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Infertility in Males

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Male infertility affects millions of couples worldwide, arising from various factors that impact different stages of the reproductive process. An endocrine imbalance resulting from conditions like hypogonadism, Klinefelter syndrome, or pituitary disorders can disrupt hormone levels and reduce sperm production. Testicular defects, such as tumors, cryptorchidism, atrophic testes, abnormal sperm morphology, and low sperm count or motility, may arise due to genetic factors, structural...

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The Y Chromosome Determines Maleness

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Related Experiment Video

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Isolation of Sertoli Cells and Peritubular Cells from Rat Testes

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Published on: February 8, 2016

Testicular function in Klinefelter syndrome.

Anne M Wikström¹, Leo Dunkel

¹Hospital for Children and Adolescents, Helsinki University Central Hospital, University of Helsinki, Helsinki, Finland. anne.wikstrom@fimnet.fi

Hormone Research

|May 28, 2008

Summary

Klinefelter syndrome (KS), the most common genetic cause of male hypogonadism, typically presents after puberty. While early development is normal, midpuberty reveals hormonal imbalances, leading to androgen deficiency and potential infertility, though assisted reproductive technologies offer hope for fatherhood.

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Area of Science:

Endocrinology
Genetics
Reproductive Medicine

Background:

Klinefelter syndrome (47,XXY) is the leading genetic cause of male hypogonadism.
Phenotypic expression, particularly hormonal changes, becomes apparent after puberty.

Purpose of the Study:

To detail the progression of pituitary-gonadal dysfunction in individuals with Klinefelter syndrome.
To describe testicular histopathology in Klinefelter syndrome.
To highlight reproductive outcomes and therapeutic options for affected males.

Main Methods:

Analysis of pituitary-gonadal function markers (FSH, LH, inhibin B, testosterone) during different pubertal stages.
Review of testicular biopsy findings in prepubertal and adult males with Klinefelter syndrome.
Evaluation of reproductive outcomes using assisted reproductive technologies.

Main Results:

Prepubertal testicular histology shows normal cells but reduced germ cells; adult testes exhibit fibrosis and hyalinization.
From midpuberty, subjects show elevated FSH/LH, decreased inhibin B, and low-normal testosterone.
Testicular sperm extraction with ICSI enables non-mosaic Klinefelter syndrome males to achieve fatherhood.

Conclusions:

Klinefelter syndrome leads to progressive hypergonadotropic hypogonadism and varying androgen deficiency.
Testosterone replacement therapy is standard for managing symptoms.
Advanced reproductive techniques offer significant fertility options for affected individuals.