6.2.2 Hypogonadotrophic hypogonadism
Aetiology, diagnosis and therapeutic management
Hypogonadotrophic hypogonadism is caused either by hypothalamic or pituitary diseases.
The failure of hormonal regulation can easily be determined [3].
Endocrine deficiency leads to a lack of spermatogenesis and testosterone secretion due to decreased
secretion patterns of LH and FSH. The therapy of choice is human chorionic gonadotrophin (hCG) treatment,
with the later addition of human menopausal globulin (hMG), dependent on initial testicular volume [4].
If hypogonadotrophic hypogonadism is hypothalamic in origin, a 1-year therapy with pulsatile gonadotrophin
releasing hormone (GnRH) is as effective as gonadotrophins in stimulating spermatogenesis [5].
Once pregnancy has been induced, patients will go back to testosterone substitution (see below).
Conclusion
Effective
drug therapy is available to achieve fertility in men with
hypogonadotrophic hypogonadism.
6.2.3 Hypergonadotrophic hypogonadism
Aetiology, diagnosis and therapeutic management
Common conditions associated with hypergonadotrophic hypogonadism in younger men include injury to and
loss of the testicles (e.g. after bilateral testicular cancer) (Table 11). More recently it has been recognized that
hypogonadism may occur after extensive testicular biopsy to recover sperm for IVF/ICSI [6]. Men with Klinefelter's syndrome are at risk for spontaneous hypogonadism with ageing. Those undergoing extensive testicular biopsy in the context of IVF/ICSI will almost certainly have an exacerbated risk [7]. Hypergonadotrophic hypogonadism may occur spontaneously in the elderly, in patients with erectile dysfunction [8], and after LHRH treatment or surgical castration for prostatic cancer [9]. All these conditions are not clinically significant for infertile men. Hypogonadism may be associated with osteoporosis [10]. The laboratory diagnosis of hypergonadotrophic hypogonadism is based on decreased serum testosterone and increased LH levels [2]. Additional prolactin measurement is suggested.
Testosterone
supplementation is only indicated in men with levels consistently
lower than normal (< 12nmol/l
= 300 ng/dl).
Injectable,
oral and transdermal testosterone preparations are available for
clinical use [2]. The best preparationis
the one that maintains serum testosterone levels as close to
physiological concentrations as possible [11].
6.2.4 Conclusion
There is general agreement that patients with primary or secondary hypogonadism should receive testosterone substitution therapy.
6.2.5 References
1. Nachtigall LB, Boepple PA, Pralong FP, Crowey WF Jr.
Adult-onset idiopathic hypogonadotropic hypogonadism - a treatable form of male infertility. New Engl J Med 1997; 336: 410-415.
2. Nieschlag E, Behre HM.
Testosterone: Action, Deficiency, Substitution, 2nd edition. Springer: Berlin, 1998.
3. World Health Organization.
WHO manual for the standardized investigation, diagnosis and management of the infertile male. Cambridge University Press, 2000.
4. Burris AS, Rodbard HW, Winters SJ, Sherins RJ.
Gonadotropin therapy in men with isolated hypogonadotropic hypogonadism: the response to human chorionic gonadotropin is predicted by initial testicular size. J Clin Endocrinol Metab 1988; 66: 1144-1151.
5. Schopohl J, Mehltretter G, von Zumbusch R, Eversmann T, von Werder K.
Comparison of gonadotropin-releasing hormone and gonatropin therapy in male patients with idiopathic hypothalamic hypogonadism. Fertil Steril 1991; 56: 1143-1150.
6. Manning M, Junemann KP, Alken P.
Decrease in testosterone blood concentrations after testicular sperm extraction for intracytoplasmic sperm injection in azoospermic men. Lancet 1998; 352: 37.
Tournaye H, Staessen C, Liebaers I, van Assche E, Devroey P, Bonduelle M, Van Steirteghem A. Testicular sperm recovery in nine 47,XXY Klinefelter patients. Hum Reprod 1996; 11: 1644-1649.
Gray A, Jackson DN, McKinlay JB.
The relation between dominance, anger, and hormones in normally aging men: results from the Massachusetts Male Aging Study. Psychosom Med 1991; 53: 375-385.