|Year : 2017 | Volume
| Issue : 1 | Page : 6-10
Reproductive hormonal profile patterns among male partners of infertile couples at the University of Ilorin teaching hospital
Waliu Olatunbosun Oladosu1, Sikiru Abayomi Biliaminu2, Ishola Musbau Abdulazeez2, Gbagirimojo Ganiyu Aliyu2, Ademola Adelekan2, Adekunle Bashiru Okesina2
1 Department of Pathology, Federal Medical Centre, Abeokuta, Ogun State, Nigeria
2 Department of Chemical Pathology, University of Ilorin, Nigeria
|Date of Web Publication||10-Sep-2018|
Waliu Olatunbosun Oladosu
Department of Chemical Pathology, Federal Medical Centre, Idi-Aba, Abeokuta, Ogun State
Source of Support: None, Conflict of Interest: None
Background: Seminal fluid analysis (SFA) is the most important investigation of the infertile males but limited in revealing the etiologies of the various spermatozoa abnormalities observed on microscopy. Increasing prevalence of male infertility and the challenges of diagnosis require biochemical investigations such as reproductive hormonal profile. Aims: The aim of this study is to determine the reproductive hormonal profile patterns among infertile males in Ilorin. Settings and Design: This was a descriptive, cross-sectional study. Materials and Methods: A total of 130 male partners of infertile couples served as subjects and 50 fertile males as controls. Serum reproductive hormonal assay was done using ELISA method. Statistical Analysis Used: Statistical Package for the Social Sciences (SPSS) version 20.0 (SPSS Inc., Chicago, IL, USA) was used. Normally distributed data were expressed as mean ± standard deviation. Results: The mean age of the subjects who were majorly civil servants was 38.6 ± 6.6 years. The prevalence of reproductive endocrinopathies in this study was 46.9%. Mean serum concentrations of follicle-stimulating hormone, luteinizing hormone, and prolactin were elevated in our subjects than control. Mean serum testosterone concentration was significantly lower in our infertile subjects. Patterns of hormonal profile abnormalities among our subjects were 2 (1.5%) with hypogonadotropic hypogonadism, 15 (11.5%) with hypergonadotropic hypogonadism, 23 (17.7%) with hypergonadotropic normogonadism, 21 (16.2%) with normogonadotropic hypogonadism, and 69 (53.1%) with normogonadotropic normogonadism. This showed 59 (45.4%) subjects with primary testicular failure/resistance and 2 (1.5%) with secondary testicular failure. Twenty (15.4%) of the subjects had hyperprolactinemia. Conclusions: Reproductive hormonal profiling of male partners of infertile couples is an important adjuvant to SFA, in diagnosis and monitoring responses to treatment.
Keywords: Male infertility, patterns, reproductive hormones
|How to cite this article:|
Oladosu WO, Biliaminu SA, Abdulazeez IM, Aliyu GG, Adelekan A, Okesina AB. Reproductive hormonal profile patterns among male partners of infertile couples at the University of Ilorin teaching hospital. Afr J Infertil Assist Concept 2017;2:6-10
|How to cite this URL:|
Oladosu WO, Biliaminu SA, Abdulazeez IM, Aliyu GG, Adelekan A, Okesina AB. Reproductive hormonal profile patterns among male partners of infertile couples at the University of Ilorin teaching hospital. Afr J Infertil Assist Concept [serial online] 2017 [cited 2020 Aug 8];2:6-10. Available from: http://www.afrijiac.org/text.asp?2017/2/1/6/241010
| Introduction|| |
Male fertility abnormalities are diagnosed by physical examination, evaluation of endocrine parameters, and semen fluid analysis (SFA). Majority of the structural defects in SFA can be attributable to reproductive endocrine disorders.,
A normal functioning reproductive endocrine system is a prerequisite for normal male fertility. Reproductive hormonal profiling of infertile patients is not only an important diagnostic tool for evaluation but can also explain the body's pattern of compensatory response in nonhormonal causes of male infertility.
10%–15% of couples are considered infertile, and male causes of infertility account for 40%–50% of infertility among couples. Furthermore, male infertility occurs in approximately 7% of all men. Male infertility is commonly due to defective semen quality and quantity. The majority of the studies on infertility focused more on female infertility with little attention on male infertility, more so in the developing countries, including Nigeria. This study seeks to assess the patterns of reproductive endocrine disorders among infertile males.
| Materials and Methods|| |
The study was conducted at the Departments of Chemical Pathology and Immunology, University of Ilorin Teaching Hospital (UITH), Ilorin, Kwara State, North-Central Nigeria. The hospital receives referrals of infertile male patients from Kwara State and other neighboring states. The Hospital has a General Outpatient Department (GOPD) which serves as a referral point for infertile couples, Specialist Gynaecological and Urology Clinics attending to female and male infertility cases, respectively, as well as an Assisted Reproductive Technology Unit. The Department of Microbiology receives request for SFA of about 400/year from Gynaecology, Urology, and GOPD Clinics in the hospital as part of evaluation of infertile couples.
The study population included male partners of infertile couples who were referred for reproductive hormonal assay from the above-mentioned clinics.
This was a descriptive, cross-sectional study of consecutive male partners of infertile couples. The study was conducted using the convenient recruitment method. One hundred and thirty male partners of infertile couples were selected as research subjects and 50 fertile participants served as control.
Recruitment into the study was preceded by obtaining informed consent from all participants. The process was repeated for consecutive patients until the required sample size was achieved.
Included in this study were consenting male partners of infertile couples presenting at UITH for management while controls were volunteering, age-matched males of fertile couples. Subjects on hormonal therapy were excluded from this study. Written consent for inclusion into the study was obtained after explanation of the study and the procedure before samples were taken from the patients.
Blood samples were drawn from patients after 10–12 h overnight fasting. Samples were allowed to clot for 2 h at room temperature before centrifugation for 15 min at 1000 ×g. The supernatant (serum) was collected and stored at −20°C to avoid the loss of bioactivity and contamination.
Reproductive hormones (follicle-stimulating hormone [FSH], luteinizing hormone [LH], prolactin, and testosterone) were assayed using Accubind ELISA kits. Calibration curves were generated using the absorbances obtained for the calibrators against their concentrations. Concentrations of the subjects' serum hormone levels were generated from their absorbances read-off the calibration curves.
Clearance was obtained from the ethical committee of the UITH for the study.
Statistical analysis was done with the Statistical Package for the Social Sciences (SPSS) version 20.0 (IBM, Armonk, NY, United States of America). Normally distributed data were expressed as mean ± standard deviation, while nonnormally distributed data were expressed as median and interquartile range or transformed logarithmically, and categorical variables were reported as percentages.
Reference intervals of reproductive hormones in males
- Testosterone 2.5–10.0 ng/ml
- Prolactin 1.8–17.0 ng/ml
- FSH 1.0–14.0 mIU/ml
- LH 0.7–7.4 mIU/ml.
| Results|| |
A total of 180 participants, comprising 130 male partners of infertile couples and 50 age-matched fertile males, were recruited for this study. The mean age of the subjects was 38.6 ± 6.6 years, while the mean age of controls was 37.0 ± 5.8 years. The subjects and controls were mainly within the age group 31–40 years, comprising 73 (56.2%) and 28 (56.0%), respectively [Figure 1].
|Figure 1: Age group distribution among male partners of infertile couples and controls |
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The subjects and controls were mainly civil servants consisting of 63 (48.5%) and 28 (56%) of male partners of infertile couples and fertile controls, respectively [Figure 2].
|Figure 2: Frequencies of occupation among male partners of infertile couples and controls|
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Mean serum levels of reproductive hormones among fertile males and male partners of infertile couples
[Table 1] shows a comparison of reproductive hormones in fertile males and male partners of infertile couples. The mean serum concentration of FSH was significantly higher among male partners of infertile couples compared to fertile males (17.8 ± 2.2 mIU/ml vs. 5.2 ± 3.3 mIU/ml; P< 0.001). LH was similarly significantly higher among male partners of infertile couples compared to controls (8.8 ± 7.6 mIU/ml vs. 5.0 ± 3.1 mIU/ml). However, mean testosterone level was significantly lower among male partners of infertile couples compared to controls (5.3 ± 4.1 ng/ml vs. 8.9 ± 3.7 ng/ml; P< 0.001).
|Table 1: Mean serum reproductive hormones levels among male partners of infertile couples and controls using Mann-Whitney U-test|
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The mean serum prolactin was higher among male partners of infertile couples than controls but not statistically significant (10.2 ± 9.9 ng/ml vs. 8.3 ± 4.8 ng/ml; P> 0.05).
The distribution of serum reproductive hormones in subjects and controls are shown in the [Table 2]. The prevalence of hyperprolactinemia was 15.4% in subjects compared to 2% in controls.
|Table 2: Serum reproductive hormones distribution among subjects and controls using Chi-square test|
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Frequencies of reproductive endocrinopathies among subjects
As shown in [Figure 3], 61 (46.9%) of the 130 subjects had one or more abnormal biochemical patterns of reproductive hormonal profile, consisting of 2 (1.5%) with hypogonadotropic hypogonadism (hh), 15 (11.5%) with hypergonadotropic hypogonadism (Hh), 21 (16.2%) with normogonadotropic hypogonadism (Nh), and 23 (17.7%) with hypergonadotropic normogonadism (HN). While 69 (53.1%) of the subjects had normogonadotropic normogonadism, all the 50 (100%) controls had normogonadotropic normogonadism.
|Figure 3: Patterns of reproductive endocrinopathies among male partners of infertile couples|
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| Discussion|| |
Reproductive hormonal abnormalities are important causes of male infertility. 61 (46.9%) of subjects in this study have abnormal hormonal profile patterns. This is similar to a study by Emokpae et al., where 40% prevalence of hormonal abnormalities was found among male partners of infertile couples but significantly lower than 80.1% found by Ozoemena et al. in Kano, Northwest Nigeria, and Enugu, Southeast Nigeria, respectively. The observed differences may be due mainly to differences in inclusion criteria for subjects and controls selection in the various studies. The study by Emokpae et al. involved azoospermic men only while the study by Ozoemena et al. was among clinically diagnosed infertile males.
Hypothalamo–pituitary–gonadal axis is central to the development, functioning, and regulation of the reproductive system in human. Male factors infertility of endocrinological origin can manifest as various patterns of hormonal imbalance that can be obtained by carrying out hormonal profiling of patients.
The mean serum concentrations of FSH and LH among male partners of infertile couples in this study were significantly higher than in controls (P<0.05), while the mean serum testosterone concentration was lower among the controls compared with male partners of infertile couples with statistically significant difference (P<0.001). These findings of significantly elevated mean serum gonadotropins (FSH and LH) and reduced mean serum testosterone level in infertile subjects compared to the control group in this study, which is consistent with the findings in previous studies by Emokpae et al., Uhuonrenren et al., and Jurasovićet al. Studies by Babu et al., DhananjayandRoshan, and Olooto et al. also found significantly elevated gonadotropins among male partners of infertile couples compared to normal control, but no significant mean difference between serum testosterone levels in the two groups was observed. The finding of insignificant difference in the mean serum testosterone levels of controls and male partners of infertile couples in those studies may be due to testicular damage not involving the Leydig cells, responsible for androgen synthesis or compensatory androgen synthesis from extragonadal sources.
Thirty-eight (29.2%) subjects had hypergonadotrophism comprising 15 (11.5%) with Hh and 23 (17.7%) with HN, suggesting primary testicular failure and resistance, respectively. 21 (16.2%) of subjects show Nh, showing a transient stage preceding primary testicular failure. There is therefore a total of 59 (45.4%) subjects with biochemical features of primary testicular failure/resistance (Hh, HN and Nh). This is similar to a study by Geidam et al. and Ozoemena et al., where 41.7% and 54.3% of male partners of infertile couples, respectively, had biochemical feature of primary testicular failure. This finding is significant because it suggests damage to the seminiferous tubules and/or the Leydig cells. Sperm retrieval and in vitro fertilization using intracytoplasmic sperm injection may be successful in these patients. Yaman et al. found significantly elevated serum gonadotropin among infertile males with histologic diagnosis of Sertoli cell-only syndrome, where germinal cells are absent and patients are azoospermic. The observed increases in the FSH and LH levels were attempt to stimulate the Sertoli and Leydig cells, respectively, for proportionate synthesis and secretion of testosterone to enhance spermatogenesis. The increase in serum FSH level among male partners of infertile couples may reflect decreased testicular activity, resulting in changes in normal feedback mechanism between the testes and the hypothalamic–pituitary axis. It must be noted however that serum level of gonadotropins within reference interval does indicate normal spermatogenesis in all cases.
In this study, 2 (1.5%) of the subjects had hh, which is biochemically suggestive of secondary testicular failure. This is slightly lower than 4.2% of cases reported in a similar study by Geidam et al. hh is an androgen insufficiency/deficiency of hypothalamic or pituitary origin. It is a deficiency of gonadotropins required to support adequate testosterone synthesis. Important causes of hh such as obesity, type 2 diabetes mellitus, AIDS, and chronic renal failure  are common diseases with increasing prevalence, which can cause suppression of FSH and LH and consequently reduce testosterone synthesis.
Twenty (15.4%) of our subjects have hyperprolactinemia compared to 1 (2%) of controls. This similar to 11% obtained by Masud et al. and 12.2% by Soler Fernández etal. but lower than 5.1% by Ozoemena et al. Hyperprolactinemia is a relatively common and treatable cause of male infertility. Hyperprolactinemia impact negatively on spermatogenesis and steroidogenesis by acting directly on prolactin receptors present in Sertoli cells More Details and Leydig cells in testes and produces primary hypogonadism or causes secondary hypogonadism by disrupting pulsatile release of gonadotropins. De Rosa et al. observed that symptoms directly related to hypogonadism are prevalent among men with hyperprolactinemia and these include impaired libido, erectile dysfunction, diminished ejaculate volume, and oligospermia. They found 16% of hyperprolactinemic patients with erectile dysfunction and about 11% of men with oligospermia. Seminal fluid abnormalities rapidly improve with cabergoline treatment to reduce serum prolactin levels, while other dopaminergic compounds require longer periods of treatment.
| Conclusions|| |
This study showed various biochemical patterns of reproductive hormone abnormalities and their relative proportions and prevalence in our patients. It also showed that reproductive hormonal disorders are relatively common and important in etiopathogenesis of male infertility. It is therefore suggested that reproductive hormonal profile should be incorporated into the routine evaluation of male partners of infertile couples.
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Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3]
[Table 1], [Table 2]