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Main Authors: Osimiri-Eugene, C., Ikaraoha, C. I., Nwadike, C., Nnodim, J.
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Published: Zenodo 2025
Online Access:https://doi.org/10.5281/zenodo.17528455
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author Osimiri-Eugene, C.
Ikaraoha, C. I.
Nwadike, C.
Nnodim, J.
author_facet Osimiri-Eugene, C.
Ikaraoha, C. I.
Nwadike, C.
Nnodim, J.
contents <p><span>This study thoroughly assessed the semen profile of male infertile individuals and specific subgroups exhibiting defined sperm abnormalities; oligospermia, asthenozoospermia, asthenoteratozoospermia,oligoasthenozoospermia, oligoasthenoteratozoospermia (OAT), and azoospermia—relative to normozoospermic controls, to clarify the extent of spermatogenic dysfunction and its clinical ramifications. A total of 72 male infertile individuals and 72 age-matched controls were evaluated for total sperm count (TSC), progressive motility, total motility, and morphology utilising standard semen analysis techniques.The results showed that the quality of semen was much lower in male subjects who were infertile than in controls. The progressive motility was 14.76 ± 9.46% vs. 55.75 ± 8.68%, the total motility was 19.75 ± 12.91% vs. 65.75 ± 8.68%, the morphology was 4.86 ± 4.66% vs. 56.80 ± 9.35%, and the TSC was 25.84 ± 15.68 × 10⁶ vs. 66.91 ± 5.12 × 10⁶ sperm cells/ejaculate (p = 0.001). Subgroup studies revealed a steady decline in semen parameters throughout the various clinical groups.Men with oligospermia had significantly reduced total sperm count (TSC) (25.66 ± 3.44 × 10⁶), progressive motility (24.66 ± 3.55%), and morphology (6.33 ± 1.77%) compared to controls (p = 0.001). Individuals with asthenozoospermia and asthenoteratozoospermia demonstrated similar reductions in sperm motility and morphology, with values of 5.00 ± 0.73% and 2.75 ± 0.45%, respectively (p = 0.001). Individuals with oligoasthenozoospermia had significant deficiencies across many metrics, with total sperm count (TSC) at 23.91 ± 6.52 × 10⁶, progressive motility at 13.66 ± 6.80%, and morphology at 12.58 ± 5.66% (p = 0.001). The OAT group exhibited the most significant multiparameter deficits among the non-azoospermic cohorts (TSC = 18.00 ± 1.04 × 10⁶; progressive motility = 11.50 ± 2.61%; morphology = 2.50 ± 0.52%; p = 0.001), indicating severe combined quantitative, motility, and structural problems. Azoospermic men showed no sperm cells, motility, or morphology , which means that spermatogenesis completely failed. There were statistically significant differences (p < 0.05) between all infertile subgroups and controls. In general, these results show a distinct range of spermatogenic failure, from partial impairment in oligospermia to total absence of spermatozoa in azoospermia. All of these diseases make it very hard to get pregnant naturally, however men with oligospermia and OAT still have some fertility potential that can be used clinically through assisted reproductive technologies. The study emphasises the diagnostic and predictive significance of complete semen analysis as a fundamental component in the evaluation and treatment of male infertility</span> </p>
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publisher Zenodo
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spellingShingle Pattern of some sperm profiles in infertile male subjects in Owerri
Osimiri-Eugene, C.
Ikaraoha, C. I.
Nwadike, C.
Nnodim, J.
<p><span>This study thoroughly assessed the semen profile of male infertile individuals and specific subgroups exhibiting defined sperm abnormalities; oligospermia, asthenozoospermia, asthenoteratozoospermia,oligoasthenozoospermia, oligoasthenoteratozoospermia (OAT), and azoospermia—relative to normozoospermic controls, to clarify the extent of spermatogenic dysfunction and its clinical ramifications. A total of 72 male infertile individuals and 72 age-matched controls were evaluated for total sperm count (TSC), progressive motility, total motility, and morphology utilising standard semen analysis techniques.The results showed that the quality of semen was much lower in male subjects who were infertile than in controls. The progressive motility was 14.76 ± 9.46% vs. 55.75 ± 8.68%, the total motility was 19.75 ± 12.91% vs. 65.75 ± 8.68%, the morphology was 4.86 ± 4.66% vs. 56.80 ± 9.35%, and the TSC was 25.84 ± 15.68 × 10⁶ vs. 66.91 ± 5.12 × 10⁶ sperm cells/ejaculate (p = 0.001). Subgroup studies revealed a steady decline in semen parameters throughout the various clinical groups.Men with oligospermia had significantly reduced total sperm count (TSC) (25.66 ± 3.44 × 10⁶), progressive motility (24.66 ± 3.55%), and morphology (6.33 ± 1.77%) compared to controls (p = 0.001). Individuals with asthenozoospermia and asthenoteratozoospermia demonstrated similar reductions in sperm motility and morphology, with values of 5.00 ± 0.73% and 2.75 ± 0.45%, respectively (p = 0.001). Individuals with oligoasthenozoospermia had significant deficiencies across many metrics, with total sperm count (TSC) at 23.91 ± 6.52 × 10⁶, progressive motility at 13.66 ± 6.80%, and morphology at 12.58 ± 5.66% (p = 0.001). The OAT group exhibited the most significant multiparameter deficits among the non-azoospermic cohorts (TSC = 18.00 ± 1.04 × 10⁶; progressive motility = 11.50 ± 2.61%; morphology = 2.50 ± 0.52%; p = 0.001), indicating severe combined quantitative, motility, and structural problems. Azoospermic men showed no sperm cells, motility, or morphology , which means that spermatogenesis completely failed. There were statistically significant differences (p < 0.05) between all infertile subgroups and controls. In general, these results show a distinct range of spermatogenic failure, from partial impairment in oligospermia to total absence of spermatozoa in azoospermia. All of these diseases make it very hard to get pregnant naturally, however men with oligospermia and OAT still have some fertility potential that can be used clinically through assisted reproductive technologies. The study emphasises the diagnostic and predictive significance of complete semen analysis as a fundamental component in the evaluation and treatment of male infertility</span> </p>
title Pattern of some sperm profiles in infertile male subjects in Owerri
url https://doi.org/10.5281/zenodo.17528455