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It was determined whether all the different neuroendocrine actions of estrogen are competitively antagonized by phenothiazines to test the putative analogy between the 2 types of molecular receptor. 12 men aged 22-25 years were tested on 3 days and then given 2 X 20 mg ethinylestradiol (EE) for 4 days with either 2 X 50 mg chlorpromazine (6 cases) or a placebo (6 cases). Neurohypophyseal activity and adenohypophyseal activity were tested. There was a lack of significant changes in pulse, blood pressure, body weight, and psychosexual factors. Blood alkaline phosphatases decreased in all 12 men after estrogen, and an inhibitory effect of estrogens alone was seen on blood FSH and on the 2 and 5 fraction of urinary 17-keto-steroids. The neurophysine basal level and the growth hormone peak response to hypoglycemia showed a stimulatory effect. There was no effect on FSH by chlorpromazine or on the inhibition of 17-keto-steroids due to estrogens. However, chlorpromazine lessened the neurophysine increase and abolished the facilitatory effect of estrogens on growth hormone responsibeness to hypoglycemia. In 60% of the cases TSH blood levels were undetectable and unvaried.

The release of gonadotropin following the injection of synthetic LH- RH was studied in various physiological and experimental circumstances. In the male 25 mcg of LH-RH led to simultaneous release of FSH and LH prior to and during puberty. In adults on the other hand the same dose led only to an increase in LH while FSH levels remained unchanged. At higher doses there was FSH release and an increase in LH proportional to the amount of LH-RH injected. When FSH was released the increase was clearly less than that of LH and often occurred considerably later. In the female 25 mcg of LH-RH led to a clear-cut considerably later. In the female 25 mcg of prior to puberty. After the onset of puberty the degree of response was inverted; the increase in LH was greater than that of FSH. In normally menstruating women the FSH and LH response was greater during the luteal phase than during the preovulatory phase. Treatment with nonsequential hormonal contraceptives blocked FSH and LH release normally produced by the injection of 50 mcg of LH-RH. There was no effect when a dose of 100 mcg was injected. In postmenopausal women only LH rose following the administration of 25 mcg of LH-RH. After 5 days of treatment with 200 mcg ethinly estradiol the same dose of LH-RH led to simultaneous release of LH and of FSH. It is concluded that the secretory response of the gonadotropins to LH-RH is influenced by the endocrine equilibrium and more particularly by the interaction of the gonadal steroids which can alter the synthesis and/or the release of the pituitary gonadotropins.

Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels, the sperm count and the histologic appearance of the testis were studied in 56 patients with azoospermia or oligospermia. FSH is elevated in those cases of azoospermia where gametogenesis is arrested prior to spermatid differentiation. Serum FSH is normal, however, in most patients in whom spermatids and spermatozoa are detectable on testicular biopsy. There is no relationship between the sperm count and the concentration of serum FSH. No correlation exists between serum LH and either the sperm count or the stage of spermatogenesis as evaluated on testicular biopsy.

Publisher Summary This chapter deals with psycboendocrine problems in patients with a late diagnosis of congenital adrenal hyperplasia. The chapter emphasizes particularly on the psychologic disturbances that were shown by different tests. Congenital hyperplasia of the adrenals is the most common cause of female pseudohermaphroditism. Although some cases are detected at birth, others are so similar morphologically to males that recognition of true sex may be made only in childhood or even adolescence. In fact, even in the presence of androgenic hormones, our patient presents the “hermaphrodite identity” as described by Stoller.” This suggests that early hormonal impregnation and sociological impacts are not the only two factors that cause the male psychological differentiation in man.

Publisher Summary This chapter discusses gonadotropin levels in infertile patients. The assays of follicle stimulating hormone (FSH) and luteinizing hormone (LH) are of interest in the investigation of infertile patients for two reasons. First, the FSH and the LH concentrations provide an etiological diagnosis of the infertility, especially when the latter is one symptom of hypogonadism. Second, the FSH and the LH levels may be correlated with the endocrine function of the testis and with the degree of maturation of the germ cell in such patients. In hypogonadism, because of testicular lesions, there is often an extensive or complete loss of germ cell production. In the cases of azoospermia, because of abnormal spermatogenesis, the FSH levels are often greater than normal, indicating that the primary lesion is at the germinal epithelial level and that the pituitary responds to this deficiency by increasing its FSH secretion. In hypogonadism, because of the gonadal lesions, when there is an extensive or complete loss of germ cell production, the FSH levels are invariably elevated and the LH levels may be either normal or high depending on the degree to which sex steroid production is involved. By contrast, in patients with organic pituitary lesions, the FSH and the LH are sometimes below the limits of sensitivity of the assays usually employed but may be detectable, in which case they are generally low but occasionally normal.

Psychogenic impotency is a frequent disease whose neuroendocrine and partic ularly androgenic component is not perfectly understood. It is known that in man late castration or testicular organic disease does not necessarily alter the sexual potency; this agrees well with the common clinical observations of the poor efficiency of exogenous testosterone in the treatment of “impotentia coeun-di”. Nevertheless, a net decrease of urinary testosterone excretion has been noticed by Ismail et al. (1970) in a group of 28 impotent patients; in that study, individual values were very widespread. This work has also shown a lack of responsiveness of testes to exogenous HCG in 4 cases tested; however, to our knowledge, no sensitive LH assay has been realized until now, so that the central response to that peripheric insufficiency is not known.