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Physiopathology of spermatogenic arrest
1Département de Gynécologie et d'Obstétrique, Hôpital Cantonal Universitaire, Geneva, Switzerland.
Objective:
To review the world literature on the etiology, physiopathology, and treatment of spermatogenesis arrest.
Study Selection:
All the pertinent literature on spermatogenic arrest has been selected. Most studies related to this topic have been identified through Medline and through published literature.
Patients:
Spermatogenic arrest has been diagnosed by testicular biopsy in men of reproductive age who had either severe oligospermia (partial arrest) or azoospermia (complete arrest), normal testicular volume, and depending on the etiology normal, high, or low levels of gonadotropins.
Interventions:
The effects of heat, radiotherapy, and chemotherapy have been reported. Depending on the etiology of spermatogenic arrest, different hormonal treatments have been tested.
Main Outcome Measure:
Level of interruption of germ cell differentiation in testicular biopsy have been determined. Improvement of the sperm count or appearance of mature sperm after an hormonal treatment have been observed.
Results:
Spermatogenic arrest can occur at spermatogonial level in case of gonadotropin insufficiency or after germ cell damage due to chemotherapy or radiotherapy. The arrest is most frequently observed at primary spermatocyte level. Reversible arrest at that level can be due to heat, infections, hormonal and nutritional factors. Irreversible arrest at primary spermatocyte or spermatid level have a genetic origin due to chromosomes anomalies either in somatic cells or in germ cells.
Conclusions:
Spermatogenic arrest is usually due to genetic factors resulting in irreversible azoospermia. However some cases may be consecutive to hormonal, thermic, or toxic factors and may be reversible either spontaneously or after a specific treatment.