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The high prevalence of men with varicoceles who by history are fertile has led some to question the suggested causal relationship between a varicocele and male infertility. However, testicular function in these fertile men has not previously been studied in detail. Fifty-five normal fertile men, 42 fertile men with varicoceles, and 24 infertile men with varicoceles and normal female partners were studied. Semen analyses were done, baseline serum testosterone and gonadotropin levels tested and the gonadotropin response to luteinizing hormone-releasing hormone (LH-RH) measured. The infertile men with varicoceles exhibited lower sperm counts, abnormal sperm morphologic features, increased baseline serum gonadotropins, and increased gonadotropin responses to LH-RH, compared with the normal fertile men. The fertile men with varicoceles showed similar abnormalities, although this was not statistically significant in all cases. That semen and hormone abnormalities were observed in both the fertile and infertile men with varicoceles suggests that the presence of a varicocele is associated with some degree of primary testicular dysfunction, regardless of present fertility status.

Fourteen patients with hypogonadotrophic eunuchoidism (HE), 10 males and 4 females, received luteinizing hormone-releasing hormone (LH-RH) as 4-h intravenous infusions of 0.2 μg/min or as subcutaneous (sc) injections of 200 μg. Repeated LH-RH administration over 4 days (200 μg sc daily) was undertaken in 8 patients. Eight of the 10 males and all 4 of the females were found to have definite elevations of luteinizing hormone (LH) and follicle stimulating hormone (FSH) following their first exposure to exogenous LH-RH. The patients included 2 males and 1 female with variant forms of HE, all of whom showed responses of both gonadotrophins.When the first exposure of HE patients to exogenous LH-RH was as a 4-h infusion, the biphasic pattern of LH increase characteristic of normal adults was not found. Instead, a monophasic and qualitatively small LH increase occurred, similar to that found in pre-pubertal children and in anorexia nervosa. In 2 patients with an initially abnormal LH response, a 4-h LH-RH infusion following 4 days of LH-RH injections (200 μg sc/day) produced a normal biphasic LH increase. These results imply that maintenance of the two pools of pituitary LH demonstrable in normal adults depends on adequate production of endogenous LH-RH.Increases in FSH following the initial exposure to LH-RH were generally as great or greater than those of normal adults in spite of the fact that LH responses tended to be smaller than those of adults. Four days of LH-RH administration (200 sc daily) did not lead to consistent increases in gonadotrophin responsiveness. Increases of testosterone or oestradiol production could not be demonstrated, even with 4 to 5 days of LH-RH administration. Exogenous sex hormone therapy markedly inhibited gonadotrophin responsiveness to LH-RH.

In order to study the ability of the sperm penetration assay (SPA) to correctly classify the fertility status of men, we prospectively examined the results of the SPA performed on the semen of three groups of men of known fertility status. The groups included 67 normal men without varicoceles whose wives were pregnant (VARN), 51 men with a palpable varicocele whose wives were pregnant (VARF), and 30 infertile men with varicoceles (VARI). Two SPAs were done on each subject. Ninety-seven percent of the VARIs showed<15% penetration on a single test, and 91% showed<15% on both tests. On a single test 61% of the VARNs and 68% of the VARFs were<15%. If 0 penetration were used as the criteria of infertility, then 40% of the VARIs, 27% of the VARFs, and 12% of the VARNs would be classified as being infertile. These data suggest that the SPA cannot independently define male fertility status and should be used in conjunction with the standard semen analysis and clinical evaluation of the couple to assess male fertility potential.

Three men who volunteered as normal subjects were found to have abnormally high levels of serum follicle-stimulating hormone (FSH) despite having normal seminal fluid analyses and fertility. Two of the men had a history of previous orchitis, and one had an atrophic testis. Serum luteinizing hormone and testosterone levels were normal. These cases appear to represent compensated primary testicular disease, with normal sperm counts and fertility maintained at the expense of chronically elevated FSH levels. These results imply that in certain situations, the measurement of serum FSH levels may be a more sensitive index of testicular disease than the performance of seminal fluid analyses.

Ocular symptoms developed in four out of 58 patients during clomiphene citrate administration. Ophthalmologic examination revealed scotomata development which disappeared after drug was discontinued in one subject. It recurred with readministration of clomiphene citrate but not with a placebo.The ocular symptoms in three subjects were reversed by discontinuance of clomiphene citrate. The symptoms disappeared while the drug was still being administered to the fourth patient.

Testicular biopsy specimens from fifteen normal adult men were analysed histologically, using Clermont's classification for the germ cell types. After corrections were made for differences in nuclear size and life-span, spermatid/primary spermatocyte ratios ranging from 0·87 to 3·82 (average 2·58) were found. This represents a marked reduction from the theoretical ratio of 4·0 which would be expected. The significance of this attrition rate, or the point at which loss occurs, is not known.

In 1935, Collip and Anderson (1) observed that animals treated with anterior pituitary extracts became refractory after an initial period of stimulation. Serum from refractory animals inhibited the actions of hormone administered to untreated animals. These inhibitory substances have been termed »antihormones«. Most of the information concerning the antihormone phenomenon has been obtained during the past two decades from experiments involving the administration of gonadotrophic hormones. The antihormones which form as a result of administering gonadotrophic hormones are called antigonadotrophins.Antihormones do not form spontaneously; they have not been demonstrated in untreated individuals. Moreover, with rare exceptions, antihormones do not form when recipient and donor of the hormone are of the same species. Antihormones may be passively transferred; the injection of a treated animal's plasma which contains antihormones can prevent the action of the hormone administered to previously untreated animals. The mechanisms governing the formation of antihormones are

The presence of an extra chromosome in the cells of patients with 47,XXY Klinefelter's syndrome and hypogonadism appears to be related phenomena. Testicular histopathology and function were compared in six patients with a 47,XXY karyotype and six patients with a 46,XY/47,XXY karyotype determined upon testicular cells. In addition, the frequency of clinical, histological, and hormonal abnormalities in these two groups of patients was compared following an extensive literature review. A greater degree of damage to the seminiferous tubules and germinal epithelium was found in the 47,XXY patients than in the 46,XY/47,XXY group. These results indicate that the normal 46,XY cells modify the damaging effect to the testis of the 47,XXY cells. This evidence supports a cause-effect relationship between the extra X chromosome and spermatogenesis in Klinefelter's syndrome.

Hypogonadotropic hypogonadism with anosmia has been found in two brothers and a half sister, who are related through the same mother. Although the mother does not have the full syndrome, her history suggests she may have minor symptoms of the syndrome. X-linked inheritance seems most compatible with the familial distributions. Differences of this syndrome from other inherited hypogonadal conditions are discussed. The genetic defect is thought to directly or indirectly affect the hypothalamus which has associations with both olfaction and pituitary function. The importance of testing for anosmia in patients with abnormality in sexual development is noted.