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The Effects of Clomiphene in Impotence a Clinical and Endocrine Study

Published online by Cambridge University Press:  29 January 2018

Alan J. Cooper
Affiliation:
University of Edinburgh, Morningside Park, Edinburgh
A. A. A. Ismail
Affiliation:
Clinical Endocrinology Research Unit, 2 Forrest Road, Edinburgh EH10 5HF
T. Harding
Affiliation:
Professorial Unit, Royal Edinburgh Hospital, Morningside Terrace, Edinburgh
D. N. Love
Affiliation:
Clinical Endocrinology Research Unit, 2 Forrest Road, Edinburgh Send reprint requests to Dr. Cooper at Huntington Research Centre

Extract

Hormone treatment for impotence and impotentia ejaculandi (delayed or absent ejaculation in the presence of normal erections and desire) (Johnson, 1965) is based on two assumptions: namely—that (1) potency in the male is androgen dependent and (2) impotency is due to relative androgen deficiency (Miller, 1968; Margolis et al., 1967; Sobotka, 1969). The synthetic preparations most frequently used are methyl testosterone, various esters, including the propionate, deconate, enanthate, etc. (Tuthill, 1955; Kupperman, 1967) and more recently a number of testosterone- ‘aphrodisiac’ combinations (Margolis et al., 1967; Cooper et al., 1971, etc.). Despite some claims of therapeutic success for the various regimes, the administration of exogenous hormones has several pharmacologic disadvantages. For instance methyl testosterone, which has to be taken sublingually or bucally, may be associated with severe toxic effects such as cholestatic jaundice, etc. (Goodman and Gilman, 1965). Parenterally administered testosterone esters, although less toxic and more certainly absorbed than methyl testosterone, have all the drawbacks of the intramuscular route; also their rate(s) of tissue release may not be optimal for metabolism. Additionally, all these synthetic compounds may inhibit endogenous testosterone formation and spermatogenesis by suppressing pituitary gonadotrophins. Long term administration may result in Leydig cell inactivity and even disuse atrophy. Recently Harkness et al. (1964, 1968) have observed that clomiphene (Fig. 1), a non-steroid triethylene derivative which in females stimulates the anovulatory ovary to secrete oestrogens (Bishop, 1970), significantly raised the levels of urinary steroid metabolites, including testosterone, in a proportion of ‘normal’ and corticosteroid deficient males. This unexpected testosterone elevating effect suggested its possible ‘experimental’ use as an alternative drug treatment in impotence. Accordingly a limited pilot study on five ‘primary’ (non-organic) impotent males was conducted: its main aims were (a) to assess the potential clinical utility of the drug and (b) to study its effects on the ‘pituitary-testes-axis' as reflected by plasma testosterone levels.

Type
Research Article
Copyright
Copyright © Royal College of Psychiatrists, 1972 

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References

Bishop, P. M. F. (1970). Brit, med. Bull., 26, 27.CrossRefGoogle Scholar
Butler, P. W. P., and Besser, G. M. (1968). Lancet, i, 1234.CrossRefGoogle Scholar
Carroll, B.J. et al. (1968). Brit. med. J., 2, 285.CrossRefGoogle Scholar
Cooper, A. J. (1967). M.D. Thesis. Bristol University, England.Google Scholar
Cooper, A. J. (1969). J. psychosom. Res., 13, 143.CrossRefGoogle Scholar
Cooper, A. J. Ismail, A. A. A., Smith, C. G., and Loraine, J. A. (1970). Brit. med. J., ii, 17.CrossRefGoogle Scholar
Cooper, A. J. Ismail, A. A. A., Loraine, J. A., Smith, C. G., and Love, D. N. (1971). Journ. din. Trials (in press).Google Scholar
Gessa, C. L. et al. (1970). Nature, 616–17.CrossRefGoogle Scholar
Goodman, L. S., and Gilman, A. (Ed.) (1965). The Pharmacological Basis of Therapeutics. New York: Macmillan.Google Scholar
Harkness, R. A., Bell, E. T., Loraine, J. A., and Morse, W. I. (1964). J. Endocrin., 31, 53.CrossRefGoogle Scholar
Harkness, R. A., Bell, E. T., Loraine, J. A., Ismail, A. A. A., and Morse, W.I. (1968). Acta endocrin., 58, 38.Google Scholar
Ismail, A. A. A., and Harkness, R. A. (1967). Acta endocrin., 56, 469.Google Scholar
Ismail, A. A. A., Davidson, D. W., Loraine, J. A., Cullen, D. R., Irvine, W. J., Cooper, A. J., and Smith, C. G. (1970). In: Symposium on Reproductive Endocrinology (ed. W. J. Irvine). Livingstone: Edinburgh.Google Scholar
Ismail, A. A. A., Love, D. N., and Nieschlage, E. (1971). In: Research on Steroids, IV, 311–6.Google Scholar
Johnson, J. (1965). J. psychosom. Res., 9, 195.CrossRefGoogle Scholar
Kupperman, H. S. (1967). In: The Encyclopedia of Sexual Behaviour (ed. A. Ellis, and A. Arbarbanel). Hawthorn: New York.Google Scholar
Margolis, R., Snagree, H., Prieto, P., Stein, L., and Chinn, S. (1967). Curr. Therap. Res., 9, 213.Google Scholar
Miller, W. W. (1968). Curr. Therap. Res., 10, 354.Google Scholar
Sobotka, J. J. (1969). Curr. Therap. Res., 11, 87.Google Scholar
Tagliamonte, A., Tagliamonte, P., Gessa, A., and Brodie, B. B. (1969). Science: N.Y., 166, 1433.CrossRefGoogle Scholar
Tuthill, J. F. (1955). Lancet, i, 124.CrossRefGoogle Scholar
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