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Use and misuse of androgen.

Use and misuse of androgen. Abdulrahman Alshaikh. Introduction.

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Use and misuse of androgen.

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  1. Use and misuse of androgen. Abdulrahman Alshaikh.

  2. Introduction. • Steroid misuse/abuse has become common in the past decade or two. Prominent among the reasons for abuse are athletic performance and look good. Abuse in girls is rising and is correlated with other risky behaviors. New regulations at the national level have been developed to curb this abuse and legislation to educate youth has become law.

  3. What are Androgens? Androgens are the sex steroids or hormones that produce changes in body shape (muscle gain, fat distribution) and secondary sexual characteristics (hair and beard growth, penile growth) typical of men. Androgens play a major and essential role in reproductive and sexual function in the mature male. The most important androgen in men is testosterone.

  4. What are Steroids? The synthetic derivative of androgens (male sex hormones) are commonly referred to as 'anabolic-androgenic steroids'. (Street name: 'roids'). Anabolic effects include the promotion of skeletal muscle growth Androgenic effects refer to the development and maintenance of male sexual characteristics

  5. When are Androgens misused or abused? The medical misuse of androgens may occur in such settings as male infertility, male sexual dysfunction and 'male menopause'. There is no good evidence to show that testosterone treatment is effective and safe for older men where androgen deficiency has not been clinically proven. Until further evidence is available, such treatment can not be recommended. In the wider community, misuse of androgens in sport is also an issue with some athletes using androgens outside the rules of their particular governing body and without knowledge of the long-term affects on the body. Disqualification may occur if androgens are used in this setting.

  6. Causes of androgen deficiency. • Testicular disease as testicular damage and klinefelters syndrome. • Pituitary diseases. • Chronic diseases, severe illness, drug use, ageing, can lead to combined pituitary and testicular diseases.

  7. Testicular causes: Classical androgen deficiency Testicular disorders Klinefelter’s syndrome and variants (mosaic) Cryptorchidism and defects of testis development Orchitis Orchidectomy (advanced prostate cancer, bilateral testicular cancer) Toxin exposure (cancer chemotherapy or radiotherapy, environmental, occupational and domestic toxins)

  8. Pituitary causes Hypothalamic–pituitary dysregulation Idiopathic hypogonadotropic hypogonadism and variants: Kallmann’s syndrome (associated with anosmia and midline cranial defects; caused by mutations in the KAL1 or FGRF1 [fibroblast growth factor receptor 1] genes) Other genetic causes (including inactivating mutations in the DAX-1 [adrenal hypoplasia congenita], GnRH-receptor or GPR54 [G protein-coupled receptor] genes) Pituitary tumour and treatment (surgery, irradiation) Haemochromatosis Craniopharyngioma

  9. Partial or transient androgen deficiency Constitutional delay of puberty Acute critical illness, burns, major trauma or surgery Drug use (eg, opiates, glucocorticoids, anabolic steroids) Chronic disease and its treatment Ageing (“late-onset” androgen deficiency)

  10. Clinical features. • During fetal life; disrupts male sexual differentiation and somatic development. • In adolescence ; incomplete or late sexual and somatic maturation. • In adult life; deficiency of some features of virilization, reduce sense of well-being, mood changes, decrease libido, rarely flushing, weight gain, loss muscle mass,

  11. Medical uses of androgen. • Delayed puberty in male. • Primary or secondary androgen deficiency in adults. Androgen replacement • Elderly patients with androgen deficiency with no pituitary diseases – controversy. • Very debilitated illness – controversy.

  12. General principles of testosterone treament. • Should be giving only to man who is hypogonadal. • Testosterone can be replaced satisfactory whether the testosterone deficiency either due to primary or secondary hypogonadism. • Testosterone replacement due to ageing is uncertain.

  13. Testosterone preparations. • Alkylated preparations. • Testosterone ester. • Transdermal. • Gel. • Buccal tablet.

  14. Androgen therapy. • Life long and should be started after androgen deficiency has been proved. • Testosterone rather synthetic androgens should be used. • 17- alkylated androgen are hepatotoxic and should not be used for ART.

  15. USE OF ANDROGENS AND OTHER DRUGS BY ATHLETES *TO IMPROVE THEIR PERFORMANCE *THEY ARE MOTIVATED TO WIN. *1950 USED BY BODY BUILDER..

  16. How this area of medicine is different? • Athletes often obtain the medications from sources other than physician. • Athletes obtain information from other athletes, trainer, magazine, and the internet. • Take several medication simultaneously. • They discontinue it periodically to ovoid detection. • Physician who see the athletes are often unaware that they are taken these medication. • Physician knowledge of the possible effects of these medications is poor.

  17. EPIDEMIOLOGY. IT IS DIFFICULT. 10 OUT OF 26 OF POWER LIFFTING.(baltimor1996) 9% OF MALE AND 2% OF FEMALE IN GYMNASIA IN ENGLAND (int.j sport med 1997) SOUTH AFRICA SCHOOLCHILDERN 3% OF MALE AND .1% OF FEMALE.(s afr. Med j 1998)

  18. HISTORY. 1930 MAINTAIN AGING. 1950 ATHELET BEGAN TO USE IT. ILLEGAL BY LAW. 1990 WERE ADDED TO PROHIBITED DRUDS. (SCHEDULE I.). 1-5 YEAR IN PRISON UP TO 25000 DOLLARS.

  19. EFFICACY. INCREASE MASS AND MUSCLE STRENGTH. 43 NORMAL MEN ASSIGNED TO 4 GROUPS WITH OR WITHOUT EXERCISE AND WITH TESTOSTERONE OR WITH PLACEBO. TESTOSTERONE TREATED GROUP INCREASED FATE –FREE MASS AND MUSCLE STRENGTH AND MORE IN THOSE WHO EXERCISED (N ENGL J MED 1996) NOT WITH ANDROSTENEDIONE. (JAMA 1999)

  20. SIDE EFFECTS. SUPPRESSION OF ENDOGENNOUS TEST. FU. GYNEACOMATSIA. ERYTHROCYTOSIS. HEPATOTOXICITY. PSYCHOLOGICAL DISORDER. CARDIAC DISEASE. SERUM LIPIDS. VIRILIZATION. PREMATURE EPIPHYSEAL FUSION. INFECTION.

  21. TESTICULAR FUNCTION. SUPPRESS GONADOTROPIN SECRETION. SUPPRESS ENDOGENOUS TESTICULAR FUN. REDUCED SPERMATOGENESIS AND FERTIL. SPERM COUNT RETURN WITHIN 4 MONTHS. TESTICULAR SIZE DEREASED. GONADOTROPIN AND TEST. REMAIN LOW FOR MONTHS.) (fertil steril 1989)

  22. GYNECOMASTIA. TESTERONE CONVERTED TO ESTRADIOL VIA AROMATASE ENZYME. DEHYDROTESTOSTERONE DO NOT CAUSE.

  23. ERTHOCYTOSIS. COMMON. ALL ANDROGEN. DIRECT STIMULATION OF ERYTHROCYTOSIS.

  24. COAGULATION ACTIVATION OF HEMOSTATIC SYSTEM. HIGH THROMBIN –ANTITHROMBIN COMPLEXES IN PLASMA. INCREASE PLASMA PROTHROMBIN FRAGMENT, ANTITHROMBIN-III AND PROTIEN - S. TISSUE PLASMINOGEN ACTIVATOR AND ITS INHIBITOR. INCREASED PLATELET AGGREGATION

  25. INFECTION. LOCAL ABSCESS. SEPTIC ARTHRITIS. HIV INFECTION. IMMUNOGLOBULIN AND T CELL CHANGES.

  26. HEPATOTOXCICTY. 17 ALPHA-ALKYLATED ANDROGEN. ELEVATED LIVER ENZYMES.(clin.chm act 1962) CHOLESTATIC JAUNDICE. PLIOSIS.(med sci sports exerc 1994) HEPATOMA.

  27. CARDIAC. SUDDEN DEATH. HIGH BLOOD PRESSURE. MYOCARDITIS. THROMBOTIC COMPLICATION. FLUID RETENTION.

  28. LIPIDS. INCREASE LDL. DECREASE HDL.

  29. NEUROLOGICL CHANGES. CEREBROVASCULAL HEMORRHAGE. INCREASE INTRACRANIAL HYPERTENSION. TIA.

  30. PSYCHOLOGICAL. MAJOR MOOD DISORDER. AGGRESSIVE BEHAVIOR.

  31. STUNTING GROWTH. PREMATURE EPIPHYSEAL CLOSURE.

  32. DETECTION. SUSPECTED CLINICALY AND LAB. IN WOMEN: HIRSUTISM, ACNE, IRREGULAR MENSES, DECREASE BREAST AND UTERUS SIZES. CHROMATOGRAPHY AND MASS SPECTROSCOPY FOR OTHER THAN TESTO.

  33. DETECTION IN MALE. QUICK WEIGHT AND MUSCLE GAIN. PURPLE AND RED PURPULE SPOTS. SWELLING OF THE FEET AND LEGS. TREMBLING. DARKENING OF SKIN. BAD BREATH. AGGRESSIVE BEHAVIOR.

  34. TESTOSTERONE. CANNOT BE DISTINGUISHED FROM ENDOGENOUS. URINARY RATIO OF TES. TO ITS ENDOGENOUS EPIMER WILL BE HIGH (urinary ratio of testosterone to epitetosterone <6:1 but in those patients the ratio increased). (cli chem1992). RATIO OF URINE TEST. TO LH >30 (clini chm 1997)

  35. OTHER DRUGS. STIMULANTS. ETHROPOIETIN. GROWTH HORMONE. ISULIN. CREATINE.

  36. STIMULANTS. AMPHETAMINE. CAFFEINE. DETECTED EASLY. LESS REGULATED EVENTS.

  37. GROWTH HORMONE. MORE MUSCL LESS FAT. IT IS NOT YET TESTED FOR. EFFICACY NOT YET DEMONSTRATED. LITTL INFORMATION ABOUT DETECTION. IGF-1 (j clin endocrinol metab 2000) PROCALLAGEN TYPIII AND OSTEOCALCIN.(j clin endocrinology metabolism2000)

  38. CREATINE. • PROFESSIONAL. • 48% OF MALE AND 4% OF FEMAL (clin j sport med 1999) • ENHANCES PERFORMANCE IN SHORT DURATION. • WT GAIN ,ACUTE INTERSTITIAL NEPHRITIS,PROGRESSION RENAL DISEASE.

  39. CYPROHEPTADINE. SEROTONIN AND HISTAMINE ANTAGONIST. INCREASE LH AND TESTOSTERONE.

  40. AMINO ACID. NITROGEN RETENTION AND ENHANCE PROTEIN FORMATION>MUSCLE GROWTH. NO CLINICAL DATA SUPPORT BENEFIT. POSSIBLE RENAL DAMAGE.

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