睾丸腫瘍患者の睾丸機能に関する研究

抄録

It is known that cryptorchidism, testicular atrophy of post mumps orchitis, and various immature, dysgenetic testis are more likely to develop a tumor than normal testis.
Testicular atrophy and immature testis are believed to especially predispose tumor development.
Conversely, the function of the testis of a patient with a testicular tumor may be hypoactivated and may become immature, dysgenetic and atrophic. Therefore, I investigated from various approaches the functions of the testis of patients with testicular tumors who are under our care. I also investigated pituitary gonadotropin, to observe how it is related to the hypofunction of the testis. The 45 testicular tumor patients, from 20 to 39 of age, who are under care of the Department of Urology, Yokohama City University, School of Medicine and its affiliated hospitals.
1) Size of the opposite testis of a testicular tumor patient was measured.
The mean was 11.4±5.53ml (normal, 11.08-21.23ml), which was smaller than normal.
2) The semen of a testicular tumor patient was examined. The volume of the semen of a testicular tumor patient tended to be less than normal.
As for the number of the sperma, 80% of the patients examined had oligospermia or azoospermia.
3) In the orchiectomy of a testicular tumor patient, biopsy of the opposite testis was made in order to explore it histologically.
(1) Most of the seminiferous tubules examined (80%) were found to be with hypospermatogenesis. However, only a few of them showed such severeness as fibrosis and hyalinization of the tissue.
(2) The interstitial cell showed a slight proliferation.
(3) Hypertrophy of the wall of the blood vessel was milder than that of the normal blood vessel.
4) An examination was made of the fertility of a testicular tumor patient, before the discovery of the tumor.
(1) Infertility for over three years was found in about 20% of the patients examined.
(2) There was a tendency that even a patient, who had normal fertility and successfully impregnated, developed tumors after more than two years of infertility.
5) Pre-operative determination of hormones in the urine of a testicular tumor patient was made.
(1) Most of 1705, 17OHCS, estorogen in the urine was within a normal range.
(2) Pituitary gonadotropin in the urine was apt to be high.
Judging from the fact that a testicular tumor is developed in cryptorchidism at a high rate, that a tumor is often developed in testicular atrophy of post mumps orchitis, that a tumor is often developed in the immature, dysgenetic testis and that an experimental testicular tumor formation is related to testicular atrophy, it can be said that the development of a testicular tumor has a close causal relation with testicular hypofunction. In conformity with the above and in addition to the data obtained, I would like to state the following:
1) The testicular function, especially spermatogenesis of a testicular tumor patient is apt to be hypoactivated regardless of a definite cause such as cryptorchidism, immature and dygenetic testis and post mumps orchitis testicular atrophy.
2) Hypospermatogenesis precedes the development of a tumor.
3) Hypersecretion of FSH is developed for hypospermatogenesis.
4) I infer that under the conditions of hypospermatogenesis, a germ cell is stimulated by hypercrinism of FSH, and its proliferation is activated. At this point I can say that there is some unknown cause which directs the proliferation of the cell wrongly to result in a tumor.