Mohsin K. AL-Murshidi
University of Kufa, Faculty of Science, Department of Biology, Najaf-Iraq
*Corresponding Author E-mail: Mohsin.almurshidi@uokufa.edu.iq
ABSTRACT:
Aim: To investigate the relationship between semen volume and serum follicle — stimulating hormone (FSH), Luteinizing hormone (LH), testosterone (T), and prolactin (PRL) in azoospermic infertile patients.
Methods: Serum FSH, LH, testosterone and prolactin levels of 25 male infertile azoospermic patients were assayed by radioimmunoassay (RIA) and their data was analyzed for significant correlation with the same parameters of 25 control cases.
Results: 25 infertile patients had azoospermic. The values of serum FSH, LH, and prolactin were significantly raised (P < 0.05) while the serum testosterone significantly lower (P < 0.05). The semen volume in the azoospermic patients was negative strongly correlated to serum FSH, LH and serum prolactin. FSH (r = 0.93), LH (r = 0.95) prolactin (r = 93).
The semen volume was positive strongly correlated to serum testosterone (r = 0.90). Conclusion: high levels of serum FSH, LH, prolactin and low levels of serum testosterone can cause infertility by azoospermic directly.
KEYWORDS: Semen volume, FSH, LH, Prolactin, Azoospermia.
INTRODUCTION:
Azoospermia, defined as complete absence of sperm from the ejaculate, is present in about 1% of all, men (1, 2) and in approximately 15% of infertile men (2). Azoospermia is different from aspermia, in that aspermia is the complete absence of seminal fluid emission upon ejaculation (3).
Azoospermia can be categorized as either: pre — testicular azoospermia (2% of men with azoospermia, due to a hypothalamic or pituitary abnormality diagnosed with hypogonadism), testicular failure or non—obstructive azoospermia (49% to 93%) this term indicate acomplete absence of spermatogenesis and post — testicular obstruction or retrograde ejaculation ( 7% to 51% ) (1, 2).
The causes of azoospermia such as of spermatogenesis and obstruction of ductal system particularly the vas deferens. (4, 5).
Normal semen volume : 1.5 to 5 ml, the semen volume is calculated abnormal when it is less than 1.5 ml (3) when vassal agenesis and testicular atrophy are not present, semen volume and serum FSH are key factors in determining the etiology of the azoospermia (6). Azoospermic patients with low semen volume and normal sized testes may have ejaculatory dysfunction or ejaculatory obstruction (7).
Various hormones have their role which affect the spermatogenesis. Testosterone secreted by leydig cells in testis is essential for growth and division of germinal cells in forming spermatozoa (8). Luteinizing hormone (LH) secreted by anterior pituitary gland stimulates the leydig cells to secreted testosterone. Follicle stimulating hormone (FSH) secreted by anterior pituitary gland, stimulate spermatide to spermatozoa will not accure (9). The successful and completely. Male germ cell development is dependent on the balanced endocrine interplay of hypothalamus pituitary and the testis. Gonadotropin releasing hormone (GnRH) secreted by the hypothalamus elicits the release of gonadotrophins i.e, follicle stimulating hormone (FSH) and luteinizing: hormone (LH) from the pituitary gland (10). FSH binds with receptors in the sertoli cells and stimulates spermatogenesis while LH stimulates the production of testosterone in leydig cells, which in turn may act on the sertoli and peritubular cells of the seminiferous tubules and stimulates spermatogenesis (11). The failure of pituitary to secret FSH and LH will result in disruption of testicular function Leading to infertility. Testosterone estradiol and inhibit control the secretion of gonadotrophins through feedback mechanism (12). Absences or decrease in sperm density, eventually leading to azoospermia, has been found to be associated with raised FSH, LH, prolactin and normal or low testosterone level (13). Prolactin also plays a direct role in spermatogenesis and steroidogenesis as prolactin receptors have been detected in sertoli cells and leydig cells in testes (14,15). Higher serum levels of prolactin proving a role in gametogenesis that is independent of gonadotropins (16).
MATERIAL AND METHODS:
This study was carried out in the center of fertility in Najaf city. A total number of 50 males were included in these study 25 healthy males and 25 azoospermic infertile males. All semen samples were obtained by masturbation after 3 days of sexual abstinence. Semen analysis was don for semen volume was measured in a graduated tube according to WHO criteria (8). Serum FSH, LH, prolactin and serum testosterone levels were estimated by radioimmunoassay (RIA) Mean and standard error (SE) of each variable in the control and test group was calculated. Student's ((t)) test was applied to compare the results of the control and test group. Difference of results was considered as significant for P < 0.05. Correlation coefficients were used to determine correlation between semen volume and serum FSH, LH, prolactin and serum testosterone levels.
RESULTS:
We found twenty five cases of azoospermia. The mean ±SE semen volume and the mean ± SE serum FSH, LH, prolactin and serum testosterone in the 25 azoospermic infertile patients and control are presented in table 1 and 2. The mean semen volume was 1.526 ± 0.11 in azoospermic infertile males and the mean FSH, LH, prolactin and testosterone in azoospermic infertile males were 21.53 ± 3.11, 22.22 ± 4.21, 21.66 ± 3.23 and 1.98 ± 0.13 respectively, where as in controls, the mean ± SE semen volume, FSH, LH, prolactin and testosterone levels were 4.24 ± 0.81, 6.88 ± 0.91, 5.7 ± 0.89, 7.26 ± 0.96 and 4.2 ± 0.61 respectively. In the table 1 FSH, LH, and prolactin levels showed significant increase (P < 0.05) in azoospermic infertile males compared to the control group. The mean testosterone level in azoospermic infertile males were significant decrease (P < 0.05) compared to control group.
There was a negative strong correlation (r = 0.93, 0.95 and 0.93) (P < 0.05) respectively between semen volume and serum FSH, LH and serum prolactine. While was a positive strong correlation (r = 0.90, p < 0.05) between semen volume and serum testosterone (Table 2).
Table 1: Comparison of semen volume, serum FSH, serum LH, serum prolactin and serum testosterone levels in the control and azoospermia group.
|
Variable |
Control group n = 25 |
Azoospermia group n = 25 |
P value |
|
Semen volume (ml) |
4.24 ± 0.81 |
1.526 ± 0.11 |
< 0.05* |
|
FSH (NHU/m1) |
6.88 ± 0.91 |
21.53 ± 3.11 |
< 0.05* |
|
LH (MIU/m1) 5.7 ± 0.89 |
|
22.22 ± 4.21 |
< 0.05* |
|
Prolactin (MEJ/m1) |
7.16 ± 0.96 |
21.66 ± 3.33 |
< 0.05* |
|
Testosterone (ng/ml) |
4.2 ± 0.61 |
1.98 ± 0.13 |
< 0.05* |
* significant < 0.05
Table 2: Correlation of semen volume with serum FSH, LH, porolactin and serum testosterone levels
|
Variable |
Control group |
n = 25 |
Azoospermia group (n = 25) |
|
|
R vale |
P value |
R vale |
P value |
|
|
Semen volume vs. serum FSH |
0.11 |
> 0.05 |
0.93 |
< 0.05* |
|
Semen volume vs. serum LH |
0.15 |
> 0.05 |
0.95 |
< 0.05* |
|
Semen volume vs. serum prolactin |
0.21 |
> 0.05 |
0.93 |
< 0.05* |
|
Semen volume vs. serum testosterone |
0.09 |
> 0.05 |
0.90 |
< 0.05* |
* significant < 0.05
Non-significant > 0.05
The azoospermic patients in this study present with low volume ejaculate. Ejaculatory duct dysfunction may be due to either failure of emission or retrograde ejaculation. Retrograde ejaculation present with low ejaculate volume (17). The secretions of the bulbo — urethral gland, which normally comprise a small part of normal semen, may be ejaculated in an antegrade manner separate from the rest of the ejaculate so that the patient may notice small semen which shows azoospermia (18). Ejaculatory dysfunction may vary from one clinic to other, retrograde ejaculation in 18% of men with azoospermia was reported (19). There is a general consensus that defective spermatogenesis and genital tract obstruction are the main causes of azoospermia.
In the present study, gondotropin FSH, LH, and prolactin levels were significantly (p<0.05) elevated in azoospermia males when compared with the levels in proven fertile controls, and the results showed negative strong correlation between semen volume and serum FSH, LH and serum prolactin. While the testosterone levels significantly (p<0.05) decrease in azoospermic males and appositive strong correlation between semen volume and serum testosterone.
FSH, LH and testosterone evaluation is useful in the management of male infertility (20). For initiation of spermatogenesis and maturation of spermatozoa, FSH is necessary. In the infertile men, higher concentration of FSH is considered to be a reliable indicator of germinal epithelial damage (21), whereas LH stimulates spermatogenesis indirectly via testosterone (22). The measurement of FSH in serum may used with advantage in the diagnosis of spermatogenic dysfunction also to differentiate between secretary and excretory azoospermia (23). In various studies elevated levels of LH in azoospermic males when compared to normal fertile men, were also documented which matches our findings (24).
Prolactin also plays a direct role in spermatogenesis and steroidogensis as prolactin receptors have been detected in sertoli cells and leydig cells in testes (25). This produces primary hypogonadism (low testosterone and high FSH, LH levels). Elevated levels of prolaction is usually cause by hyperscretion from lactotrophes in interior pituitary (26). Higher serum levels of gonadotropins show relatively higher serum levels of prolactin which lead to low semen volume ejaculate in azoospermia (27). The role of prolactin in gametogenesis that is independent of gonadotropins (28).
The suppression of testosterone secretion in infertile men could be due to deficiency of hypothalamic GnRH, result on in the impairment of Gonadotropin secretion from pituitary. The deficiency of LH and FSH prevents the gonads from either producing sperm or sufficient quality of testosterone (29). Where decreased level of testosterone was observed in infertile males (30), as sometimes there is a loss of germinal epithelium but leydig cells of testes remain intact (31).
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Received on 06.12.2017 Modified on 27.01.2018
Accepted on 06.03.2018 © RJPT All right reserved
Research J. Pharm. and Tech. 2018; 11(3): 1169-1171.
DOI: 10.5958/0974-360X.2018.00218.4