남성 성선기능부전증의 임상적 고찰

Abstract

[한글]

남성 성선기능부전증은 정자형성의 이상, 남성홀몬 분비의 감소 또는 위 모두의 경우와, 또는 이차성징 발현의 장애등을 나타내는 진단명으로 과거로부터 많은 임상적 연구가 되어왔다.

1980년 5월부터 1982년 7월까지 연세의대부속 세브란스병원 비뇨기과로 내원하여 남성 성선기능부전증 진단을 받은 환자 29례를 대상으로 임상적 고찰 및 홀몬변화를 측정하여 다음과 같은 결론을 얻었다.

1. 환자의 이학적 소견은 내원시기의 사춘기 전후에 따라 달랐다.

2. 중요한 임상소견은 남성 이차성징의 발현이 늦어지는 것이었으며, 그외에 여성형 유방이 7례, 무후각증과 무고환증이 각각 4례, 정류고환이 3례, 지능박약이 1례 있었다.

3. 고환 용적은 환관증의 경우 2.5±0.8mg였고, 유환관증의 경우 2.4 ± 1.8㎖ 였다.

4. 음경 길이는 환관증의 경우 4.4±1.2cm였고, 유환관증의 경우 2.8 ± 1.4cm 였다.

5. 환관증의 혈청 FSH는 62.4±20.5mIU/㎖, LH는 65.0±23.6mIU/㎖, testosterone은 1.6±1.4ng/㎖, prolactin은 10.2±4.2ng/㎖였고, 유환관증의 혈청 FSH는 3.5±1.9mlU/㎖, LH는 5.3± 2.8mIU/㎖, testosterone은 0.9±0.6ng/㎖였다.

6. 환관증의 원인으로는 klinefelter씨 증후군이 5례로 가장 많았으며, 이차적으로 생긴 무고환증이 4례, 이하선염성 고환염의 과거력이 있는 고환위축이 2례, 외상으로 인한 고환위축이 1례, 원인을 모르는 경우가 3례였다.

7. 유환관증의 경우 kallmann씨 증후군으로 생각된 예가 4레, 뇌하수체 병변으로 생각된 예가 2례, 성선자극홀몬결핍과 GH결핍이 동반된 예가 2례였다.

8. 환관증의 경우 남성홀몬 치료로 이차성징의 발현, 성교능력의 증가와 유지가 가능하였다.

9. 유환관증의 경우 치료후 추후관찰 기간이 짧아 조정기능은 언급할 수 없으나, 성교능력을 유지하고, 조정기능을 유발하여, 유지할 수 있는 가장 좋은 방법은 human chorionic, gonadotropin과 human menopausal gonadotropin 병용치료인 것으로 생각되었다.

이상의 결과로 보아 남성 성선기능부전증 환자에서도 적절한 홀몬요법으로 정상인과 같은 성생활을 유지할 수 있고 특히 유환관증의 경우 장기간의 홀몬요법으로 정상적인 성생활과 생식도 가능한 것으로 생각된다.

Clinical investigation of male hypogonadism

Jae Yup Hong

Department of Medical Science The Graduate School Yonsei University

(Directed by Prof. Moo Sang Lee, M.D.)

Male hypogonadism refers to decrease in Leydig cell function, diminished or

absent spermatogenesis, or both defects in tandem.

The results of clinical investigation on 29 patients with male hypogonadism seen

in urology department of Severance hospital from May, 1980 to August, 1982 are

reported.

The results were as follows ;

1. Physical findings varied according to whether onset occurred before or after

puberty.

2. The major physical finding was delay in sexual maturation.

In addition, gynecomastia was found in 7 cases, hyposmia or anosmia in 4 cases,

secondary bilateral anorchia in 4 cases, cryptorchidism in 3 cases and mental

retardation in 1 case.

3. In patients with hypergonadotropic hypogonadism(eunuch group), testicular

volume was 2.5 : 0.8㎖.

In patients with hypogonatotropic hypogonadism(eunuchoid group), testicular

volume was 2.4 ± 1.8㎖.

4. In patients with hypergonadotropic hypogonadism, penile length was 4.4 ±

1.2cm.

In patients with hypogonadotropic hypogonadism, penile length was 2.8 ± 1.4cm.

5. In patients with hypergonadotropic hypogonadism, plasma FSH was 62.4 ±

20.5mIU/㎖, plasma LH 65.0 ± 23.6mIU/㎖, plasma testosterone 1.6 ± 1.4ng/㎖ and

plasma prolactin 10.2 ± 4.2ng/㎖.

In patients with hypogonadotropic hypogonadism, plasma FSH was 3.5 ± 1.9mIU/㎖,

plasma LH 5.3 ± 2.8mIU/㎖ and plasma testosterone 0.9 ± 0.6ng/㎖,

6. The cause of hypergonadotropic hypogonadism was Klinefelter's syndrome in 5

cases, prepubertal traumatic bilateral anorchisms in 2 cases, postpubertal

bilateral anorchisms for seminoma or torsion in 2 cases. Testicular atrophy was

found in 3 cases, 2 cases having past history of mumps orchitis and 1 case having

past history of trauma. In 3 cases, no etiology could be identified.

7. The cause of hypogonadotropic hypogonadism was a Kallamnn's syndrome in 4

cases. In two other cases, a pituitary lesion was suspected but could not be

confirmed due to absence of pituitary hormone reserve function test. Two cases were

identified as gonadotropin deficiency with growth hormone deficiency.

8. In patients with hypergonadotropic hypogonadism, androgen replacement therapy

with a testosterone preparation was performed. After the treatment, improvement of

male secondary sex characteristics such as hair growth, voice change ,enlargement

of penis size and scrotum size was noted.

Promotion and maintenance of sexual potency was also noted.

9. The patients with hypogonadotropic hypogonadism were treated with androgens,

HCG or HCG and HMG. However, due to the short period of therapy and follow-up, no

firm conclusions about treatment efficacy in this group can be drawn. Howeverl, the

best therapy to promote fertility should have been human chorionic gonadotropin

combined with human menopausal gonadotropin.

In conclusion, it appears that long-term treatment with androgen preparation

promotes sexual potency and improves male secondary sex characteristics in

hypergonadotropic hypogonadism.

In addition, long-term treatment with human chorionic gonadotropin combined with

human menopausal gonadotropin may provide an efficient means of treating paitients

with hypogonadotropic hypogonadism to obtain potency and fertility.

[영문]

Male hypogonadism refers to decrease in Leydig cell function, diminished or absent spermatogenesis, or both defects in tandem.

The results of clinical investigation on 29 patients with male hypogonadism seen in urology department of Severance hospital from May, 1980 to August, 1982 are reported.

The results were as follows ;

1. Physical findings varied according to whether onset occurred before or after puberty.

2. The major physical finding was delay in sexual maturation.

In addition, gynecomastia was found in 7 cases, hyposmia or anosmia in 4 cases, secondary bilateral anorchia in 4 cases, cryptorchidism in 3 cases and mental retardation in 1 case.

3. In patients with hypergonadotropic hypogonadism(eunuch group), testicular volume was 2.5 : 0.8㎖.

In patients with hypogonatotropic hypogonadism(eunuchoid group), testicular volume was 2.4 ± 1.8㎖.

4. In patients with hypergonadotropic hypogonadism, penile length was 4.4 ± 1.2cm.

In patients with hypogonadotropic hypogonadism, penile length was 2.8 ± 1.4cm.

5. In patients with hypergonadotropic hypogonadism, plasma FSH was 62.4 ± 20.5mIU/㎖, plasma LH 65.0 ± 23.6mIU/㎖, plasma testosterone 1.6 ± 1.4ng/㎖ and plasma prolactin 10.2 ± 4.2ng/㎖.

In patients with hypogonadotropic hypogonadism, plasma FSH was 3.5 ± 1.9mIU/㎖, plasma LH 5.3 ± 2.8mIU/㎖ and plasma testosterone 0.9 ± 0.6ng/㎖,

6. The cause of hypergonadotropic hypogonadism was Klinefelter's syndrome in 5 cases, prepubertal traumatic bilateral anorchisms in 2 cases, postpubertal bilateral anorchisms for seminoma or torsion in 2 cases. Testicular atrophy was found in 3 cases, 2 cases having past history of mumps orchitis and 1 case having past history of trauma. In 3 cases, no etiology could be identified.

7. The cause of hypogonadotropic hypogonadism was a Kallamnn's syndrome in 4 cases. In two other cases, a pituitary lesion was suspected but could not be confirmed due to absence of pituitary hormone reserve function test. Two cases were identified as gonadotropin deficiency with growth hormone deficiency.

8. In patients with hypergonadotropic hypogonadism, androgen replacement therapy with a testosterone preparation was performed. After the treatment, improvement of male secondary sex characteristics such as hair growth, voice change ,enlargement

of penis size and scrotum size was noted.

Promotion and maintenance of sexual potency was also noted.

9. The patients with hypogonadotropic hypogonadism were treated with androgens, HCG or HCG and HMG. However, due to the short period of therapy and follow-up, no firm conclusions about treatment efficacy in this group can be drawn. Howeverl, the

best therapy to promote fertility should have been human chorionic gonadotropin combined with human menopausal gonadotropin.

In conclusion, it appears that long-term treatment with androgen preparation promotes sexual potency and improves male secondary sex characteristics in hypergonadotropic hypogonadism.

In addition, long-term treatment with human chorionic gonadotropin combined with human menopausal gonadotropin may provide an efficient means of treating paitients with hypogonadotropic hypogonadism to obtain potency and fertility.