Clinical Investigation of Male Hypogonadism.
- Author:
Jae Yup HONG
1
;
Moo Sang LEE
Author Information
1. Department of Urology, Yonsei University, College of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
male hypogonadism
- MeSH:
Adolescent;
Atrophy;
Chorionic Gonadotropin;
Cryptorchidism;
Fertility;
Follow-Up Studies;
Gonadotropins;
Growth Hormone;
Gynecomastia;
Hair;
Humans;
Hypogonadism*;
Intellectual Disability;
Kallmann Syndrome;
Klinefelter Syndrome;
Male*;
Mumps;
Olfaction Disorders;
Orchitis;
Penis;
Prolactin;
Puberty;
Scrotum;
Seminoma;
Sex Characteristics;
Sexual Maturation;
Spermatogenesis;
Testosterone;
Treatment Outcome;
Urology;
Voice
- From:Korean Journal of Urology
1983;24(4):653-660
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Male hypogonadism refers to decrease in Leydig cell function, diminished or absent spermatogenesis, or both 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 hypergonadotrophic hypogonadism (eunuch group), testicular volume was 2.5 +/- 0.8 ml. In patients with hypogonadotrophic hypogonadism (eunuchoid group), testicular volume was 2.4 +/- 1.8ml. 4. In patients with hypergonadotrophic hypogonadism, penile length was 4.4 +/- 1.2cm. In patients with hypogonadotrophic hypogonadism, penile length was 2.8 +/- 1.4cm. 5. In patients with hypergonadotrophic hypogonadism, serum FSH was 62.4 +/- 20.5mlU/ml, serum LH 65.0 +/- 23.6mlU/ml, serum testosterone 1.6 +/- 1.4ng/ml and serum prolactin 10.2 +/- 4.2ng/ml. In patients with hypogonadotrophic hypogonadism, serum FSH was 3.5 +/- l.9mlU/ml, serum LH 5.3 +/- 2.8mlU/ml and serum testosterone 0.9 +/- 0.6ng/ml. 6. The cause of hypergonadotrophic 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 causes of hypogonadotrophic hypogonadism was a kallmann'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 hypergonadotrophic 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 hypogonadotrophic hypogonadism were treated with androgen, 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. However, 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 hypergonadotrophic hypogonadism. In addition, long-term treatment with human chorionic gonadotropin combined with human menopausal gonadotropin may provide an efficient means of treating patients with hypogonadotrophic hypogonadism to obtain potency and fertility.
