSD), and therefore shows a high ratio of anabolic to androgenic activity.[3] As a DHT derivative, drostanolone is not a substrate for aromatase and hence cannot be aromatized into estrogenic metabolites.[3] While no data are available on the progestogenic activity of drostanolone, it is thought to have low or no such activity similarly to other DHT derivatives.[3] Since the drug is not 17α-alkylated, it is not known to cause hepatotoxicity.[3]
Chemistry[edit]
Drostanolone, also known as 2α-methyl-5α-dihydrotestosterone (2α-methyl-DHT) or as 2α-methyl-5α-androstan-17β-ol-3-one, is a synthetic androstane steroid and a derivative of DHT.[1][2][3] It is specifically DHT with a methyl group at the C2α position.[1][2][3]
History[edit]
Drostanolone and its ester drostanolone propionate were first described in 1959.[3][5] Drostanolone propionate was first introduced for medical use in 1961.[6]
Society and culture[edit]
Generic names[edit]
Drostanolone is the generic name of the drug and its INN, BAN, and DCF.[1][2] It has also been referred to as dromostanolone.[1][2]
Legal status[edit]
Drostanolone, along with other AAS, is a schedule III controlled substance in the United States under the Controlled Substances Act.[7]
References[edit]
- ^ Jump up to:a b c d e f Elks J (14 November 2014). The Dictionary of Drugs: Chemical Data: Chemical Data, Structures and Bibliographies. Springer. pp. 652–. ISBN 978-1-4757-2085-3.
- ^ Jump up to:a b c d e f Index Nominum 2000: International Drug Directory. Taylor & Francis. January 2000. pp. 377–. ISBN 978-3-88763-075-1.
- ^ Jump up to:a b c d e f g h i j k Llewellyn W (2011). Anabolics. Molecular Nutrition Llc. pp. 517–. ISBN 978-0-9828280-1-4.
- ^ Bennett MB, Helman P, Palmer P (November 1975). “Hormonal therapy of breast cancer with special reference to Masteril therapy”. South African Medical Journal = Suid-Afrikaanse Tydskrif vir Geneeskunde. 49 (49): 2036–40. PMID 1242823.
- ^ Ringold HJ, Batres E, Halpern O, Necoechea E (1959). “Steroids. CV.12-Methyl and 2-Hydroxymethylene-androstane Derivatives”. Journal of the American Chemical Society. 81 (2): 427–432. doi:10.1021/ja01511a040. ISSN 0002-7863.
- ^ William Andrew Publishing (22 October 2013). Pharmaceutical Manufacturing Encyclopedia, 3rd Edition. Elsevier. pp. 1402–. ISBN 978-0-8155-1856-3.
- ^ Karch SB (21 December 2006). Drug Abuse Handbook, Second Edition. CRC Press. pp. 30–. ISBN 978-1-4200-0346-8.
External links[edit]
- Cyclopentanols
- Androgens and anabolic steroids
- Androstanes
- Ketones
- World Anti-Doping Agency prohibited substances
Effect of drostanolone propionate on the binding of oestradiol and dihydrotestosterone by normal and malignant target tissues
Abstract
The influence of drostanolone propionate, an anticancer agent, was tested on the binding of 17 β-oestradiol and dihydrotestosterone to specific receptor proteins in tissue of normal and neoplastic target organs. Steroid binding capacity was measured by agar gel electrophoresis of tissue extracts.
Drostanolone was found to compete with androgen binding sites but not with oestrogen receptors. Therefore it is unlikely that the growth inhibitory effect of drostanolone propionate in human breast cancer is mediated through interaction with oestradiol binding proteins as suggested earlier by other authors.
Drostanolone is a DEA Schedule III controlled substance. Substances in the DEA Schedule III have a potential for abuse less than substances in Schedules I or II and abuse may lead to moderate or low physical dependence or high psychological dependence.
Drostanolone (also known as dromostanolone) is a potent synthetic androgenic anabolic steroid similar to testosterone. Drostanolone is indicated in postmenopausal women with recurrent breast cancer, in a combined hormone therapy.
Dromostanolone is a synthetic anabolic steroid related to dihydrotestosterone that has antiestrogenic effects. Dromostanolone inhibits the growth of estrogen receptor-presenting breast cancers; its virilizing effects limit its clinical usefulness. (NCI04)
Drostanolone
Drostanolone International Programme on Chemical Safety Poisons Information Monograph 901 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 Drostanolone 1.2 Group ATC Classification: A14 (Anabolic Agents for Systemic Use) A14A (Anabolic steroids) 1.3 Synonyms Compound 32379; Dromostanolone Propionate (USAN); 2-alpha-Methyldihydrotestosterone Propionate; NSC-12198 1.4 Identification numbers 1.4.1 CAS number 58-19-5 1.4.2 Other numbers CAS: 521-12-0 (drostanolone propionate) 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: Drostanolone: 17-beta-Hydroxy-2alpha-methyl-5alpha- androstan-3-one Drostanolone acetate: 17-beta-Hydroxy-2alpha-methyl- 5alpha-androstan-3-one propionate. Molecular formula Drostanolone: C20H32O2 Drostanolone acetate: C23H36O3 Molecular Weight Drostanolone acetate: 360.5 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. 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. 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: 487-490. Reynolds Ed. (1992) Martindale-The Extra Pharmacopeia. The Pharmaceutical Press. London. Roberts JT, & Essenhigh DM. (1986) Adenocarcinoma of prostate in 40-year old body builder. Lancet 2: 742. Ross RB, & Deutsch S I.(1990) Hooked on hormones. JAMA 263: 2048-2049. Ryan A J. (1981) Anabolic steroids are fool's gold. Fed Proc 40: 2682-2688. Schurmeyer T, Belkien L, Knuth UA, & Nieschlag E. (1984) Reversible azoospermia induced by the anabolic steroid 19-nortestosterone. Lancet i: 417-420. Soe KL. Soe M. & Gluud C. (1992). Liver pathology associated with the use of anabolic-androgenic steroids. Liver 12: 73-9. Schulte HM, Hall MJ, & Boyer M. (1993). Domestic violence associated with anabolic steroid abuse. Am J Psychiatr 150: 348. Spano F, & Ryan W G. (1989) Tamoxifen for gynecomastia induced by anabolic steroids? New Engl J Med 311: 861-862. Strauss RH, Liggett MT, & Lanese RR. (1984) Anabolic steroid use and perceived effects in 10 weight-trained women athletes JAMA 253: 2871-2873. Su T-P, Pagliaro M, Schmidt PJ, Pickar D, Wolkowitz O, & Rubinow DR. (1993) Neuropsychiatric effects of anabolic steroids in male normal volunteers. JAMA 269: 2760-2764. Wagner JC (1989). Abuse of drugs used to enhance athletic performance. Am J Hosp Pharm 46: 2059-2067 Webb O L, Laskarzewski P M, & Glueck, CJ. (1984) Severe depression of high-density lipo protein cholesterol levels in weight lifters and body builders by self-administered exogenous testerone and anabolic-andorgenic steroids. Metabolism 33: 971-975. Wilson J D. (1992). Androgens. In: Goodman Gilman A., Rall T W, Nies A S, & Taylor P. Goodman and Gilman's Pharmacological Basis of Therapeutics. McGraw-Hill, Toronto. Pages 1413-1430.


There are no reviews yet.