4.1. Age of the Population
In a study population of 628 patients, the mean age was 37.5 ± 9.28 years, and the predominant age group was 31 - 40 years at 43.31% of cases, followed by 41 - 50 years at 24.2% of cases. Studies conducted in Senegal by Diao et al. (2006), Niang et al. (2009), Faye et al. (2000), Diallo et al. (2015), and Kane (2021) had already found that the mean age of patients consulting for a spermogram was between 30 and 45 years [13]-[15][19][20]. Similarly, elsewhere—in Morocco with Kbirou et al. in 2021, in Algeria with Bouchelaghem in 2017, in the DRC with Kadima et al. in 2023, and in Niger with Halidou et al. in 2022—the mean age of patients was 37.5 years, 37.4 years and 36.39 years respectively, with a predominance of patients aged 30 - 39 years (35.9%) and 40 - 49 years (24.54%), and 34 years with patients aged 30 - 40 years most frequently observed [21]-[24]. This mean age could be explained by the psychological complex some men feel about their infertility and therefore about consulting. But it also reflects that infertility would concern an increasingly young population, since the most represented age group was 31 - 40 years, and it highlights the impact of the media and advances in communication about male infertility in recent years, which have convinced young men to consult early, as well as the fact that the desire to procreate generally arises at this age.
4.2. Sperm Parameters
Our results highlight an alteration of sperm parameters to varying degrees, in order of frequency: morphological abnormalities (49.04%), followed by vitality (46.18%), sperm concentration (42.99%) and motility (41.08%).
4.2.1. Volume
Normospermia in our study was observed in 81.6% of patients, while hypospermia was found in 14% of patients. These data are similar to those found in 2009 and 2015 in Senegal by Niang et al. and Diallo et al., with hypospermia of 11.9% and 10.5%, respectively [14][19]. This contrasts with the results of Diao et al. in 2006 in Senegal, Traore et al. in 2008 in Mali, and Kadima et al. in 2023 in the DRC, where high rates of hypospermia were recorded in 28%, 44% and 34.1% of patients, respectively, although semen volume remained normal in the majority of cases [13][23][25]. These results could be explained, on the one hand, by the variance in the semen analysis methods used—in our study, we used the WHO 2021 references, whereas some authors such as Diallo et al. used those of 2010, and Diao et al. as well as Traore et al. used the WHO 1999 human semen analysis standards. On the other hand, by a long abstinence period or by anatomical and functional impairments of the seminal glands and ducts in cases of hypospermia, since semen volume essentially reflects the secretory capacity of the seminal glands; and, having been unable to assay the biochemical markers, we unfortunately cannot give with precision the causes of the hypospermia. Although a downward trend in sperm parameters is currently demonstrated, this trend was not observed in our study regarding semen volume, which remained unchanged, as in Nigeria between 2010 and 2019 among infertile men [26].
4.2.2. Motility
Sperm motility is known to be an essential factor in male fertility. Infertile patients had asthenozoospermia, whether isolated or in association, in 41.08% of cases. This result is in line with those of Kadima et al., who found asthenozoospermia at 60%, and Diallo et al. in 2015, who found that 74.4% of patients had low motility. This contrasts with the studies conducted by Halidou et al. in 2022, which showed asthenozoospermia at 6.9%. This rate could be explained by the analyses performed by Kadima et al., who found semen infections in 20.5% of patients and sexually transmitted infections in 32.7% of patients, with a predominance of Staphylococcus aureus (39.9%) and Neisseria gonorrhoeae (20.9%); Diallo et al. found leucocytospermia in 57.8% of samples; likewise Schuppe et al. in Germany showed in 2017 that asymptomatic inflammations of the genital tract affecting the epididymis, as well as chronic prostatitis, were responsible for the reduction in progressive sperm motility [19][23][24][27]. Indeed, leucocytospermia in our study was present in 28.68% of cases.
4.2.3. Vitality
In this study, 46.18% of patients had necrozoospermia. These results are close to those of Diallo et al., who found a prevalence of 76.2% of necrozoospermia in a cohort of 262 patients, among whom 42.5% had varicoceles, 37.2% had urogenital infections and 17.7% had testicular trauma [19]. In our study, necrozoospermia was often associated with leucospermia, so the responsibility of urogenital infections is preponderant.
4.2.4. Concentration
Analysis of the various semen parameters showed that, with regard to concentration, the mean was 39.57 million spermatozoa/mL of semen. In more than a quarter of patients, oligozoospermia was found (26.11%), and azoospermia was estimated in 13.69% of patients. Our rates are lower than those of Diao et al. (2006), who found oligozoospermia at 46.5%—isolated in 10% of cases—and azoospermia in 23% of cases. Halidou et al. in Niger, for their part, found azoospermia in 50% of patients. These rates would be explained by the results obtained on semen culture, which were positive in 59.38% of patients in Niger and in 21.3% of patients in Senegal. Moreover, in the study conducted by Diallo et al. in 2015, azoospermia was estimated at 14.5% and urogenital infections accounted for 37.2% of cases. According to Schuppe et al. (2017), about 10% of men who have had acute epididymitis subsequently develop persistent azoospermia and 30% develop oligozoospermia. However, the disruption of spermatogenesis may be due to various factors, including exposure to vibration, emotional stress, and an increase in scrotal temperature during prolonged sitting [13][19][24][27][28]. Indeed, sperm concentration decreased by 40% for a 1˚C increase above the median (CI: 8% - 71%) [29], and two hours of driving would raise scrotal temperature by 2˚C [30]. Male infertility often has multiple causes, and infectious causes are among the most common; the infectious agents involved are most often bacterial or viral, which can lead to inflammation and increased oxidative stress, thereby altering semen analysis parameters and increasing sperm DNA fragmentation [31].
4.2.5. Morphology
Nearly half of the patients (49.04%) had teratozoospermia. Our rate is lower than that found in 2015 by Diallo et al., which was 80.9%. This variation in results would be explained, on the one hand, by the method used to assess sperm morphology. Indeed, in 2015, Diallo et al. morphology was assessed according in David scale where the percentage of normal forms was 32% or more (WHO, 2010 guidelines), whereas in our study, the percentage of the normal forms was 4% or more Kruger criteria (WHO, 2021 guidelines). On the other hand, intra-individual, inter-individual and inter-laboratory variation exists in the assessment of sperm morphology [19][32][33].
4.2.6. Cytospermiological Profile
The cytospermiological profile of the abnormalities showed a predominance of oligo-astheno-terato-necrozoospermia (18.15%), followed by azoospermia (13.69%), astheno-terato-necrozoospermia (9.4%) and astheno-necrozoospermia (5.73%). This profile is similar to that found by Diallo et al. (2015). Furthermore, abnormalities associated with necrozoospermia and/or teratozoospermia were dominant and associated with leucocytospermia. This profile reflects the frequency of urogenital infections in our countries [19].
4.3. Influence of Age on Sperm Parameters
Several factors are responsible for sperm alterations. A study carried out in India by Kumar et al. (2017) found that age had a negative effect on semen volume, motility and sperm morphology, but had no effect on sperm concentration [34]. These results are close to those observed in our study, where a negative correlation is found between age and vitality, but also between age and sperm concentration. Other authors, however, find a significant effect of age on ejaculate volume in South Africa, and a moderate negative correlation of age on morphology and progressive motility in the semen of Nigerian and South African patients [26].
Patients over 35 years of age show a late impairment of semen volume and morphology, and an early impairment of motility, concentration and vitality. Count, motility and morphology were also decreased in the study by Kumar et al. (2017) [34]. Although maternal aging contributes significantly to human infertility and men continue to produce spermatozoa even at an advanced age, paternal age may also contribute to human infertility [35]. Thus, advanced paternal age has been implicated in an increased frequency of miscarriages, autosomal dominant disorders, aneuploidies and other diseases [36][37]. It has also been associated with an increase in the prevalence of genomic and epigenomic abnormalities, which would explain infertility in patients with no alteration of sperm parameters and the failure rate of assisted reproduction measures in these patients [38]-[40]. The early impairment of motility, concentration and vitality leads us to suppose that other associated factors, not explored in our study, may be involved in the deterioration of male fertility in Africa (genital infections, exposure to pesticides and heavy metals, tobacco and alcohol consumption, etc.), and to recognize the increase in the infertility rate in our regions.