L. Kiesel – författare

In 1920, Hirose demonstrated the luteinising effect of placental tissue and one year later, Evans and Long described luteinised ovaries in rats treated with hypophysial extracts. In 1926, Zondek and Aschheim as well as Smith, independently of each other, showed that a gonad-stimulating hormone was secreted by the adenohypophysis. In 1927, Aschheim and Zondek found their "Prolan" in human pregnancy urine and the first reliable pregnancy test was available. In the following years it could be demonstrated that the gonadotropic hormones from pituitary and from pregnancy urin were not of identical structure. During the years 1931 - 1933 Fevold and coworkers prepared follicle stimulating hormone from sheep pituitaries which were free of other hormone activities. Already in 1934, Collip found "antihormones" in animals treated with proteinhormones from animals of another species. It could be shown that they were antibodies against these hormones and this was the future basis for the immunological era starting in 1960. The quantitative determination of gonadotropins has been performed over several decades by difficult bioassays and since 1960 immunological and later radioimmunological assays became available. Since that time a new field was opened for the studies of gonadotropins. During this time, highly purified preparations of gonadotropins were available for research and clinical treatment. I recall the first successful attempt of inducing follicle growth and ovulation by Gemzell and coworkers 1958 as well as by Lunenfeld and Bettendorf at about the same time.

Atrophy of gonadotrophin producing cells Exogenously LH synthesis administered androgens and release or anabolic steroids are decreased Prostate Testes Normal function. Testosterone synthesis in The deficit of endogenously Leydig cells is decreased. The synthesized testosterone is exogenously administered compensated for by the steroid is not able to exogenously administered compensate for the deficit of steroid endogenously synthesized testosterone Figure 2 Intratesticular and serum testosterone concentrations after treatment with andro­ gens or anabolic steroids in order to substitute for the peripheral androgen deficiency and to achieve azoospermia. Because this steroid is alkylated in position 17, toxic effects on liver function can not be excluded. Danazol offers no advantages as compared with other anabolic steroids; rather, disadvantages. Numerous experiments of this type have been performed during the last 40 or 50 years. The outcome in each case was more or less identical: with a certain dose of an androgen or anabolic steroid it is possible to inhibit spermatogenesis without interfering with other androgen-dependent func­ tions, including libido (potentia coeundi) and accessory sexual glands. On the basis of this pharmacological-endocrinological background, androgens and anabolic steroids can be used for male fertility control, and several clinical trials have been performed during the last 10-15 years. Some of 1 these studies 2-23 are mentioned in Table 2.

Atrophy of gonadotrophin producing cells Exogenously LH synthesis administered androgens and release or anabolic steroids are decreased Prostate Testes Normal function. Testosterone synthesis in The deficit of endogenously Leydig cells is decreased. The synthesized testosterone is exogenously administered compensated for by the steroid is not able to exogenously administered compensate for the deficit of steroid endogenously synthesized testosterone Figure 2 Intratesticular and serum testosterone concentrations after treatment with andro­ gens or anabolic steroids in order to substitute for the peripheral androgen deficiency and to achieve azoospermia. Because this steroid is alkylated in position 17, toxic effects on liver function can not be excluded. Danazol offers no advantages as compared with other anabolic steroids; rather, disadvantages. Numerous experiments of this type have been performed during the last 40 or 50 years. The outcome in each case was more or less identical: with a certain dose of an androgen or anabolic steroid it is possible to inhibit spermatogenesis without interfering with other androgen-dependent func­ tions, including libido (potentia coeundi) and accessory sexual glands. On the basis of this pharmacological-endocrinological background, androgens and anabolic steroids can be used for male fertility control, and several clinical trials have been performed during the last 10-15 years. Some of 1 these studies 2-23 are mentioned in Table 2.